Lauric acid and its easters studies

Lauric acid and its easters studies

Enhancer of transdermal delivery and lipophilicity of hydrophillic compound like EGCG, cinnamic, caffeic acids, ascorbic acid, genistein.

antimicrobial~s.aureus 0.1% glyceryl laurate

anti-inflammation

small molecular, readily absorbed by skin

The MCT fatty acids from coconut oil converts to starage tryglycerides by enzyme DGAT1 (expressed in liver and instestine)

　

What is the difference between palm oil and palm kernel oil?

They both come from palm trees, but there the similarity ends. Palm oil comes from the palm fruit, while palm kernel oil is extracted from the palm seed. And while over 80 percent of the fat in palm kernel oil is saturated, only 50 percent of palm oil is, making it easier on arteries. Palm oil's reddish or golden color is a clue that it also contains a fair amount of heart-healthy carotenoids. Some research even suggests that the fatty acids in palm oil don't raise cholesterol the way saturated fats traditionally do.

Palm Oil vs. Palm Kernel Oil | EatingWell
https://www.eatingwell.com/article/290687/palm-oil-vs-palm-kernel-oil/

　

Journal of Animal Science and Biotechnology volume 11, Article number: 89 (2020)
Development of an in vitro macrophage screening system on the immunomodulating effects of feed components

Department of Animal Sciences and Industry, Kansas State University, Manhattan, 66506, USA

Background
While feed components capable of modulating the immune system are highly sought after and marketed, often little evidence is available to support functional immune response claims. Thus, a high-throughput in vitro cell screening system was developed to test these compounds for innate immune signaling effects, using Saccharomyces cerevisiae and its cell wall components in addition to lauric acid and its esters as models in two separate experiments. This screening system utilized RAW 264.7 murine macrophages to assess live S. cerevisiae cells and S. cerevisiae-derived cell wall components β-glucan, mannan, and zymosan (a crude cell wall preparation containing both β-glucan and mannan). D-mannose was also evaluated as the monomer of mannan. We also examined the effect of a saturated fatty acid (C12:0, lauric acid) and its esters (methyl laurate and glycerol monolaurate) on innate immune cell activation and cellular metabolism. RAW cells were transfected with a vector that drives expression of alkaline phosphatase upon promoter activation of nuclear factor κ-light-chain-enhancer of activated B cells (NFκB), a major inflammatory/immune transcription factor. RAW cells were incubated with 0.01, 0.1 or 1 mg/mL of yeast compounds alone or RAW cells were challenged with LPS and then incubated with yeast compounds. In a separate experiment, RAW cells were incubated with 0, 0.5, 2.5, 12.5, 62.5, and 312.5 μmol/L of lauric acid, methyl laurate, or glycerol monolaurate alone, or RAW cells were challenged with LPS and then incubated with fatty acid treatments.

Results
Treatment with zymosan or β-glucan alone induced NFκB activation in a dose-dependent manner, whereas treatment with D-mannose, mannan, or live S. cerevisiae cells did not. Post-treatment with mannan after an LPS challenge decreased NFκB activation, suggesting that this treatment may ameliorate LPS-induced inflammation. Slight increases in NFκB activation were found when fatty acid treatments were applied in the absence of LPS, yet substantial reductions in NFκB activation were seen when treatments were applied following an LPS challenge.

Conclusions
Overall, this cell screening system using RAW macrophages was effective, high-throughput, and sensitive to feed components combined with LPS challenges, indicating modulation of innate immune signaling in vitro.

体外巨噬细胞筛选系统对饲料成分免疫调节作用的开发

背景
尽管人们强烈寻求并销售能够调节免疫系统的饲料成分，但很少有证据支持功能性免疫应答。因此，开发了高通量体外细胞筛选系统来测试这些化合物的先天免疫信号传导作用，除了两个月桂酸及其酯作为模型外，还使用酿酒酵母及其细胞壁成分作为模型。该筛选系统利用RAW 264.7鼠巨噬细胞评估活啤酒酵母细胞和啤酒酵母来源的细胞壁成分β-葡聚糖，甘露聚糖和zymosan（含有β-葡聚糖和甘露聚糖的粗制细胞壁制剂）。还评价了D-甘露糖作为甘露聚糖的单体。我们还检查了饱和脂肪酸（C12：0，月桂酸）及其酯（月桂酸甲酯和甘油单月桂酸酯）对先天免疫细胞活化和细胞代谢的影响。 RAW细胞用一种载体转染，该载体在启动子激活活化的B细胞核因子κ-轻链增强子（NFκB）时启动碱性磷酸酶的表达，NF-B是一种主要的炎症/免疫转录因子。 RAW细胞仅与0.01、0.1或1μg/ mL的酵母化合物一起孵育，或者RAW细胞用LPS攻击，然后与酵母化合物一起孵育。在另一个实验中，将RAW细胞分别与0、0.5、2.5、12.5、62.5和312.5μmol/ L的月桂酸，月桂酸甲酯或单月桂酸甘油酯孵育，或者用LPS攻击RAW细胞，然后与脂肪酸孵育治疗。

结果
单独用酵母聚糖或β-葡聚糖处理可诱导剂量依赖性的NFκB活化，而用D-甘露糖，甘露聚糖或活的酿酒酵母细胞则不会。 LPS攻击后用甘露聚糖进行后处理可降低NFκB活化，表明该治疗可改善LPS诱导的炎症。当在不存在LPS的情况下进行脂肪酸治疗时，发现NFκB的激活略有增加，但是在受到LPS攻击后进行治疗时，NFκB的激活却显着降低。

结论
总的来说，这种使用RAW巨噬细胞的细胞筛选系统是有效的，高通量的，并且对饲料成分和LPS刺激敏感，表明体外先天免疫信号的调节。

Development of an in vitro macrophage screening system on the immunomodulating effects of feed components | Journal of Animal Science and Biotechnology | Full Text
https://jasbsci.biomedcentral.com/articles/10.1186/s40104-020-00497-4

　

Bull Exp Biol Med. 2003 Dec;
Effect of lauric acid on transdermal penetration of phenazepam in vivo

1I I Metcnhikov Odessa National University, Odessa.
We studied the effect of lauric acid on transdermal penetration of phenazepam in vivo. It was found that treatment with lauric acid 3-fold increased the maximum anticonvulsive effect of phenazepam applied in a transdermal therapeutic system in comparison with the control. Study of the pharmacokinetics of phenazepam transdermal therapeutic system showed its higher bioavailability in the presence of lauric acid (f=0.9).

