亚麻籽的抗炎作用
Anti-Inflammatory Benefits of Flaxseed
鲑鱼靠边，甘蓝让路，为亚麻籽腾出空间，它是健康食品俱乐部的合法成员。它甚至被证明可以缓解关节炎，尤其是在类风湿性关节炎、狼疮和雷诺氏症中。
“虽然亚麻籽已经使用了很长一段时间——希波克拉底在公元前500年吃过和记录过亚麻籽——只有在过去的10年里,研究人员才专注于亚麻籽的健康好处,”说乔斯林Mathern, 注册营养师和亚麻木酚素信息局咨询委员会的成员, 在明尼阿波利斯的一个消费者教育组织。
仅仅两汤匙的亚麻籽含有超过140%每日推荐量的OMEGA-3脂肪酸和更多的木酚素，一种抗癌的植物化学物质，比地球上任何其他植物食物都多。要了解这颗营养之星，看看里面有什么。
必需脂肪酸。亚麻籽油中57%的脂肪酸是阿尔法-亚麻酸(ALA)，是3种奥米茄-3脂肪酸之一。当使用的时候，ALA会转化成作用更强的OMEGA-3脂肪酸—二十二碳六烯酸(DHA)和二十碳五烯酸(EPA)。亚麻籽中含有ALA，但亚麻籽油含量最高。在一项研究中，志愿者们连续四周食用亚麻籽油，这种抗炎物质显著降低了促炎症化合物的含量。
木酚素(LIGNAN)。在亚麻籽壳中发现，这些植物化学物质在消化道转化为植物雌激素。研究表明，它们可以预防多种癌症，预防心脏病和缓解更年期症状。整个亚麻仁必须被磨碎，或者作为木酚素的食物，被身体吸收。一旦打开，一包亚麻籽应该被存放在冰箱的密闭容器中，以防止它变质。亚麻籽油不含整粒或磨碎的亚麻籽中的木酚素物质，所以要寻找添加了木酚素物质的品牌。
类黄酮（BIOFLAVONOIDS)。这些化合物存在于所有的亚麻籽中，具有降低低密度脂蛋白(LDL)或“坏”胆固醇的作用。高水平的低密度脂蛋白与更高的心脏病风险有关。
纤维(FIBER)。膳食纤维占研磨亚麻籽成分的28%。可溶性纤维被证明可以降低胆固醇和降低癌症的风险，而不可溶性纤维可以帮助防止消化道问题。
注意:使用血液稀释剂的人应避免使用亚麻籽油，因为它可能会增加出血; 服用降胆固醇药物的人应该小心，因为它可能会降低过高的胆固醇水平。
Anti-Inflammatory Benefits of Flaxseed
Step aside, salmon. Scoot over kale. Make room for flaxseed, a rightful member of the healthiest foods club. It has even been shown to ease arthritis, especially in rheumatoid arthritis, lupus and Raynaud’s phenomenon.
“Although flaxseed has been used for a long time – Hippocrates ate and wrote about it in 500 B.C. – it’s only been in the past 10 years that researchers have focused on flaxseed’s health benefits,” says Jocelyn Mathern, a registered dietitian and member of the Flax Lignan Information Bureau Advisory Board, a consumer education organization in Minneapolis.
Just two tablespoons of ground flaxseed contain more than 140% daily value of the inflammation-reducing omega-3 fatty acids and more lignans, a cancer-fighting plant chemical, than any other plant food on the planet. To understand this nutritional star, take a look at what’s inside.
Essential fatty acids. Fifty-seven percent of the total fatty acids in flaxseed oil is alpha-linoleic acid (ALA), one of three omega-3 fatty acids. When consumed, ALA is converted into the other, more powerful omega-3s, docosahexaeonic (DHA) and eicosapentaenoic (EPA) acids. Ground flaxseed has ALA, but flaxseed oil contains the highest amount. In a study where volunteers consumed flaxseed oil for four weeks, the ALAs significantly decreased pro-inflammatory compounds.
Lignans. Found in flaxseed hulls, these plant chemicals convert to plant estrogen in the digestive tract. Research suggests they may protect against several forms of cancer, prevent heart disease and alleviate menopause symptoms. Whole flaxseed must be ground or bought as meal for lignans to be absorbed by the body. Once opened, a package of flaxseed should be stored in airtight containers in the refrigerator to keep it from going rancid. Flaxseed oil does not have the lignans of whole or ground flaxseeds, so look for brands that have added lignans.
