College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, China.
College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, China.
Eur J Pharmacol. 2021 Jan 15;891:173652. doi: 10.1016/j.ejphar.2020.173652. Epub 2020 Oct 15.
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.
本研究旨在通过抑制细胞凋亡和炎症反应，确定脱落酸 (ABA) 是否可以通过抑制细胞凋亡和炎症反应来预防硫代乙酰胺 (TAA) 在体内诱导的肝纤维化。为此，每周三次向小鼠腹腔内注射 TAA（200mg/kg）8 周以诱导肝纤维化。在治疗的第四周，检测组织学变化、血清生化指标、炎症和肝细胞凋亡因子（如半胱氨酸天冬氨酸蛋白酶-3、B 细胞淋巴瘤 2 [Bcl-2]、Bcl-2 相关 X [Bax]），以阐明其潜在机制。结果清楚地表明，ABA 可改善 TAA 诱导的小鼠肝损伤和胶原积累。此外，ABA 通过调节半胱氨酸天冬氨酸蛋白酶-3 和 Bcl-2、α-平滑肌肌动蛋白和胶原 I 显著减轻肝纤维化。ABA 抑制核因子 kappa B 途径，显著减轻氧化应激和炎症细胞因子。因此，ABA 可能是预防肝损伤的潜在治疗剂。
