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白花丹素可预防四氯化碳诱导的小鼠肝损伤和纤维化。

Byakangelicin protects against carbon tetrachloride-induced liver injury and fibrosis in mice.

机构信息

State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin, China.

Tianjin Key Laboratory of Molecular Drug Research, Tianjin International Joint Academy of Biomedicine, Tianjin, China.

出版信息

J Cell Mol Med. 2020 Aug;24(15):8623-8635. doi: 10.1111/jcmm.15493. Epub 2020 Jul 9.

DOI:10.1111/jcmm.15493
PMID:32643868
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7412405/
Abstract

Liver fibrosis is a disease caused by long-term damage that is related to a number of factors. The current research on the treatment of liver fibrosis mainly focuses on the activation of hepatic stellate cell, in addition to protecting liver cells. byakangelicin has certain anti-inflammatory ability, but its effect on liver fibrosis is unclear. This study aims to explore whether byakangelicin plays a role in the development of liver fibrosis and to explore its mechanism. We determined that byakangelicin has a certain ability to resist fibrosis and reduce liver cell damage in a model of carbon tetrachloride-induced liver fibrosis in mice. Thereafter, we performed further verification in vitro. The signalling pathways of two important pro-fibrotic cytokines, transforming growth factor-β and platelet-derived growth factor, were studied. Results showed that byakangelicin can inhibit related pathways. According to the hepatoprotective effect of byakangelicin observed in animal experiments, we studied the effect of byakangelicin on 4-HNE-induced hepatocyte (HepG2) apoptosis and explored its related pathways. The results showed that byakangelicin could attenuate 4-HNE-induced hepatocyte apoptosis via inhibiting ASK-1/JNK signalling. In conclusion, byakangelicin could improve carbon tetrachloride-induced liver fibrosis and liver injury by inhibiting hepatic stellate cell proliferation and activation and suppressing hepatocyte apoptosis.

摘要

肝纤维化是一种由多种因素引起的长期损伤相关疾病。目前，肝纤维化治疗的研究主要集中在肝星状细胞的激活上，此外还包括保护肝细胞。byakangelicin 具有一定的抗炎能力，但它对肝纤维化的作用尚不清楚。本研究旨在探讨 byakangelicin 是否在肝纤维化的发展中起作用，并探讨其机制。我们确定 byakangelicin 在四氯化碳诱导的小鼠肝纤维化模型中具有一定的抗纤维化能力，并减轻肝损伤。此后，我们在体外进行了进一步验证。研究了两种重要的促纤维化细胞因子转化生长因子-β和血小板衍生生长因子的信号通路。结果表明，byakangelicin 可以抑制相关通路。根据动物实验中观察到的 byakangelicin 的保肝作用，我们研究了 byakangelicin 对 4-HNE 诱导的肝细胞（HepG2）凋亡的影响，并探讨了其相关通路。结果表明，byakangelicin 通过抑制 ASK-1/JNK 信号通路减轻 4-HNE 诱导的肝细胞凋亡。总之，byakangelicin 可以通过抑制肝星状细胞增殖和活化以及抑制肝细胞凋亡来改善四氯化碳诱导的肝纤维化和肝损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/2a80cbc58ad0/JCMM-24-8623-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/e409ba2fc839/JCMM-24-8623-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/103c10d6de13/JCMM-24-8623-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/004dc84aa9c7/JCMM-24-8623-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/219768aa56d8/JCMM-24-8623-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/81cecc52269e/JCMM-24-8623-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/2a80cbc58ad0/JCMM-24-8623-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/e409ba2fc839/JCMM-24-8623-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/103c10d6de13/JCMM-24-8623-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/004dc84aa9c7/JCMM-24-8623-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/219768aa56d8/JCMM-24-8623-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/81cecc52269e/JCMM-24-8623-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c08b/7412405/2a80cbc58ad0/JCMM-24-8623-g006.jpg

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