月桂酸对苯扎西trans体内透皮渗透的影响

我们研究了月桂酸对苯扎西m（phenazepam)体内透皮渗透的影响。已经发现，与对照相比，用月桂酸治疗3倍增加了在透皮治疗系统中应用的非那西(phenazepam)最大抗惊厥作用。 Phenazepam透皮治疗系统的药代动力学研究表明，在月桂酸存在下，其生物利用度更高（f = 0.9）。

Effect of lauric acid on transdermal penetration of phenazepam in vivo - PubMed
https://pubmed.ncbi.nlm.nih.gov/15500077/

　

[PDF]Exerts Anti-Proliferation E cacy through Induction of Cell ...
https://www.mdpi.com/2072-6643/12/1/92/pdf
2.2. Preparation of Crude EGCG Derivative LEGCG was prepared according to the literature [17]. Brieﬂy, EGCG and lauric acid were mixed at a mole ratio of 1:1 in ethanol, and then 5% of Lipozyme TLIM (5% w/w) was added. The mixture was heated at 45 C for 12 h in a screw-capped glass bottle. The reaction was terminated by the removal of

Cited by: 3
Publish Year: 2019
Author: Jun Chen, Linli Zhang, Changhong Li, Ruochen Ch

Effect of fatty acids on the permeation of melatonin across rat and pig skin in-vitro and on the transepidermal water loss in rats in-vivo

University of Minnesota
Transdermal delivery of melatonin would be advantageous in the treatment of sleep disorders considering the short biological half-life of melatonin and its variable bioavailability via the oral route. This study looked at suitable penetration enhancers for the transdermal permeation of melatonin. The permeation of melatonin was enhanced by all saturated and unsaturated fatty acids across both rat and porcine skin. There was a parabolic relationship between the carbon chain length of saturated fatty acids and the enhancement of melatonin permeation across rat and porcine skin. For rat skin, the maximum flux was observed with undecanoic acid (45.33 μg cm-2 h-1) which enhanced the flux of melatonin 8.6 times compared with the control, whereas lauric acid produced the maximum flux of melatonin (24.98 μg cm-2 h-1; 4.7 times) across porcine skin. An increase in the number of double bonds in cis-9-octadecanoic acid increased the flux of melatonin across rat skin. In contrast, with porcine skin, the flux of melatonin decreased as the number of double bonds increased, although the flux values were not statistically significant. Treatment of rats with undecanoic acid, oleic acid and linolenic acid for 3 h using Hill top chamber enhanced the transepidermal water loss significantly. The maximum transepidermal water loss was observed with undecanoic acid and linolenic acid among saturated and unsaturated fatty acids, respectively. Nonanoic acid and myristic acid did not cause a significant change in the transepidermal water loss. The enhancement effect of saturated fatty acids on the permeation of melatonin was dependent on the chain-length of the fatty acid in both rat and porcine skin. While an increase in the number of double bonds in the fatty acid increased the flux of melatonin in rat skin, no significant difference in the flux was observed with porcine skin. The permeation enhancement of melatonin by saturated and unsaturated fatty acids across rat skin was significantly higher than that of porcine skin. A positive correlation was observed between the permeation enhancement effect of the fatty acids across rat skin in-vitro and the transepidermal water loss in rats in-vivo, suggesting that there is a similarity in the mechanism by which fatty acids enhance the permeation of melatonin and in the enhancement of transepidermal water loss. We conclude that saturated fatty acids such as undecanoic acid or lauric acid which showed maximum permeation across rat and porcine skin, respectively, may be used as potential penetration enhancers in the development of a transdermal delivery system for melatonin.

脂肪酸对褪黑激素在大鼠和猪皮肤中的体外渗透及对大鼠体内表皮失水的影响

明尼苏达大学
考虑到褪黑激素的短生物半衰期及其通过口服途径的可变生物利用度，褪黑激素的透皮递送在治疗睡眠障碍中将是有利的。这项研究寻找了适合褪黑激素透皮渗透的渗透促进剂。大鼠和猪皮肤中所有饱和和不饱和脂肪酸均会增强褪黑激素的渗透。在大鼠和猪皮肤中，饱和脂肪酸的碳链长度与褪黑激素渗透的增强之间存在抛物线关系。对于大鼠皮肤，十一烷酸（45.33μgcm-2 h-1）观察到最大通量，与对照组相比，褪黑素通量增加了8.6倍，而对于猪皮肤，月桂酸产生了最大的通量褪黑素（24.98μgcm-2 h-1； 4.7倍）。顺式9-十八烷酸中双键数目的增加增加了褪黑激素在大鼠皮肤中的通量。相反，对于猪皮，褪黑素的通量随着双键数量的增加而降低，尽管通量值在统计学上不显着。希尔顶室用十一烷酸，油酸和亚麻酸处理大鼠3小时，明显增加了表皮水分流失。在饱和和不饱和脂肪酸中，十一烷酸和亚麻酸分别观察到最大的表皮水分流失。壬酸和肉豆蔻酸并未引起表皮水分流失的显着变化。饱和脂肪酸对褪黑激素渗透的增强作用取决于大鼠和猪皮肤中脂肪酸的链长。尽管脂肪酸中双键数量的增加增加了大鼠皮肤中褪黑激素的通量，但在猪皮中通量却没有显着差异。饱和和不饱和脂肪酸在大鼠皮肤中对褪黑激素的渗透增强作用明显高于猪皮肤。脂肪酸在体外大鼠皮肤中的渗透增强作用与大鼠体内表皮水分流失之间存在正相关关系，这表明脂肪酸增强褪黑激素和黑色素的渗透的机理相似。在增加表皮水分流失。我们得出的结论是，饱和脂肪酸（如十一酸或月桂酸）分别在大鼠和猪皮肤上表现出最大的渗透性，可在褪黑素透皮给药系统的开发中用作潜在的渗透促进剂。

Effect of fatty acids on the permeation of melatonin across rat and pig skin in-vitro and on the transepidermal water loss in rats in-vivo — Experts@Minnesota
https://experts.umn.edu/en/publications/effect-of-fatty-acids-on-the-permeation-of-melatonin-across-rat-a

　

Published: 22 November 2020
A Novel Eutectic-Based Transdermal Delivery System for Risperidone

This paper reports for the first time the possible formation of a novel room temperature therapeutic deep eutectic solvent (THEDES) of risperidone (RIS) with some fatty acids, namely capric acid (C10; CA), lauric acid (C12; LA), and myristic acid (C14; MA). All mixtures of RIS and MA yielded a solid or pasty-like solid and were readily discarded. Some of the prepared THEDESs from RIS and CA or LA have spontaneously transformed into a transparent liquid, without any precipitate at room temperature by simple physical mixing of the components. From the DSC thermograms, phase diagrams of the eutectic systems were constructed and the lowest obtained melting point for a RIS:CA mixture was 17°C at 40:60% w/w ratio. While 22°C was recorded as the lowest melting point for RIS:LA at a ratio of 30:70% w/w, solubility improvement of RIS was up to 70,000-fold compared with water. Freeze-drying microscopy provided valuable information regarding the phase change and transitions the drug undergoes as a function of temperature and it clarifies the interpretation of the DSC results and provides valuable evidence of drug crystals co-melting within the fatty acid base. The presence of natural fatty acid as one component of THEDES and the depression in the melting point significantly (P < 0.05) enhanced RIS skin permeation. Rheological studies showed a viscosity temperature dependency of the DES and well fitted to the Arrhenius equation. Application of the obtained THEDES on the shaved skin of rats revealed the absence of any irritation or edema effects.

