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D-chiro-inositol enriched Fagopyrum tataricum (L.) Gaench extract alleviates mitochondria' malfunction and inhibits ER stress/JNK associated inflammation in the endothelium

文献类型： 外文期刊

作者： Zhang, Bobo 1 ; Gao, Caifeng 1 ; Li, Yunlong 2 ; Wang, Min 1 ;

作者机构： 1.Northwest A&F Univ, Coll Food Sci & Engn, Yangling 712100, Peoples R China

2.Shanxi Acad Agr Sci, Inst Agr Prod Proc, Taiyuan 030031, Shanxi, Peoples R China

关键词： D-chiro-inositol enriched tartary buckwheat extract;Mitochondrial malfunction;ER stress;JNK;Caspase-3

期刊名称：JOURNAL OF ETHNOPHARMACOLOGY （ 影响因子：4.36； 五年影响因子：4.488 ）

ISSN： 0378-8741

年卷期： 2018 年 214 卷

页码：

收录情况： SCI

摘要： Ethnopharrnacological relevance: Tartary buckwheat is a food medicine dual-use crop with healing effects on cardiovascular diseases and type2 diabetes. It has been proposed that endothelial dysfunction is the initial lesion in these diseases and it's associated with mitochondria] dysfunction, endoplasmic reticulum (ER) stress and inflammation. D-chiro-inositol (DCI) is a bioactive compound of Tartary buckwheat and is always deficit in type2 diabetes. However, it remains unknown whether DCI-enriched Tartary buckwheat extract can ameliorate mitochondrial dysfunction, ER stress and inflammation in the endothelium. Material and methods: Endothelial cells were treated with palmitic acid (PA) and mice were fed with high fat diet (HFD). The effects of DCI-enriched Tartary buckwheat bran extract (TBBE) on superoxide anion generation, dynamin-related protein 1 (Drpl), mitofusin2 (Mfn2), inositol-requiring enzyme-1 alpha (IRE1 alpha) and Jun n-terminal kinase (JNK) activation and inflammation in the endothelium against lipotoxicity were investigated. Results: In endothelial cells, TBBE significantly inhibited oxidative stress. Meanwhile, in HFD-fed mice and PA induced cells, TBBE regulated Drpl phosphorylation and inhibited its activation, implying the protective effect of TBBE on mitochondrial morphology. As a result, TBBE protected mitochondrial function. Additionally, TBBE inhibited ER stress and reduced the production of IL-6 and VCAM-1, associated with JNK pathway, thereby inhibiting the caspase-3 activation in vivo and in vitro. Conclusions: Taken together, this study indicated the beneficial role of TBBE in endothelial inflammation, with emphasis on mitochondria, dysfunction, ER stress and JNK activation.

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