Flavonoids. These compounds are found in all flaxseed and lower levels of low-density lipoprotein (LDL), or “bad” cholesterol. High LDL levels have been linked to a greater risk of heart disease.
Fiber. Dietary fiber accounts for 28%of ground flaxseed’s composition. Soluble fiber has been shown to lower cholesterol and reduce the risk of cancer, while insoluble fiber can help prevent digestive problems.
Note: Flaxseed oil should be avoided by those taking blood-thinners because it may increase bleeding; it should be taken with care by those taking cholesterol-lowering medication because it could lower cholesterol levels too far.
http://blog.arthritis.org/living-with-arthritis/health-benefits-flaxseed-anti-inflammatory/
Eur J Transl Myol. 2016 Dec 15; 26(4): 6033.
α-Linolenic Acid Reduces TNF-Induced Apoptosis in C2C12 Myoblasts by Regulating Expression of Apoptotic Proteins
Felicia Carotenuto,(1)(2) Dario Coletti,(3)(4) Paolo Di Nardo,(1) and Laura Teodori(2)
Author information Copyright and License information Disclaimer
(1) Department Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, Rome, Italy
(2) Diagnostics and Metrology Laboratory, FSN-TECFIS-DIM, ENEA-Frascati, Rome, Italy
(3) Department of Biological Adaptation and Aging B2A, University Pierre et Marie Curie Paris 06, Paris, France
(4) Section of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic and Orthopaedic Sciences, Sapienza University of Rome, Italy
Abstract
Impaired regeneration and consequent muscle wasting is a major feature of muscle degenerative diseases. Nutritional interventions such as adjuvant strategy for preventing these conditions are recently gaining increasing attention. Ingestion of n3-polyunsaturated fatty acids has been suggested as having a positive impact on muscle diseases. We recently demonstrated that a diet enriched with plant derived n3-fatty acid, α-linolenic acid (ALA), exerts potent beneficial effects in preserving skeletal muscle regeneration in models of muscle dystrophy. To better elucidate the underlying mechanism we here investigate on the expression level of the anti- and pro-apoptotic proteins, as well as caspase-3 activity, in C2C12 myoblasts challenged with pathological levels of tumor necrosis factor-α (TNF). The results demonstrated that ALA protective effect on C2C12 myoblasts was associated with a decrease in caspase-3 activity and an increase of the Bcl-2/Bax ratio. Indeed, the effect of ALA was directed to rescuing Bcl-2 expression and to revert Bax translocation to mitochondria both affected in an opposite way by TNF, a major pro-inflammatory cytokine expressed in damaged skeletal muscle. Therefore, ALA counteracts inflammatory signals in the muscle microenvironment and may represent a valuable strategy for ameliorating skeletal muscle pathologies.
Key Words: myoblasts, apoptotic proteins, muscle wasting, inflammation, phytochemicals
α-Linolenic Acid Reduces TNF-Induced Apoptosis in C2C12 Myoblasts by Regulating Expression of Apoptotic Proteins
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5220214/
Alpha-linolenic acid confers protection on mice renal cells against cisplatin-induced nephrotoxicityErman Salih İstifli, Erkan Demir, Halil Mahir Kaplan, Kıvılcım Eren Ateş, Figen Doran
Alpha-linolenic acid protects against lipopolysaccharide-induced acute lung injury through anti-inflammatory and anti-oxidative pathways
Author links open overlay panelXuejiaoZhua1BingWangb1XinyiZhangcd1XiaChendJialiZhudYunZoubJinbaoLib
a Department of Anesthesiology, The Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou, Jiangsu, 215004, China
b Department of Anesthesiology, The 950th Hospital of CPLA Ground Force, Yecheng, Xinjiang Uygur Autonomous Region, 844900, China
c Department of Anesthesiology, Weifang Medical University, Weifang, Shandong, 261000, China
d Department of Anesthesiology, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, 200080, China
Received 30 June 2019, Revised 17 February 2020, Accepted 17 February 2020, Available online 18 February 2020.
Highlights
• ARDS are the major causes of respiratory failure in the intensive care unit worldwide.
• ALA is one of the two essential fatty acids, which are indispensible for health.
• ALA showed anti-inflammatory and anti-oxidative effects in mice with LPS-induced ALI.
