Wu Zheng-Rong, Bai Zhong-Tian, Sun Ying, Chen Peng, Yang Zhi-Gang, Zhi De-Juan, Li Yang, Wang Xing, Du Jing-Jing, Yang Rui, Cui Peng, Zhang Yu, Li Hong-Yu
School of Pharmaceutics, Lanzhou University, 222 Tian Shui South Road, Lanzhou 730000, People's Republic of China.
The First Hospital of Lanzhou University, People's Republic of China.
Bioorg Med Chem Lett. 2015 Nov 15;25(22):5424-6. doi: 10.1016/j.bmcl.2015.09.003. Epub 2015 Sep 5.
In our searching for novel antioxidants from natural sources, N-trans-Caffeoyldopamine which was from natural product was found to be a potential compound for its remarkable antioxidant activity. Isoniazid (INH) and Rifampicin (RFP) is widely used for the treatment of Tuberculosis (TB) as the first line drugs, have been known to be potentially hepatotoxic and may lead to drug-induced liver injury. Oxidative stress has been regarded as the major mechanism of the hepatotoxicity. Therefore, in this study, the possible protective effects of N-trans-Caffeoyldopamine was investigated in the hepatotoxicity caused by INH and RFP in rats. Results showed that serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and hepatic malondialdehyde (MDA) content were reduced dramatically, and hepatic superoxide dismutase (SOD) activity and glutathione (GSH) content were restored remarkably by N-trans-Caffeoyldopamine co-administration, as compared to the INH-RFP treated rats (p<0.01). Moreover, the histopathological damage of liver and the number of apoptotic hepatocytes were also significantly ameliorated by the treatment. It is therefore suggested that N-trans-Caffeoyldopamine can provide a definite protective effect against acute hepatic injury caused by INH and RFP in rats, which may mainly be associated with its antioxidative effect. Mechanisms studies indicated that it inhibited the lipid peroxidation through the cytochrome P450 2E1 (CYP2E1) downregulation.
在我们从天然来源寻找新型抗氧化剂的过程中,发现天然产物中的N-反式咖啡酰多巴胺因其显著的抗氧化活性而成为一种潜在的化合物。异烟肼(INH)和利福平(RFP)作为一线药物被广泛用于治疗结核病(TB),已知它们具有潜在的肝毒性,可能导致药物性肝损伤。氧化应激被认为是肝毒性的主要机制。因此,在本研究中,我们研究了N-反式咖啡酰多巴胺对INH和RFP诱导的大鼠肝毒性的可能保护作用。结果表明,与INH-RFP处理的大鼠相比,联合给予N-反式咖啡酰多巴胺可显著降低血清天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)水平以及肝脏丙二醛(MDA)含量,并显著恢复肝脏超氧化物歧化酶(SOD)活性和谷胱甘肽(GSH)含量(p<0.01)。此外,该处理还显著改善了肝脏的组织病理学损伤和凋亡肝细胞的数量。因此,提示N-反式咖啡酰多巴胺对INH和RFP诱导的大鼠急性肝损伤具有明确的保护作用,这可能主要与其抗氧化作用有关。机制研究表明,它通过下调细胞色素P450 2E1(CYP2E1)抑制脂质过氧化。