Authors
Feng Li, Zhehao Liu, Bi Wang, Jinqiang Liang, Jiaxiu Liu, Xiaobin Wei
Published in
Molecular and cellular biochemistry. Jul 01, 2026. Epub Jul 01, 2026.
Abstract
Liver fibrosis is usually accompanied by abnormal activation of hepatic stellate cells. Exosomal microRNAs play important roles in the development of liver fibrosis. Our previous study confirmed that Ellagic acid (EA) is one of the main bloodstream components of Scutellaria barbata, a traditional Chinese medicinal herb. This study aimed to explore the effects of EA on hepatic stellate cells in liver fibrosis. First, a CCl4-induced mouse model of liver fibrosis was used to evaluate the effects of EA administration on the histopathology and histochemical staining of liver tissue in mice with liver fibrosis, while simultaneously assessing serum markers of liver function; Second, RT-PCR was used to detect fibrosis-related genes, inflammation-related genes and matrix metalloproteinase-related genes. Third, exosome-enriched fraction miRNAs from liver tissues were sequenced and PCR-verified for differential expression. Finally, in vitro experiments were performed on murine hepatic stellate cells (JS-1) and human hepatic stellate cells (LX-2) using flow cytometry and Western blotting (WB) to apoptosis-related proteins. Animal studies demonstrated that Scutellaria barbata and its natural active component EA can significantly ameliorate hepatic histopathology in the mouse model of liver fibrosis. Furthermore, EA effectively improves serum liver function parameters, reduces the expression of fibrosis-related, inflammation-related and matrix metalloproteinase-related genes, and markedly reduces elevated miR-182-5p expression in the fibrotic model. Cellular experiments demonstrated that inhibition of miR-182-5p promotes the expression of proteins associated with apoptosis in hepatic stellate cells, thereby accelerating apoptosis in these cells. In summary, EA from S. barbata may accelerates hepatic stellate cell apoptosis during liver fibrosis by inhibiting miR-182-5p.
PMID:
42384345
Bibliographic data and abstract were imported from PubMed on 01 Jul 2026.
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