• NF-κB pathway may be involved in ALA mediated protective effects.
Abstract
Alpha-linolenic acid (ALA), an important component of polyunsaturated fatty acids (PUFAs), possesses potent anti-inflammatory properties. To date, the effects of ALA on acute lung injury (ALI) remains unknown.
This study was designed to investigate the potential protective effects of ALA on LPS-induced ALI and the underpinning mechanisms. An animal model of ALI was established via intratracheally injection of lipopolysaccharide (LPS, 1 mg/kg).
We found that lung wet/dry weight ratio and protein concentration in Bronchoalveolar lavage fluid (BALF) were dramatically decreased by ALA pretreatment. Treatment with ALA significantly alleviated the infiltration of total cells and neutrophils, while increased the number of the macrophages. ALA significantly inhibited the secretion of proinflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) and increased anti-inflammatory cytokine.
Moreover, we found that the levels of myeloperoxidase (MPO) and malondialdehyde (MDA) were highly increased in LPS-induced ALI, while the activities of glutathione (GSH) and superoxide dismutase (SOD) were decreased, which were reversed by ALA.
ALA attenuated LPS-induced histopathological changes and apoptosis. Furthermore, ALA significantly inhibited the phosphorylation of IκBα and NF-κB (p65) activation in ALI. ALA showed anti-inflammatory effects in mice with LPS-induced ALI. NF-κB pathway may be involved in ALA mediated protective effects.
3.6. ALA suppressed the activation of NF-κB in LPS-induced ALI
It is believed that NF-κB activation is required for the production of inflammatory cytokines. The phosphorylation and degradation of IκBα and the translocation of NF-κB/p65 into the nucleus were determined using western blotting (Fig. 5A). As shown in Fig. 5, LPS significantly induced NF-κB activation (Fig. 5B) and IκBα degradation (Fig. 5C). Pre-treatment with ALA dose-independently inhibited LPS-induced NF-κB activation.
Fig. 5. ALA inhibited the activation of NF-κB on LPS-induced acute lung injury. (A) Protein levels of p-p65, p-IκB, p65 and IκB were evaluated by western blotting analysis. (B&C) Densitometric analysis displayed that the levels of phosphorylated p65 and IκB-α were significantly upregulated after LPS challenge. ALA pretreatment effectively supressed the phosphorylation of p65 and IκB-α. **P < 0.01 vs. Sham group, ##P < 0.01vs. LPS group.
Alpha-linolenic acid protects against lipopolysaccharide-induced acute lung injury through anti-inflammatory and anti-oxidative pathways - ScienceDirect
https://www.sciencedirect.com/science/article/pii/S0882401019311763
Published: 26 August 2017
Alpha-Linolenic Acid Treatment Reduces the Contusion and Prevents the Development of Anxiety-Like Behavior Induced by a Mild Traumatic Brain Injury in Rats
Taiza H. Figueiredo, Carolina L. Harbert, Volodymyr Pidoplichko, Camila P. Almeida-Suhett, Hongna Pan, Katia Rossetti, Maria F. M. Braga & Ann M. Marini
Molecular Neurobiology volume 55, pages187–200(2018)Cite this article
Abstract
Approximately, 1.7 million Americans suffer a TBI annually and TBI is a major cause of death and disability. The majority of the TBI cases are of the mild type and while most patients recover completely from mild TBI (mTBI) about 10% result in persistent symptoms and some result in lifelong disability. Anxiety disorders are the second most common diagnosis post-TBI. Of note, TBI-induced anxiety disorders are difficult to treat and remain a chronic condition suggesting that new therapies are needed. Previous work from our laboratory demonstrated that a mild TBI induced an anxiety-like phenotype, a key feature of the human condition, associated with loss of GABAergic interneurons and hyperexcitability in the basolateral amygdala (BLA) in rodents 7 and 30 days after a controlled cortical impact (CCI) injury. We now confirm that animals display significantly increased anxiety-like behavior 30 days after CCI. The anxiety-like behavior was associated with a significant loss of GABAergic interneurons and significant reductions in the frequency and amplitude of spontaneous and miniature GABAA-receptor-mediated inhibitory postsynaptic currents (IPSCs) in the BLA. Significantly, subchronic treatment with alpha-linolenic acid (ALA) after CCI prevents the development of anxiety-like behavior, the loss of GABAergic interneurons, hyperexcitability in the BLA and reduces the impact injury. Taken together, administration of ALA after CCI is a potent therapy against the neuropathology and pathophysiological effects of mTBI in the BLA.
