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多糖通过抑制氧化应激和肠道渗漏来预防酒精诱导的肝损伤和炎症。

polysaccharide prevents alcohol-induced hepatic injury and inflammation by repressing oxidative stress and gut leakiness.

作者信息

Jiang Yue-Hang, Wang Lei, Chen Wei-Dong, Duan Yu-Ting, Sun Ming-Jie, Huang Jia-Jing, Peng Dai-Yin, Yu Nian-Jun, Wang Yan-Yan, Zhang Yue

机构信息

School of Pharmacy, Anhui University of Chinese Medicine, Hefei, China.

MOE-Anhui Joint Collaborative Innovation Center for Quality Improvement of Anhui Genuine Chinese Medicinal Materials, Hefei, China.

出版信息

Front Nutr. 2022 Aug 17;9:963598. doi: 10.3389/fnut.2022.963598. eCollection 2022.

DOI:10.3389/fnut.2022.963598
PMID:36061887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9428680/
Abstract

Alcoholic liver disease (ALD) is a major worldwide chronic liver disease accompanied by hepatic inflammation, gut leakiness, and abnormal oxidative stress. Our previous study demonstrated substantial hepatoprotective activity of the active polysaccharide (PCP-1C). The present study explored whether PCP-1C protects against ALD among hepatic inflammation, gut leakiness, and abnormal oxidative stress. The results showed that PCP-1C significantly improved alcohol-induced liver injury by decreasing serum biochemical parameters, alleviating hepatic steatosis, and reducing lipid accumulation caused by ALD. Moreover, PCP-1C treatment reduced hepatic inflammation by inhibiting the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) signaling pathway and also improved hepatocyte apoptosis by inhibiting the cytochrome P450 2E1 (CYP2E1)/reactive oxygen species (ROS)/mitogen-activated protein kinases (MAPKs) signaling pathway. Regarding intestinal protection, PCP-1C could repair the intestinal barrier and reduce lipopolysaccharide (LPS) leakage. Generally, PCP-1C exerts a positive therapeutic effect on ALD, which may play a pivotal of decreasing inflammatory factor release, inhibiting oxidative stress and apoptosis, and improving intestinal barrier injury.

摘要

酒精性肝病(ALD)是一种全球性的主要慢性肝病,伴有肝脏炎症、肠道通透性增加和异常氧化应激。我们之前的研究表明活性多糖(PCP-1C)具有显著的肝脏保护活性。本研究探讨了PCP-1C在肝脏炎症、肠道通透性增加和异常氧化应激方面是否对ALD具有保护作用。结果表明,PCP-1C通过降低血清生化参数、减轻肝脏脂肪变性和减少ALD引起的脂质积累,显著改善了酒精诱导的肝损伤。此外,PCP-1C治疗通过抑制Toll样受体4(TLR4)/核因子-κB(NF-κB)信号通路减轻肝脏炎症,并通过抑制细胞色素P450 2E1(CYP2E1)/活性氧(ROS)/丝裂原活化蛋白激酶(MAPKs)信号通路改善肝细胞凋亡。关于肠道保护,PCP-1C可以修复肠道屏障并减少脂多糖(LPS)泄漏。总体而言,PCP-1C对ALD具有积极的治疗作用,这可能在减少炎症因子释放、抑制氧化应激和细胞凋亡以及改善肠道屏障损伤方面发挥关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/0a7c25217099/fnut-09-963598-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/ca1749cf6693/fnut-09-963598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/923d5daf9961/fnut-09-963598-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/5e3b5c64acbd/fnut-09-963598-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/49efaa467585/fnut-09-963598-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/0a7c25217099/fnut-09-963598-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/ca1749cf6693/fnut-09-963598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/923d5daf9961/fnut-09-963598-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/5e3b5c64acbd/fnut-09-963598-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/49efaa467585/fnut-09-963598-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f81/9428680/0a7c25217099/fnut-09-963598-g005.jpg

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