Guangxi Medical University, Nanning 530021, China.
The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning 530023, China.
Int Immunopharmacol. 2014 Apr;19(2):365-72. doi: 10.1016/j.intimp.2014.02.009. Epub 2014 Feb 21.
A compound was isolated from Potentilla chinensis, and it was identified as tormentic acid (TA) based on its physicochemical properties and spectral data. The hepatoprotective effect of TA was evaluated using an acute liver failure model induced by lipopolysaccharide (LPS)/D-galactosamine (D-GalN). The results revealed that TA significantly prevented LPS/D-GalN-induced fulminant hepatic failure, as evidenced by the decrease in serum aminotransferase and total bilirubin activities and the attenuation of histopathological changes. TA alleviated the pro-inflammatory cytokines including TNF-α and NO/iNOS by inhibiting nuclear factor-κB (NF-κB) activity. Moreover, TA strongly inhibited lipid peroxidation, recruited the anti-oxidative defense system, and increased HO-1 activity. In addition, TA significantly attenuated increases in TUNEL-positive hepatocytes through decreasing the levels of cytochrome c, as well as caspases-3, 8 and 9, while augmenting the expression of Bcl-2. In conclusion, TA protects hepatocytes against LPS/D-GalN-induced injury by blocking NF-κB signaling pathway for anti-inflammatory response and attenuating hepatocellular apoptosis. Consequently, TA is a potential agent for preventing acute liver injury and may be a major bioactive ingredient of Potentilla chinensis.
从委陵菜中分离得到一种化合物，根据其理化性质和光谱数据鉴定为没食子酸（TA）。采用脂多糖（LPS）/D-半乳糖胺（D-GalN）诱导的急性肝衰竭模型评价 TA 的肝保护作用。结果表明，TA 可显著预防 LPS/D-GalN 诱导的暴发性肝衰竭，血清转氨酶和总胆红素活性降低，组织病理学变化减轻。TA 通过抑制核因子-κB（NF-κB）活性，减轻 TNF-α 和 NO/iNOS 等促炎细胞因子。此外，TA 还能强烈抑制脂质过氧化，募集抗氧化防御系统，并增加 HO-1 活性。此外，TA 通过降低细胞色素 c 以及 caspase-3、8 和 9 的水平，同时增加 Bcl-2 的表达，显著减少 TUNEL 阳性肝细胞的增加，从而减轻 LPS/D-GalN 诱导的肝细胞凋亡。综上所述，TA 通过阻断 NF-κB 信号通路的抗炎反应和减轻肝细胞凋亡来保护肝细胞免受 LPS/D-GalN 诱导的损伤。因此，TA 是一种预防急性肝损伤的潜在药物，可能是委陵菜的主要生物活性成分。