Alpha-Linolenic Acid Treatment Reduces the Contusion and Prevents the Development of Anxiety-Like Behavior Induced by a Mild Traumatic Brain Injury in Rats | SpringerLink
https://link.springer.com/article/10.1007%2Fs12035-017-0732-y
Journal of Analytical and Applied Pyrolysis
Volumes 58–59, 1 April 2001,
Thermally assisted hydrolysis and methylation-pyrolysis-gas chromatography/mass spectrometry of light-aged linseed oil
panelDominiqueScalaroneMassimoLazzariOscarChiantoreepartment of Chemistry IPM, University of Torino, Via Giuria 7, 10125 Torino, Italy
Abstract
Drying and photooxidative ageing of thin films of linseed oil has been investigated under solar light accelerated ageing conditions by means of thermally assisted hydrolysis and methylation–pyrolysis–gas chromatography/mass spectrometry. The main pyrolysis product after the ageing process was found to be azelaic acid, in agreement with results reported in literature on naturally aged samples. The kinetic of azelaic acid formation during degradation has been determined from the pyrolysis experiments, and the results are fully compatible with those previously obtained by Fourier transform infrared spectroscopy. In this work the method for quantitative determination of azelaic acid from aged linseed oil, proposed by Chiavari et al., 1993 [G. Chiavari, G.C. Galletti, G. Lanterna, R. Mazzeo, J. Anal. Appl. Pyrolysis, 24 (1993) 227] is shown to be also valid under more strenuous ageing conditions than those occurring in typical indoor expositions.
Thermally assisted hydrolysis and methylation-pyrolysis-gas chromatography/mass spectrometry of light-aged linseed oil - ScienceDirect
https://www.sciencedirect.com/science/article/pii/S0165237000001273
Antibacterial activity of hydrolysed linseed oil and linolenic acid against methicillin-resistant Staphylococcus aureus.
Author(s) : Mcdonald, M. I. ; Graham, I. ; Harvey, K. J. ; Sinclair, A.
Correspondence : Lancet 1981 Vol.2 pp.1056
Abstract : The antibacterial activity of hydrolysed linseed oil against methicillin-resistant Staphylococcus aureus (MRSA) was compared with that of linolenic acid. At a concentration of 0.025% both linolenic acid and hydrolysed linseed oil inhibited all 91 strains of MRSA tested. The authors suggest that preparations containing hydrolysed linseed oil could be useful in the eradication of the staphylococcal carrier state and in prophylaxis. Antonnette A. Wieneke.
Antibacterial activity of hydrolysed linseed oil and linolenic acid against methicillin-resistant Staphylococcus aureus.
https://www.cabdirect.org/cabdirect/abstract/19822701462
Lipids Health Dis. 2016; 15: 206.
Published online 2016 Nov 25. doi: 10.1186/s12944-016-0377-2
Combination of aspirin with essential fatty acids is superior to aspirin alone to prevent or ameliorate sepsis or ARDS
Undurti N Dascorresponding author1,2
Abstract
It has been suggested that aspirin may be of benefit in treating sepsis and ARDS in view of its ability to block cyclo-oxygenase-1 (COX-1) and COX-2 activities; inhibit nuclear factor kappa B (NF-κB); enhance the production of endothelial nitric oxide (eNO) and lipoxin A4 (LXA4). Our previous studies revealed that plasma phospholipid content of arachidonic acid (AA) and eicosapentaenoic acid (EPA) is low in patients with sepsis. This implies that beneficial actions of aspirin in sepsis and ARDS is unlikely to be obtained in view of deficiency of AA and EPA, the precursors of LXA4 and resolvins respectively that are potent anti-inflammatory compounds and enhancers of eNO generation. In view of this, I propose that a combination of aspirin and AA and EPA (and possibly, docosahexaenoic acid, DHA) is likely to be superior in the management of sepsis and ARDS compared to aspirin alone. This suggestion is supported by the recent observation that trauma patients with uncomplicated recoveries had higher resolvin pathway gene expression and lower gene expression ratios of leukotriene: resolvin pathways.