发布时间：2020年11月22日
一种基于共晶的利培酮透皮给药系统

本文首次报道了利培酮（RIS）与某些脂肪酸，即癸酸（C10; CA），月桂酸（C12; LA）和新型脂肪酸的新型室温治疗性深共晶溶剂（therapeutic deep eutectic solvent，THEDES）的可能形成。肉豆蔻酸（C14; MA）。 RIS和MA的所有混合物均产生固体或糊状固体，因此很容易丢弃。通过简单地物理混合各组分，一些由RIS和CA或LA制备的THEDES已自发转变为透明液体，在室温下没有任何沉淀。根据DSC热分析图，构建了低共熔体系的相图，以40：60％w / w的比率获得的RIS：CA混合物的最低熔点为17°C。尽管以22：C记录为RIS：LA的最低熔点，比率为30：70％w / w，但与水相比，RIS的溶解度提高了70,000倍。冷冻干燥显微镜提供了有关药物随温度变化的相变和转变的有价值的信息，它阐明了DSC结果的解释，并为药物晶体在脂肪酸基体内共融提供了有价值的证据。天然脂肪酸作为THEDES的一种成分的存在和熔点的降低（P <0.05）显着增强了RIS皮肤的渗透性。流变学研究表明DES的粘度温度依赖性，并很好地符合Arrhenius方程。将获得的THEDES施用在大鼠的剃毛皮肤上表明没有任何刺激或浮肿作用。

Department of Pharmaceutics and Pharmaceutical Technology, Faculty of Pharmacy and Medical Sciences, Petra University, Amman, Jordan

A Novel Eutectic-Based Transdermal Delivery System for Risperidone | SpringerLink
https://link.springer.com/article/10.1208/s12249-020-01844-4

　

Journal of Pharmaceutical Sciences
February 1994,
Transdermal Delivery of Buprenorphine through Cadaver Skin

Cygnus Therapeutic Systems, 400 Penobscot Dr., Redwood City, CA 94306

The skin permeation of buprénorphine base and HCI salt through cadaver skin was investigated. The octanol-water partition coefficient and solubilities of both buprénorphine free base and HCI salt were determined at 32 °C. As expected, buprénorphine free base was more lipophilic than its HCI salt and was practically insoluble In aqueous buffer at pH 8.7. The drug solubility decreased exponentially as the pH of the solution increased, whereas the permeability coefficient Increased as the donor solution pH decreased. The skin flux of buprenorphlne-HCI was significantly higher than that of the free base from propylene glycol/laurlc acid vehicle mixtures. Buprénorphine base permeation through tape-stripped epidermis suggested that in addition to stratum corneum, viable epidermis presented a significant diffusion barrier because of the very low aqueous solubility of the free base observed. The mean steady-state skin fluxes of buprenorphlne-HCI were 20.3 and 29.7 /μg/cm2/h from propylene glycol:lauryl alcohol: ethanol (80:15:5) and propylene glycol:propylene glycol monolaurate: water (80:15:5) vehicle mixtures, respectively. The skin flux of buprenorphlne-HCI from various monolithic matrix patches was also evaluated. When capric acid, lauric acid, and lauryl alcohol were separately Incorporated into an adhesive matrix, the skin flux of buprenorphlne-HCI was enhanced by a factor of 2 to 3.5. Finally, based on the total body clearance and minimum effective concentration of buprénorphine, a transdermal delivery rate of 2.5 /μg/cm2/h from a 20-cm2 patch was estimated. The in vitro skin permeation data clearly suggest that transdermal delivery of buprénorphine Is feasible to achieve a desired systemic analgesic effect.

药物科学杂志
1994年2月，
通过尸体皮肤透皮递送丁丙诺啡

□研究了丁丙诺啡碱和HCl盐通过尸体皮肤的透皮性。在32°C下测定丁丙诺啡游离碱和HCl盐的辛醇-水分配系数和溶解度。不出所料，丁丙诺啡游离碱比其HCl盐更具亲脂性，几乎不溶于pH 8.7的水性缓冲液。药物溶解度随溶液pH的增加呈指数下降，而渗透系数随供体溶液pH的降低而增加。丁丙诺啡-HCl的皮肤通量显着高于丙二醇/月桂酸媒介混合物中游离碱的皮肤通量。丁丙诺啡碱通过带状剥离的表皮渗透表明，除了角质层以外，由于观察到的游离碱的水溶性很低，因此可行的表皮还具有明显的扩散障碍。从丙二醇：月桂醇：乙醇（80：15：5）和丙二醇：丙二醇单月桂酸酯：水（80:15:20）中，丁丙诺啡HCl的平均稳态皮肤通量为20.3和29.7 /μg/ cm2 / h 5）分别是车辆混合物。还评估了来自各种整体基质贴片的丁丙诺啡-HCl的皮肤通量。当将癸酸，月桂酸和月桂醇分别掺入粘合剂基质中时，丁丙诺啡-HCl的皮肤通量提高了2到3.5倍。最后，根据全身清除率和丁丙诺啡的最低有效浓度，估计从20平方厘米的贴剂中透皮递送速率为2.5 /μg/ cm2 / h。体外皮肤渗透数据清楚地表明，丁丙诺啡的透皮递送对于实现所需的全身镇痛作用是可行的。

Transdermal Delivery of Buprenorphine through Cadaver Skin - ScienceDirect
https://www.sciencedirect.com/science/article/abs/pii/S0022354915493669

　

Transdermal delivery of highly lipophilic drugs: in vitro fluxes of antiestrogens, permeation enhancers, and solvents from liquid formulations

Purpose: Highly lipophilic basic drugs, the antiestrogens AE 1 (log P = 5.82) and AE 2 (log P = 7.8) shall be delivered transdermally.

Methods: Transdermal permeation of drugs, enhancers, and solvents from various fluid formulations were characterized by in-vitro permeation studies through excised skin of hairless mice. Furthermore, differential scanning calorimetry (DSC) measurements of skin lipid phase transition temperatures were conducted.

