沒食子酸抗氧化與促氧化特性於促進肝星狀細胞死亡之探討

Gallic Acid-induced cell death on Hepatic Stellate Cells

林明輝(Ming-Hui Lin)

指導教授 ： 吳立真

國立暨南國際大學/科技學院/生物醫學科技研究所/碩士(2008年)

https://doi.org/10.6837/NCNU.2008.00011

摘要

無資料

關鍵字

肝星狀細胞,沒食子酸,活性氧分子

並列摘要

Liver fibrosis is a chronic liver disease, mainly attributed by a process of excess extracellular matrix, which damages the structure of liver. The progression of fibrosis can develop cirrhosis or even cancer. Activation of Hepatic stellate cells (HSCs) is critical to the development of liver fibrosis; activated HSCs express a variety of cytokines, leading to inflammation. Therefore, therapeutic strategy mostly against fibrosis is to suppress the activation of HSC to avoid with the adverse effect like induction of inflammatory response of kupffer cells & endothelial cells.
Gallic acid (GA; 3, 4, 5-trihydroxybenzoic acid) is a naturally occurring compound found in many vegetables. Its anti-oxidant & pro-oxidant properties are believed to show liver-protective effect, mainly because it inhibits cell growth on HSCs and the development of liver fibrosis.
The aim of this study is to investigate GA-induced cell death on HSCs and the signaling pathway involved. The results suggested that GA-induced reactive oxygen species (ROS) leads to cell death. The studies on type of cell death including cell cycle, DNA condensation, DNA fragmentation, change of mitochondrial membrane potential, and caspase-3 activity implied that GA induced HSC death in the process of necrosis. Moreover, catalase expression evaluated by western blotting and activity assay showed that catalase expression was regulated differently on cell types in response to scavenge ROS. The related signaling pathway may be the key to explain cell death on HSCs. HSCs cultured in Hepatocytes (HC) conditioned medium were resistant to inhibitory effect of GA. Similar result was found in HSC & HC co-culture in transwell system. The results demonstrated the role of hepatocyte in paracrine regulation of HSC proliferation. Lastly, liposomal delivery system facilitated the inhibitory effect of GA; this may lead to a new strategy of targeting HSCs.

並列關鍵字

Hepatic Stellate cell (HSC), Gallic acid (GA), ROS (Reactive Oxygen Species)

參考文獻

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