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氧化应激和炎症引发的糖尿病发病机制:小檗碱对其的抑制作用

The Pathogenesis of Diabetes Mellitus by Oxidative Stress and Inflammation: Its Inhibition by Berberine.

作者信息

Ma Xueling, Chen Zhongjun, Wang Le, Wang Gesheng, Wang Zihui, Dong XiaoBo, Wen Binyu, Zhang Zhichen

机构信息

Beijing University of Chinese Medicine, Beijing, China.

Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian, China.

出版信息

Front Pharmacol. 2018 Jul 27;9:782. doi: 10.3389/fphar.2018.00782. eCollection 2018.

DOI:10.3389/fphar.2018.00782
PMID:30100874
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6072898/
Abstract

A substantial knowledge on the pathogenesis of diabetes mellitus (DM) by oxidative stress and inflammation is available. Berberine is a biologically active botanical that can combat oxidative stress and inflammation and thus ameliorate DM, especially type 2 DM. This article describes the potential of berberine against oxidative stress and inflammation with special emphasis on its mechanistic aspects. In diabetic animal studies, the modified levels of proinflammatory cytokines and oxidative stress markers were observed after administering berberine. In renal, fat, hepatic, pancreatic and several others tissues, berberine-mediated suppression of oxidative stress and inflammation was noted. Berberine acted against oxidative stress and inflammation through a very complex mechanism consisting of several kinases and signaling pathways involving various factors, including NF-κB (nuclear factor-κB) and AMPK (AMP-activated protein kinases). Moreover, MAPKs (mitogen-activated protein kinases) and Nrf2 (nuclear factor erythroid-2 related factor 2) also have mechanistic involvement in oxidative stress and inflammation. In spite of above advancements, the mechanistic aspects of the inhibitory role of berberine against oxidative stress and inflammation in diabetes mellitus still necessitate additional molecular studies. These studies will be useful to examine the new prospects of natural moieties against DM.

摘要

关于氧化应激和炎症在糖尿病发病机制方面已有大量知识。黄连素是一种具有生物活性的植物成分,能够对抗氧化应激和炎症,从而改善糖尿病,尤其是2型糖尿病。本文描述了黄连素在对抗氧化应激和炎症方面的潜力,并特别强调其作用机制。在糖尿病动物研究中,给予黄连素后观察到促炎细胞因子和氧化应激标志物水平发生了改变。在肾脏、脂肪、肝脏、胰腺及其他多种组织中,均发现黄连素可介导氧化应激和炎症的抑制。黄连素通过一种非常复杂的机制对抗氧化应激和炎症,该机制由几种激酶和信号通路组成,涉及包括核因子κB(NF-κB)和AMP激活蛋白激酶(AMPK)在内的多种因素。此外,丝裂原活化蛋白激酶(MAPKs)和核因子红细胞2相关因子2(Nrf2)在氧化应激和炎症中也具有机制上的参与。尽管有上述进展,但黄连素在糖尿病中对抗氧化应激和炎症的抑制作用的机制仍需要更多的分子研究。这些研究将有助于探索天然成分对抗糖尿病的新前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b867/6072898/427a7cc4d3bc/fphar-09-00782-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b867/6072898/4bee50476c8e/fphar-09-00782-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b867/6072898/5c77647f28a1/fphar-09-00782-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b867/6072898/427a7cc4d3bc/fphar-09-00782-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b867/6072898/4bee50476c8e/fphar-09-00782-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b867/6072898/5c77647f28a1/fphar-09-00782-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b867/6072898/427a7cc4d3bc/fphar-09-00782-g0003.jpg

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