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Hepatology. 2022 Jan;75(1):219-228. doi: 10.1002/hep.32163. Epub 2021 Dec 10.
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Tyrosine kinase inhibitor neratinib attenuates liver fibrosis by targeting activated hepatic stellate cells.酪氨酸激酶抑制剂奈拉替尼通过靶向激活的肝星状细胞来减轻肝纤维化。
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丹皮酚通过抑制SMAD2/3和STAT3信号通路抑制肝星状细胞活化发挥肝脏保护作用。

Hepatoprotective effects of paeonol by suppressing hepatic stellate cell activation via inhibition of SMAD2/3 and STAT3 pathways.

作者信息

Jeong Hye-Jin, Koo Sooyeon, Kang Yeon-Ho, Kim Tae Won, Kim Hye Kyung, Park Yong Joo

机构信息

College of Pharmacy, Kyungsung University, Busan, 48434 Republic of Korea.

Brain Busan 21 plus Research Project Group, Kyungsung University, Busan, Republic of Korea.

出版信息

Food Sci Biotechnol. 2023 Nov 18;33(8):1939-1946. doi: 10.1007/s10068-023-01440-9. eCollection 2024 Jun.

DOI:10.1007/s10068-023-01440-9
PMID:38752108
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11091017/
Abstract

UNLABELLED

Hepatic stellate cell (HSC) activation is a key event in extracellular matrix accumulation, causing hepatic fibrosis. Therefore, identifying chemicals that inhibit HSC activation is an important therapeutic strategy for hepatic fibrosis. The aim of this study was to investigate the therapeutic effects of paeonol on HSC activation. In LX-2 cells, paeonol inhibited the expression of collagen and decreased the expression of HSC activation markers. In mice with thioacetamide-induced liver fibrosis, paeonol treatment decreased the serum levels of aspartate aminotransferase and alanine transaminase and mRNA expression of α-smooth muscle actin, platelet-derived growth factor-β, and connective-tissue growth factor. Investigation of the underlying molecular mechanism of paeonol showed that paeonol inhibits the SMAD2/3 and STAT3 signaling pathways that are important for HSC activation. On the basis of these results, paeonol should be investigated and developed further for hepatic fibrosis treatment.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s10068-023-01440-9.

摘要

未标记

肝星状细胞（HSC）激活是细胞外基质积累的关键事件，可导致肝纤维化。因此，鉴定抑制HSC激活的化学物质是肝纤维化的重要治疗策略。本研究旨在探讨丹皮酚对HSC激活的治疗作用。在LX-2细胞中，丹皮酚抑制胶原蛋白的表达并降低HSC激活标志物的表达。在硫代乙酰胺诱导的肝纤维化小鼠中，丹皮酚治疗降低了天冬氨酸转氨酶和丙氨酸转氨酶的血清水平以及α-平滑肌肌动蛋白、血小板衍生生长因子-β和结缔组织生长因子的mRNA表达。对丹皮酚潜在分子机制的研究表明，丹皮酚抑制对HSC激活很重要的SMAD2/3和STAT3信号通路。基于这些结果，应进一步研究和开发丹皮酚用于肝纤维化治疗。

补充信息

在线版本包含可在10.1007/s10068-023-01440-9获取的补充材料。