Keywords: Aspirin, Essential fatty acids, Acute respiratory distress syndrome, Sepsis, Lipoxin A4, Resolvin, Protectins, Arachidonic acid, Eicosapentaenoic acid, Docosahexaenoic acid, Nitric oxide, Cyclo-oxygenase, Lipoxygenase
Combination of aspirin with essential fatty acids is superior to aspirin alone to prevent or ameliorate sepsis or ARDS
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5124295/
Int J Mol Sci. 2019 Oct; 20(20): 5028.
Effects of Omega-3 Fatty Acids on Immune Cells
Saray Gutiérrez, Sara L Svahn, and Maria E Johansson*
Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, 405 30 Gothenburg, Sweden;
Abstract
Alterations on the immune system caused by omega-3 fatty acids have been described for 30 years. This family of polyunsaturated fatty acids exerts major alterations on the activation of cells from both the innate and the adaptive immune system, although the mechanisms for such regulation are diverse. First, as a constitutive part of the cellular membrane, omega-3 fatty acids can regulate cellular membrane properties, such as membrane fluidity or complex assembly in lipid rafts. In recent years, however, a new role for omega-3 fatty acids and their derivatives as signaling molecules has emerged. In this review, we describe the latest findings describing the effects of omega-3 fatty acids on different cells from the immune system and their possible molecular mechanisms.
Keywords: polyunsaturated fatty acids, PUFAs, omega-3 fatty acids, α-linolenic acid, ALA, eicosapentaenoic acid, EPA, docosahexaenoic acid, DHA, immune cells, immune response, phagocytosis, immune-modulation, anti-inflammatory, migration, presentation, cytokines, antibody production
Concluding Remarks
In the present review, we have summarized the main findings regarding the immunomodulatory effects of omega-3 fatty acids on the different cells that conform the immune system (summarized in Table 1). To our knowledge, from all the immune cells investigated to date, none of them has been found to be inert to dietary omega-3 fatty acids. Generally, ALA, DHA, and EPA exert an inhibitory effect on the activation of immune cells from both the innate and the adaptive branch. Interestingly, some specific immune functions are promoted by dietary omega-3 fatty acids in specific immune cell types, i.e., phagocytosis by macrophages and neutrophils or Treg differentiation, suggesting that omega-3 fatty acids do not act as unspecific immune-repressors.
Effects of Omega-3 Fatty Acids on Immune Cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834330/
Int Urol Nephrology. 2016 Aug
Effect of flaxseed oil on serum systemic and vascular inflammation markers and oxidative stress in hemodialysis patients: a randomized controlled trial
Abstract
Purpose: The aim of this study was to investigate the effects of flaxseed oil consumption on serum systemic and vascular inflammation markers, and oxidative stress in hemodialysis (HD) patients.
Methods: In this randomized, double-blind, clinical trial, 34 HD patients were randomly assigned to either the flaxseed oil or the control group. The patients in the flaxseed oil group received 6 g/day flaxseed oil for 8 week, whereas the control group received 6 g/day medium-chain triglycerides (MCT) oil. At baseline and the end of week 8, serum concentrations of high-sensitive C-reactive protein (hs-CRP), soluble intercellular adhesion molecule type 1 (sICAM-1), soluble vascular cell adhesion molecule type 1 (sVCAM-1), sE-selectin, and malondialdehyde (MDA) were measured after a 12- to 14-h fast.
Results: Serum hs-CRP, a systemic inflammation marker, and sVCAM-1, a vascular inflammation marker, reduced significantly in the flaxseed oil group at the end of week 8 compared to baseline (P < 0.05), and the reductions were significant in comparison with the MCT oil group (P < 0.05). There were no significant differences between the two groups in mean changes in serum sICAM-1, sE-selectin, and MDA.
Conclusion: This study indicates that daily consumption of 6 g flaxseed oil reduces serum hs-CRP and sVCAM-1, which are two risk factors for CVD. Therefore, the inclusion of flaxseed oil in the usual diet of HD patients can be considered as a strategy for reducing CVD risk factors.
Keywords: Flaxseed oil; Hemodialysis; Oxidative stress; Systemic inflammation; Vascular inflammation.Effect of flaxseed oil on serum systemic and vascular inflammation markers and oxidative stress in hemodialysis patients: a randomized controlled trial - PubMed
https://pubmed.ncbi.nlm.nih.gov/27115157/
.png)