Results: Transdermal flux of highly lipophilic drugs was extraordinarily enhanced by the unique permeation enhancer combination propylene glycol-lauric acid (9 + 1): steady-state fluxes of AE 1 and AE 2 were as high as 5.8 microg x cm(-2) x h(-1) and 3.2 microg x cm(-2) x h(-1), respectively. This dual enhancer formulation also resulted in a marked increase in the transdermal fluxes of the enhancers. Furthermore, skin lipid phase transition temperatures were significantly reduced by treatment with this formulation.

Conclusion: Transdermal delivery of highly lipophilic drugs can be realized by using the permeation enhancer combination propylene glycol-lauric acid. The extraordinary permeation enhancement for highly lipophilic drugs by this formulation is due to mutual permeation enhancement of these two enhancers and their synergistic lipid-fluidising activity in the stratum corneum.

高亲脂性药物的透皮给药：抗雌激素，渗透促进剂和液体制剂中溶剂的体外通量

目的：高度亲脂性基础药物，抗雌激素AE 1（log P = 5.82）和AE 2（log P = 7.8）应经皮输送。

方法：通过无毛小鼠的离体皮肤的体外渗透研究，对各种流体制剂中药物，增强剂和溶剂的透皮渗透进行了表征。此外，进行了皮肤脂质相转变温度的差示扫描量热法（DSC）测量。

结果：独特的渗透促进剂组合丙二醇-月桂酸（9 + 1）极大地增强了高度亲脂性药物的透皮通量：AE 1和AE 2的稳态通量高达5.8 microg x cm（-2） xh（-1）和3.2 microg x cm（-2）xh（-1）。这种双重增强剂制剂还导致增强剂的透皮通量显着增加。此外，通过用该制剂处理，皮肤脂质相转变温度显着降低。

结论：通过使用渗透促进剂丙二醇-月桂酸组合可以实现高度亲脂性药物的透皮给药。通过这种制剂，高度亲脂性药物的非凡渗透增强是由于这两种增强剂的相互渗透增强以及它们在角质层中的协同脂质流化活性。

Transdermal delivery of highly lipophilic drugs: in vitro fluxes of antiestrogens, permeation enhancers, and solvents from liquid formulations - PubMed
https://pubmed.ncbi.nlm.nih.gov/12069170/

　

AAPS J, 2019 May 31;
Skin Delivery and Irritation Potential of Phenmetrazine as a Candidate Transdermal Formulation for Repurposed Indications
bstract
Phenmetrazine, a selective dopamine and norepinephrine releaser, previously available as an oral anorectic, is prone to be abused. This study aimed to assess the feasibility of delivering phenmetrazine via the transdermal route for a new indication, while also minimizing its abuse potential. The passive permeation of phenmetrazine through dermatomed human cadaver skin was evaluated using static Franz diffusion cells at 10 mg/mL for the fumarate salt, and at 20, 40, and 80 mg/mL for the free base in propylene glycol for 24 h. Further, oleic acid (5% w/w), oleyl alcohol (5% and 10% w/w), and lauric acid (10% w/w) were investigated as chemical permeation enhancers to enhance the delivery. Skin irritation potential was assessed using EpiDerm™ in vitro reconstructed human epidermal model. The free base showed superior 24-h delivery (8.13 ± 4.07%, 10.6 ± 2.5%, and 10.4 ± 1.4% for groups with 20, 40, and 80 mg/mL of the free base, respectively) to phenmetrazine fumarate salt (undetectable). The successful screening of effective chemical enhancers, oleyl alcohol (5% and 10% w/w), oleic acid (5% w/w), and lauric acid (10% w/w) resulted in significant enhancement of delivery. The calculated therapeutic relevant flux for the potential indication, attention deficit hyperactivity disorder, 20 μg/cm2/h was met, where a 24-mg daily dose from a 50-cm2 patch was projected to be delivered to a 60-kg individual. Irritation study results suggest that formulations with therapeutically relevant delivery are likely to be non-irritant. In conclusion, it is feasible to deliver therapeutically relevant amounts of phenmetrazine via the transdermal route.

Keywords: Chemical permeation enhancers; Phenmetrazine; Skin irritation; Transdermal delivery.

AAPS J，2019年5月31日;
苯甲r嗪作为皮肤适应症的候选替代用途的透皮制剂。
抽象
苯丙哌嗪是一种选择性的多巴胺和去甲肾上腺素释放剂，以前可作为口服厌食药而被滥用。这项研究旨在评估通过透皮途径提供吩美拉嗪作为新适应症的可行性，同时还将其滥用潜力降到最低。使用静态Franz扩散池（富马酸盐），游离碱浓度分别为20、40和80 mg / mL，丙二醇中的24小时，评估芬太嗪通过皮肤切开的人体尸体皮肤的被动渗透。此外，研究了油酸（5％w / w），油醇（5％和10％w / w）和月桂酸（10％w / w）作为化学渗透增强剂以增强递送。使用EpiDerm™体外重建的人表皮模型评估皮肤刺激潜力。游离碱对富马酸苯甲met嗪盐具有24小时的卓越递送（分别为20、40和80 mg / mL的组，分别为8.13±4.07％，10.6±2.5％和10.4±1.4％）（无法检测））。有效筛选有效的化学促进剂，油醇（5％和10％w / w），油酸（5％w / w）和月桂酸（10％w / w）可显着提高输送效率。满足了针对潜在指征，注意缺陷多动障碍20μg/ cm2 / h的计算出的治疗相关通量，其中来自50 cm2贴片的24 mg日剂量预计将被递送给60 kg个体。刺激性研究结果表明，具有治疗相关作用的制剂可能无刺激性。总之，通过透皮途径递送治疗上相关量的吩美拉嗪是可行的。

关键字：化学渗透促进剂；苯甲r嗪;皮肤过敏;透皮递送。

Skin Delivery and Irritation Potential of Phenmetrazine as a Candidate Transdermal Formulation for Repurposed Indications - PubMed
https://pubmed.ncbi.nlm.nih.gov/31152318/

　

Lipophilized Epigallocatechin Gallate Derivative Exerts Anti-Proliferation Efficacy through Induction
of Cell Cycle Arrest and Apoptosis on DU145 Human Prostate Cancer Cells

Jun Chen, Linli Zhang, Changhong Li, Ruochen Chen, Chengmei Liu and Mingshun Chen *
State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China

Published: 28 December 2019

Abstract:

Epigallocatechin gallate (EGCG) is the predominant tea polyphenol and it exhibits a hydrophilic character. The lipophilized EGCG derivative (LEGCG) was synthesized by enzymatic esterification of EGCG with lauric acid to enhance its bioactivity. The tetralauroyl EGCG was confirmed by high-performance liquid chromatography-tandem mass spectrometry and further identified as 30, 50, 300, 500-4-O-lauroyl EGCG by 1H and 13C nuclear magnetic resonance. The anti-proliferation effect of LEGCG on DU145 human prostate carcinoma cells was evaluated by MTT assay. In addition, the underlying molecular mechanism by which LEGCG exerts anti-proliferation efficacy was elucidated by flow cytometry and immunoblot analysis. Results suggested that LEGCG exhibited a dose-dependent anti-proliferation effect on DU145 cells by G0/G1 phase arrest and induction of apoptosis. LEGCG induced cell cycle arrest via p53/p21 activation, which down-regulated the cyclin D1 and CDK4 expression. In addition, LEGCG induced apoptosis by increasing the Bax/Bcl-2 ratio, the cytochrome c release, and the caspases cleavage on DU145 cells. The results provide theoretical support to prevent prostate cancer with LEGCG.

