Abscisic acid ameliorates oxidative stress, inflammation, and apoptosis in thioacetamide-induced hepatic fibrosis by regulating the NF-кB signaling pathway in mice.

Chen, Xueyan; Ding, Chuanbo; Liu, Wencong; Liu, Xinglong; Zhao, Yingchun; Zheng, Yinan; Dong, Ling; Khatoon, Sadia; Hao, Mingqian; Peng, Xiaojuan; Zhang, Yue; Chen, Huiying

The purpose of this study was to determine whether abscisic acid (ABA) can protect against liver fibrosis induced by thioacetamide (TAA) in vivo by inhibiting apoptosis and inflammatory responses. To this end, three times per week, mice were injected intraperitoneally with TAA (200 mg/kg) for 8 weeks to induce liver fibrosis. After the fourth week of treatment, histological changes, the serum biochemical index, inflammation, and hepatocyte apoptosis factors (e.g., caspase-3, B-cell lymphoma 2 [Bcl-2], Bcl-2-associated X [Bax]) were detected to clarify its underlying mechanism. The results clearly indicated that ABA improves TAA-induced hepatic injury and collagen accumulation in mice. Otherwise, ABA significantly reduced liver fibrosis by regulating caspase-3 and Bcl-2, α-smooth muscle actin, and collagen I. ABA inhibited the nuclear factor kappa B pathway, significantly alleviating oxidative stress and inflammatory cytokines. Therefore, ABA may be a potential therapeutic agent for preventing liver damage.