肝星状细胞
时间1
癌症研究
细胞外基质
纤维化
肝硬化
化学
肝纤维化
炎症
基质金属蛋白酶
转化生长因子
细胞生物学
信号转导
细胞生长
生物
药理学
医学
基因
基因表达
生物化学
免疫学
内科学
内分泌学
作者
NULL AUTHOR_ID,Sucheewin Krobthong,Yodying Yingchutrakul,NULL AUTHOR_ID,NULL AUTHOR_ID,Krai Daowtak,NULL AUTHOR_ID,NULL AUTHOR_ID
出处
期刊:Biomolecules
[MDPI AG]
日期:2024-07-05
卷期号:14 (7): 800-800
摘要
Liver fibrosis, a consequence of chronic liver damage or inflammation, is characterized by the excessive buildup of extracellular matrix components. This progressive condition significantly raises the risk of severe liver diseases like cirrhosis and hepatocellular carcinoma. The lack of approved therapeutics underscores the urgent need for novel anti-fibrotic drugs. Hepatic stellate cells (HSCs), key players in fibrogenesis, are promising targets for drug discovery. This study investigated the anti-fibrotic potential of Citrus hystrix DC. (KL) and its bioactive compound, β-citronellol (β-CIT), in a human HSC cell line (LX-2). Cells exposed to TGF-β1 to induce fibrogenesis were co-treated with crude KL extract and β-CIT. Gene expression was analyzed by real-time qRT-PCR to assess fibrosis-associated genes (ACTA2, COL1A1, TIMP1, SMAD2). The release of matrix metalloproteinase 9 (MMP-9) was measured by ELISA. Proteomic analysis and molecular docking identified potential signaling proteins and modeled protein–ligand interactions. The results showed that both crude KL extract and β-CIT suppressed HSC activation genes and MMP-9 levels. The MAPK signaling pathway emerged as a potential target of β-CIT. This study demonstrates the ability of KL extract and β-CIT to inhibit HSC activation during TGF-β1-induced fibrogenesis, suggesting a promising role of β-CIT in anti-hepatic fibrosis therapies.
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