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多糖通过调节炎症和细胞凋亡改善四氯化碳诱导的肝纤维化。

polysaccharides ameliorated carbon tetrachloride-induced liver fibrosis through modulating inflammation and apoptosis.

机构信息

School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, 453003, PR China.

College of Life Science, Shandong Agricultural University, Taian, 271018, PR China.

出版信息

Food Funct. 2022 Oct 31;13(21):11125-11141. doi: 10.1039/d2fo01349e.

Abstract

Liver fibrosis is a serious global public health problem, owing to a lack of effective treatment. polysaccharides (CP), isolated from , possess multiple biological activities. In our work, water-soluble polysaccharides (CPa) from CP were obtained by column chromatography. We attempted to investigate the anti-liver fibrosis ability of CPa and the underlying mechanisms of its activity against liver fibrosis and , as well as its structure. results showed that CPa reduced the release of inflammatory factors and apoptosis by modulating the TLR4/MyD88/NF-κB, Bcl-2/Bax and caspase family signaling pathways, thereby attenuating serum enzymes, ROS, α-SMA, collagen III, TGFβ1, p-Smad3, and collagen volume fraction, and increasing the defense capacity of the antioxidant defense system in tetrachloride (CCl)-induced liver fibrosis mice. The result was used to verify that, , CPa regulated the TLR4/MyD88/NF-κB, Bcl-2/Bax and caspase family signaling pathways to prevent the activation of HSCs and accelerate HSCs apoptosis in activated LX-2 cells. Thus, CPa could attenuate liver fibrosis by mediating inflammation and apoptosis. Meantime, the structural analysis showed that CPa is a polysaccharide with α- and β-configurations including Fuc, Man, Gal and Glc with a of 524 kDa. These findings indicate that CPa could be developed into functional foods and drugs against liver fibrosis.

摘要

肝纤维化是一个严重的全球性公共卫生问题,由于缺乏有效的治疗方法。从 中分离得到的多糖(CP)具有多种生物活性。在我们的工作中,通过柱层析从 CP 中获得了水溶性多糖(CPa)。我们试图研究 CPa 的抗肝纤维化能力及其对肝纤维化的作用机制,以及其结构。结果表明,CPa 通过调节 TLR4/MyD88/NF-κB、Bcl-2/Bax 和半胱天冬酶家族信号通路,降低炎症因子和细胞凋亡的释放,从而减轻血清酶、ROS、α-SMA、胶原 III、TGFβ1、p-Smad3 和胶原容积分数,增强四氯化碳(CCl)诱导的肝纤维化小鼠的抗氧化防御系统的防御能力。结果用于验证 CPa 通过调节 TLR4/MyD88/NF-κB、Bcl-2/Bax 和半胱天冬酶家族信号通路来防止活化的 HSCs 激活,并加速活化的 LX-2 细胞中 HSCs 的凋亡。因此,CPa 可以通过介导炎症和凋亡来减轻肝纤维化。同时,结构分析表明,CPa 是一种具有α-和β构型的多糖,包括 Fuc、Man、Gal 和 Glc,分子量为 524 kDa。这些发现表明,CPa 可以开发成对抗肝纤维化的功能性食品和药物。

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