In our previous study, lipophilic grape seed proanthocyanidin, synthesized by grape seed proanthocyanidin and lauric acid, showed excellent anti-prostate

Preparation of Crude EGCG Derivative
LEGCG was prepared according to the literature [17]. Briefly, EGCG and lauric acid were mixed at a mole ratio of 1:1 in ethanol, and then 5% of Lipozyme TLIM (5% w/w) was added. The mixture was
heated at 45 ◦C for 12 h in a screw-capped glass bottle. The reaction was terminated by the removal of the enzyme through filter paper, and the product was concentrated to get crude LEGCG.

　

Lipophilicity of LEGCG
The high hydrophilicity of EGCG is considered as having low bioavailability and is not conducive to application in the fat food system. The structural modification, especially enzymatic esterification, is an effective means to improve lipophilicity. Many hydrophilic bioactive compounds have been lipophilized, including EGCG, cinnamic, caffeic acids, ascorbic acid, genistein [22–26], and expanding their application in a more lipophilic system.
The lipophilicity of LEGCG was evaluated by the log p. A higher log p value indicates higher lipophilicity of the compound. As expected, the log p value of LEGCG (4.63 ± 0.14) was significantly higher than their parent EGCG molecule (0.46 ± 0.02). According to the literature, the incorporation rate of tea polyphenols and lipid bilayers was positively correlated with log p value [27]. Enhancement of lipophilicity of LEGCG may increase their bioavailability and the liposome-based drug delivery capability

　

脂化的表没食子儿茶素没食子酸酯衍生物通过诱导具有抗增殖作用
细胞周期阻滞和凋亡对DU145人前列腺癌细胞的影响

陈军，张琳莉，李长虹，陈若辰，刘成美，陈明顺*
南昌大学食品科学技术国家重点实验室，南昌330047

发布时间：2019年12月28日

抽象：
表没食子儿茶素没食子酸酯（EGCG）是主要的茶多酚，具有亲水性。通过用月桂酸将EGCG酶促酯化以增强其生物活性，合成了脂化的EGCG衍生物（LEGCG）。通过高效液相色谱-串联质谱法确认了四月桂酰基EGCG，并且通过1H和13C核磁共振将其进一步鉴定为30、50、300、500-4-O-月桂酰基EGCG。通过MTT法评估了LEGCG对DU145人前列腺癌细胞的抗增殖作用。此外，流式细胞术和免疫印迹分析阐明了LEGCG发挥抗增殖功效的潜在分子机制。结果提示LEGCG通过G0 / G1期阻滞和诱导凋亡对DU145细胞表现出剂量依赖性的抗增殖作用。 LEGCG通过p53 / p21激活诱导细胞周期停滞，这下调了细胞周期蛋白D1和CDK4的表达。此外，LEGCG通过增加Bax / Bcl-2比率，细胞色素c释放和胱天蛋白酶在DU145细胞上的裂解来诱导细胞凋亡。该结果为LEGCG预防前列腺癌提供了理论支持。

在我们以前的研究中，由葡萄籽原花青素和月桂酸合成的亲脂性葡萄籽原花青素显示出优异的抗前列腺癌增殖特性。

EGCG衍生物的制备
LEGCG是根据文献[17]制备的。简而言之，将EGCG和月桂酸在乙醇中以1：1的摩尔比混合，然后加入5％的Lipozyme TLIM（5％w / w）。混合物是
在螺口玻璃瓶中于45℃加热12小时。通过滤纸除去酶来终止反应，并将产物浓缩以得到粗LEGCG。

LEGCG的亲脂性
EGCG的高亲水性被认为具有低生物利用度，并且不利于在脂肪食物系统中的应用。结构修饰，特别是酶促酯化，是改善亲脂性的有效手段。许多亲水性生物活性化合物已被亲脂化，包括EGCG，肉桂酸，咖啡酸，抗坏血酸，染料木黄酮[22-26]，并扩大了它们在亲脂性系统中的应用。
LEGCG的亲脂性通过log p评估。较高的log p值表示该化合物的亲脂性较高。不出所料，LEGCG的log p值（4.63±0.14）明显高于其母体EGCG分子（0.46±0.02）。根据文献，茶多酚和脂质双层的掺入率与log p值呈正相关[27]。 LEGCG亲脂性的增强可能会提高其生物利用度和基于脂质体的药物传递能力

Keywords: EGCG; LEGCG; DU145 cell; proliferation; apoptosis

Exerts Anti-Proliferation E cacy through Induction of Cell ...
https://www.mdpi.com/2072-6643/12/1/92/pdf
2.2. Preparation of Crude EGCG Derivative LEGCG was prepared according to the literature [17]. Brieﬂy, EGCG and lauric acid were mixed at a mole ratio of 1:1 in ethanol, and then 5% of Lipozyme TLIM (5% w/w) was added. The mixture was heated at 45 C for 12 h in a screw-capped glass bottle. The reaction was terminated by the removal of

Cited by: 3
Publish Year: 2019

　

The liver processes coconut oil differently than rapeseed oil
by University of Bonn

The inside view of a cell. Credit: (c) Johanna Spandl / Universität Bonn
Coconut oil has increasingly found its way into German kitchens in recent years, although its alleged health benefits are controversial. Scientists at the University of Bonn have now been able to show how it is metabolized in the liver. Their findings could also have implications for the treatment of certain diarrheal diseases. The results are published in the journal Molecular Metabolism.

Coconut oil differs from rapeseed or olive oil in the fatty acids it contains. Fatty acids consist of carbon atoms bonded together, usually 18 in number. In coconut oil, however, most of these chains are much shorter and contain only 8 to 12 carbon atoms. In the liver, these medium-chain fatty acids are partly converted into storage fats (triglycerides). Exactly how this happens was largely unknown until now.

