The Fifth Department of Chemotherapy, Affiliated Tumor Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Guangxi Key laboratory of Regenerative Medicine, Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Aging (Albany NY). 2020 Apr 13;12(7):6058-6066. doi: 10.18632/aging.103002.
Hepatic fibrosis arises from a sustained wound-healing response to chronic liver injury. Because the occurrence and development of hepatic fibrosis is always associated with chronic inflammation, controlling inflammation within the liver may be an effective means of controlling the development and progression of hepatic fibrosis. Aspirin is a non-steroidal anti-inflammatory drug used to relieve both inflammatory symptoms and pain. The results of our study showed that aspirin significantly attenuated hepatic inflammation and fibrosis. Aspirin effectively inhibited the activation and proliferation of hepatic stellate cells (HSCs), which led to downregulation of inflammatory factors, including IL-6 and TNF-α in those cells. Aspirin also downregulated expression of Toll-like receptor-4 (TLR4) on HSCs, as well as its downstream mediators, MyD88 and NF-κB. The results of our study demonstrate aspirin's potential to inhibit the development of hepatic fibrosis and the molecular mechanism by which it acts. They suggest aspirin may be an effective therapeutic agent for the treatment of hepatic fibrosis.
肝纤维化是由慢性肝损伤引起的持续的创伤愈合反应引起的。由于肝纤维化的发生和发展总是与慢性炎症有关，因此控制肝脏内的炎症可能是控制肝纤维化发展和进展的有效手段。阿司匹林是一种用于缓解炎症症状和疼痛的非甾体抗炎药。我们的研究结果表明，阿司匹林显著减轻了肝炎症和纤维化。阿司匹林有效抑制了肝星状细胞（HSCs）的激活和增殖，导致细胞内的炎症因子（包括 IL-6 和 TNF-α）下调。阿司匹林还下调了 HSCs 上 Toll 样受体 4（TLR4）及其下游介质 MyD88 和 NF-κB 的表达。我们的研究结果表明，阿司匹林具有抑制肝纤维化发展的潜力及其作用的分子机制。它们表明阿司匹林可能是治疗肝纤维化的有效治疗药物。