The new study now sheds light on this: "There are two enzymes in the liver for storage fat synthesis, DGAT1 and DGAT2," explains Dr. Klaus Wunderling of the LIMES Institute (the acronym stands for Life & Medical Sciences) at the University of Bonn. "We have now seen in mouse liver cells that DGAT1 processes mainly medium-chain fatty acids and DGAT2 processes long-chain ones."

In their experiments, the researchers blocked DGAT1 with a specific inhibitor. The synthesis of storage fats from medium-chain fatty acids subsequently decreased by 70 percent. In contrast, blocking DGAT2 resulted in reduced processing of long-chain fatty acids. "The enzymes therefore seem to prefer different chain lengths," concludes Prof. Dr. Christoph Thiele of the LIMES Institute, who led the study and is also a member of the Cluster of Excellence Immunosensation.

Surprising side effect

Whether fatty acids in the liver are used at all to build up storage fat depends on the current energy requirement. When the body needs a lot of energy at a particular moment, the so-called beta oxidation is fired up—the fatty acids are "burned" straight away, so to speak. Medically, this metabolic pathway is of great interest. In diabetes, for instance, it might be useful to reduce beta-oxidation. This is because the body then has to meet its energy needs from glucose instead, causing blood glucose levels to drop, with positive implications for the disease.

As early as some 40 years ago, pharmaceutical researchers therefore developed a corresponding inhibitor, etomoxir. It binds to enzymes required for beta-oxidation, bringing it to a halt. However, it quickly became apparent that etomoxir had severe side effects.

The researchers in Bonn have now discovered a possible reason for this: They used etomoxir to inhibit the beta-oxidation of medium-chain fatty acids in mice, in anticipation of using it to boost the production of storage fat. "Instead, fat synthesis also decreased significantly, but only of storage fats with medium-chain fatty acids," Wunderling explains. "We therefore suspect that etomoxir also switches off the DGAT1 enzyme." In the future, he says, it will be necessary to pay attention to such effects when developing new inhibitors of beta-oxidation.

Also interesting is a finding published a few years ago by Austrian and Dutch scientists: They had studied patients suffering from chronic diarrheal diseases. In 20 of them, they found alterations in the DGAT1 gene that rendered it nonfunctional. "We now want to find out whether the impaired processing of medium-chain fatty acids is responsible for the digestive complaints," says Wunderling. This is because the DGAT1 enzyme is active not only in the liver but also in the intestine. Perhaps this is why its disorder causes diarrhea when sufferers consume medium-chain fatty acids. Wunderling: "In this case, they could possibly be helped quite simply—with an appropriate diet."

The liver processes coconut oil differently than rapeseed oil
https://medicalxpress.com/news/2021-01-liver-coconut-oil-differently-rapeseed.html

　

Glycerol Monolaurate and Dodecylglycerol Effects on Staphylococcus aureus and Toxic Shock Syndrome Toxin-1 In Vitro and In Vivo

Background
Glycerol monolaurate (GML), a 12 carbon fatty acid monoester, inhibits Staphylococcus aureus growth and exotoxin production, but is degraded by S. aureus lipase. Therefore, dodecylglycerol (DDG), a 12 carbon fatty acid monoether, was compared in vitro and in vivo to GML for its effects on S. aureus growth, exotoxin production, and stability.

Methodology/Principal Findings
Antimicrobial effects of GML and DDG (0 to 500 µg/ml) on 54 clinical isolates of S. aureus, including pulsed-field gel electrophoresis (PFGE) types USA200, USA300, and USA400, were determined in vitro. A rabbit Wiffle ball infection model assessed GML and DDG (1 mg/ml instilled into the Wiffle ball every other day) effects on S. aureus (MN8) growth (inoculum 3×108 CFU/ml), toxic shock syndrome toxin-1 (TSST-1) production, tumor necrosis factor-α (TNF-α) concentrations and mortality over 7 days. DDG (50 and 100 µg/ml) inhibited S. aureus growth in vitro more effectively than GML (p<0.01) and was stable to lipase degradation. Unlike GML, DDG inhibition of TSST-1 was dependent on S. aureus growth. GML-treated (4 of 5; 80%) and DDG-treated rabbits (2 of 5; 40%) survived after 7 days. Control rabbits (5 of 5; 100%) succumbed by day 4. GML suppressed TNF-α at the infection site on day 7; however, DDG did not (<10 ng/ml versus 80 ng/ml, respectively).

Conclusions/Significance
These data suggest that DDG was stable to S. aureus lipase and inhibited S. aureus growth at lower concentrations than GML in vitro. However, in vivo GML was more effective than DDG by reducing mortality, and suppressing TNF-α, S. aureus growth and exotoxin production, which may reduce toxic shock syndrome. GML is proposed as a more effective anti-staphylococcal topical anti-infective candidate than DDG, despite its potential degradation by S. aureus lipase.

甘油单月桂酸酯和十二烷基甘油对金黄色葡萄球菌和毒性休克综合征毒素-1的体内和体外影响

背景
甘油单月桂酸酯（GML）是一种12碳脂肪酸单酯，可抑制金黄色葡萄球菌的生长和外毒素的产生，但会被金黄色葡萄球菌脂肪酶降解。因此，在体外和体内，将十二碳甘油单醚（DDG）（一种12碳脂肪酸单醚）与GML进行比较，以分析其对金黄色葡萄球菌生长，外毒素产生和稳定性的影响。

方法/主要发现
在体外确定了GML和DDG（0至500 µg / ml）对54株金黄色葡萄球菌临床分离株的抗菌作用，包括USA200，USA300和USA400型脉冲场凝胶电泳（PFGE）。兔子Wiffle球感染模型评估了GML和DDG（每隔一天向Wiffle球中滴入1 mg / ml）对金黄色葡萄球菌（MN8）生长（接种物3×108 CFU / ml），中毒性休克综合征毒素1（ TSST-1）的产生，肿瘤坏死因子-α（TNF-α）的浓度和7天内的死亡率。 DDG（50和100 µg / ml）在体外抑制金黄色葡萄球菌的生长要比GML（p <0.01）更有效，并且对脂肪酶降解稳定。与GML不同，TSG-1对DDG的抑制作用取决于金黄色葡萄球菌的生长。经GML处理的动物（5只中的4只； 80％）和经DDG处理的兔子（5只2中的一只； 40％）在7天后存活。对照兔（5只中的5只； 100％）在第4天死去。GML在第7天在感染部位抑制了TNF-α；在第7天，TNF-α抑制了TNF-α。但是，DDG却没有（分别小于10 ng / ml和80 ng / ml）。

结论/意义
这些数据表明，DDG对金黄色葡萄球菌脂肪酶是稳定的，并且在低于GML的体外浓度下抑制金黄色葡萄球菌的生长。但是，体内GML通过降低死亡率，抑制TNF-α，金黄色葡萄球菌的生长和外毒素的产生而比DDG更为有效，这可以减少中毒性休克综合征。尽管GML可能被金黄色葡萄球菌脂肪酶降解，但它被认为是比DDG更有效的抗葡萄球菌局部抗感染药物。

已经报道了针对金黄色葡萄球菌的GML的一系列最小抑制浓度（MIC）。在复杂培养基中，针对29株金黄色葡萄球菌的GML MIC报道为10至20 µg / ml，接种量为103至104 CFU / ml [31]。 Kabara等人报道了胰蛋白酶解毒大豆肉汤中针对金黄色葡萄球菌的GML MIC为25 µg / ml，接种量约为107 CFU / ml [30]。 Preuss等。据报道营养肉汤中接种量为63 µg / ml，接种量约为105至106 CFU / mL [32]。 Kelsey及其同事报道了针对三种金黄色葡萄球菌的GML MIC为25–50 µg / ml [33]。 MIC的可变性可能是由于培养条件，接种量和测试的金黄色葡萄球菌菌株引起的[31]。通过针对大量临床相关菌株测试化合物，我们证实了即使在同一克隆类型中，细菌菌株之间对GML的敏感性也存在差异。 GML敏感性的差异可能不能仅由菌株产生的脂肪酶水平不同来解释，因为在DDG组中也可以观察到金黄色葡萄球菌克隆类型之间的差异，而金黄色葡萄球菌脂肪酶并不会降解这种差异。我们还观察到，USA400菌株虽然对化合物具有更高的抵抗力，但其产生的脂肪酶却不比USA200菌株多（数据未显示）。金黄色葡萄球菌克隆类型对DDG和GML的反应差异背后的机制可能与细胞表面疏水性有关[34]，但是，这一假说需要在未来的研究中进行研究。

A range of minimum inhibitory concentrations (MICs) for GML against S. aureus have been reported. The MICs of GML against 29 strains of S. aureus in a complex medium were reported to be between 10 to 20 µg/ml with 103 to 104 CFU/ml inocula [31]. Kabara and colleagues reported the MIC of GML against S. aureus was 25 µg/ml with approximate 107 CFU/ml inocula in trypticase soy broth [30]. Preuss et al. reported 63 µg/ml with approximate 105 to 106 CFU/mL inocula in nutrient broth [32]. Kelsey and colleagues reported the MIC of GML against three strains of S. aureus was 25–50 µg/ml [33]. The variability in MIC is potentially due to culture conditions, inoculum size, and the S. aureus strains tested [31]. By testing the compounds against a large collection of clinical relevant strains, we confirmed that there are differences in sensitivity to GML among bacterial strains, even within the same clonal type. The differences in GML sensitivity may not be solely explained by different levels of lipase produced by the strains since the differences among S. aureus clonal types can also be observed in the DDG group, which is not degraded by S. aureus lipase. We also observed that USA400 strains do not produce more lipase than USA200 strains (data not shown), despite being more resistant to the compounds. The mechanism(s) behind the differences among S. aureus clonal types in response to DDG and GML may be related to cell surface hydrophobicity [34], however, this hypothesis will need to be investigated in future studies.

　

据报道，GML可稳定真核细胞的膜，调节促炎性细胞因子的产生，从而防止细菌外毒素对真核细胞的毒性[16]。我们以前曾提出GML作为双重作用的抗感染药的优势，1）对微生物具有预防作用，以防止其生长和/或外毒素的产生； 2）对宿主上皮细胞具有抗炎和膜稳定作用，它减少了感染后诱导促炎性细胞因子和趋化因子引起的粘膜通透性障碍的破坏[19]。尽管与直觉相反，后一种抗炎和膜稳定特性可能与抗微生物作用同等重要或更重要。我们最近报道，尽管粘膜表面GML浓度低于杀病毒浓度，但含有GML（5％）的凝胶阻止SIV在猴颈和阴道粘膜之间的传播[19]。另外，组织学研究证明对先天免疫有抑制作用。在我们的研究中，尽管细菌密度在7天内约为1×107 CFU / ml，但GML还降低了局部促炎性细胞因子的产生（通过TNF-α进行测量）。

GML has been reported to stabilize the membrane of eukaryotic cells, modulate the production of pro-inflammatory cytokines and thereby prevent the toxicity of bacterial exotoxins on eukaryotic cells [16]. We have previously suggested the benefits of GML as a dual-acting anti-infective, 1) with effects on the microbes to prevent growth and/or exotoxin production, and 2) with anti-inflammatory and membrane stabilizing effects on the host epithelial cells, which reduces the disruption in the mucosal permeability barriers caused by induction of pro-inflammatory cytokines and chemokines following infection [19]. This latter anti-inflammatory and membrane stabilizing property, although counterintuitive, may be equally important or more important than the antimicrobial effect. We reported recently that a GML (5%) containing gel prevented SIV transmission across monkey cervical and vaginal mucosa, despite mucosal surface GML concentrations being below virucidal concentrations [19]. Additionally, histological studies demonstrated an inhibitory effect on innate immunity. In our study, GML also decreased local pro-inflammatory cytokine production (as measured by TNF-α) despite bacterial densities of approximately 1×107 CFU/ml over 7 days.

Based on the collective results of this study, GML is proposed as more effective anti-staphylococcal topical anti-infective candidate than DDG, despite its potential degradation by S. aureus lipase.

Glycerol Monolaurate and Dodecylglycerol Effects on Staphylococcus aureus and Toxic Shock Syndrome Toxin-1 In Vitro and In Vivo
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0007499

　

Coconut Oil for Hair Growth: A Review of the Scientific Literature
May 10, 2019 by Sophia
Chances are:

You’ve used coconut oil before.

But, is it really working?

I’ve compiled the science we have on coconut oil for hair growth, hair health, and hair loss.

You’ll learn:

if coconut oil really works for your hair;
the research on coconut oil;
the interesting connection between Indian oil practices and hair;
and the best way to use coconut oil for your hair.
Just keep reading!

Quickly, make sure you take the free hair quiz later in this article.

What Is Coconut Oil?
Before we get into the research behind coconut oil:

Let’s talk about what coconut oil actually is.

This is crucial for understanding how coconut oil works.

Coconut oil is solid at room temperature, it’s a saturated fat.

Coconut oil scooped onto a spoon

What makes coconut oil unique from all other saturated fats is one fatty acid:

Lauric acid.

This fatty acid is what holds all the potential benefits for hair.

In the sections below, I’ll share just how lauric acid works.

Key Takeaway: Lauric acid is a key component of coconut oil.

Coconut Oil for Hair Growth and Hair Loss: How Does It Work?
So, let’s talk more about lauric acid.

There are three situations where lauric acid might just be helpful.

Coconut Oil and Androgenetic Alopecia
Androgenetic Alopecia (AGA) is a form of hair loss. It’s also known as pattern hair loss. Both men and women experience it.

Researchers are still determining exactly what causes androgenetic alopecia. But, what we do know is that most cases present with increased male hormones on the scalp (1).

There are also clear characteristics of androgenetic alopecia:

miniaturized hair follicles that produce tiny hairs, called vellus hairs (think: peach fuzz);
scarring around the follicle;
inflammation on the scalp;
decreased scalp blood flow and oxygen;
and increased sebaceous gland size.
When all of these factors come together, the result is this:

A catch-22 cycle that makes hair loss hard to overcome.

Now, there are two approved treatments for AGA:

Topical minoxidil and oral finasteride.

The issue with these is that they only work when you’re using them (2, 3).

Back to coconut oil.

What does lauric acid have to do with androgenetic alopecia?

Remember how increased sebaceous gland size and decreased oxygen are characteristics of androgenetic alopecia?

Well, this creates the perfect breeding ground for a problematic strain of bacteria:

P. acnes.

You might recognize this bacteria for its role in acne, but it might contribute to hair loss, too.

When P. acnes overgrows, it triggers the immune system (4).

As a result, inflammatory proteins come in and invade the hair follicle.

If P. acnes continues to overgrow, chronic inflammation can cause scarring, follicle miniaturization, and may contribute to the vicious cycle of androgenetic alopecia.

Interestingly, researchers have found that miniaturized hair follicles present in androgenetic alopecia have higher levels of P. acnes bacteria (5).

So, how can coconut oil help?

Well, lauric acid is a potent antimicrobial (6). Even more so than benzoyl peroxide, which is designed to specifically kill P. acnes bacteria (7).

By applying coconut oil on the scalp, it may help regulate levels of P. acnes on the scalp. This may reduce the inflammation that is associated with AGA and P. acnes overgrowth.

One study investigated this (8):

Researchers cultured P. acnes bacteria. They then treated the samples with liposomal lauric acid.

They found that the liposomal lauric acid successfully killed the P. acnes bacteria.

Although this demonstrates the power of lauric acid against P. acnes, it doesn’t necessarily mean that applying coconut oil will have the same dramatic effects.

Although, it is promising!

Key Takeaway: Lauric acid from coconut oil may benefit androgenetic alopecia by killing P. acnes bacteria. This strain can cause hair follicle inflammation which is associated with androgenetic alopecia. Androgenetic alopecia miniaturized hair follicles contain high levels of P. acnes bacteria.

Coconut Oil and Scalp Fungal Infections
Let’s talk about another form of hair loss:

Scarring alopecia.

Scarring alopecia can be a result of fungal infections in the scalp, called trichomycoses (9). If these fungal infections go untreated, it may cause chronic inflammation, leading to hair follicle scarring.

The various causes of skin fungal infections

Unfortunately, fungal infections that cause scarring alopecia are permanent.

So, the trick is prevention.

Lauric acid also acts as an anti-fungal and may be able to prevent scalp fungal infections (10).

In one 1992 study, researchers looked at just this (11):

They examined the effects of Indian hair oils like coconut, mustard, cantharidine, and amla oil on fungi.

They found that coconut, cantharidine, and amla oil were the most effective at inhibiting fungal growth.

The authors also noted how rare scalp fungal infections are in India. Although we can’t say for sure, researchers hint that it might be associated with the culture’s common hair oil practices.

These results mirrored a 1975 study (12):

Researchers found that coconut oil, mustard oil, and oleic acid oils inhibited the growth of fungi.

But, we can’t deem coconut oil as a miracle treatment for fungal infections. There are currently no studies examining coconut oil for the treatment of trichomycoses.

Key Takeaway: Lauric acid in coconut oil is antifungal. Fungal infections can cause scarring alopecia. Coconut oil may prevent fungal infections from worsening and damaging hair follicles.

Coconut Oil for Healthy Hair
Let’s go beyond the scalp:

Coconut oil can promote healthy hair, too.

A hallmark of healthy hair is reduced breakage.

The truth is:

You can’t grow long, full hair if it keeps snapping off.

So, how can you prevent breakage?

One way is to prevent the hair from damage, a.k.a protein loss (13).

Certain environmental factors like the use of heat tools, UV radiation, and chemical treatments can cause protein loss.

The good news is:

Coconut oil can protect hair from damage.

In one study, researchers put coconut oil to the test against sunflower oil and mineral oil (14).

Of the three oils, coconut oil successfully preserved the protein content of hair.

Sunflower oil and mineral oil didn’t.

Researchers believe lauric acid’s small molecular structure allows it to penetrate the hair shaft. It also binds easily to hair proteins.

So, using coconut oil regularly on your hair can protect it from damage and breakage.

Key Takeaways: Lauric acid in coconut oil preserves hair protein content, preventing damage and breakage.

The Research on Coconut Oil
Here’s the deal:

As with any product, we have to look at direct observations researchers have made on coconut oil.

Unfortunately, the only widely accepted benefit of coconut oil is its benefit for hair health.

Although the other mechanisms are promising, we can’t fully rely on them until more studies are done.

How to Use Coconut Oil for Hair
You might be wondering:

How can I take advantage of coconut oils proven and potential benefits?

Let’s get into it.

Coconut Oil for Hair Mask
Hair masks are a perfect way to take advantage of coconut oil.

A woman applying a hair mask to her hair

Here’s how:

Brush your hair to remove any knots or tangles.
Take a few tablespoons of coconut oil and melt it down on an ultra-low heat. You don’t want to damage the oil.
Pour the oil into a heat-safe applicator bottle.
Test the oil on your wrist to make sure you don’t burn yourself.
If the oil is cool enough, apply coconut oil until your scalp is coated.
Using your fingertips, massage the coconut oil into your scalp.
Then, take a hairbrush (preferably a no-snag brush) and brush through to the ends to evenly distribute the coconut oil to the ends of your hair.
If you have long hair, you can secure your hair to the top of your head to avoid oil stains.
Leave the oil mask on for a minimum of twenty minutes. You can even leave coconut oil in your hair overnight.
Then, wash out the oil using shampoo and conditioner.
Using this method, it will allow the lauric acid to penetrate the hair shaft and follicle. The longer you leave it on, the greater the chances of deepest penetration you get.

Put simply: leave it on for as long as you can!

Key Takeaway: Use coconut oil as a hair mask and let it sit for an extended period of time for maximum penetration.

Coconut Oil for Hair Growth: A Review of the Scientific Literature - Hair Science
https://www.hairscience.com/coconut-oil-for-hair-growth/

　