Much research has indicated that alcoholic liver disease (ALD) is associated with oxidative stress and inflammation induced by ethanol, and that numerous antioxidants could effectively alleviate such injuries. Moreover, recent studies have identified andrographolide (AD) as having strong anti-inflammatory and antioxidant activities, which can block oxidative damage associated with nuclear factor kappa B (NF-κB)-mediated inflammation. However, the biological role and potential mechanism of AD in its protection against ALD have not been fully characterized. To observe the possible effect of AD, male C57BL/6J mice received ethanol through intragastrical gavage for 12 weeks in this study. The ethanol group was separated into five subgroups: (1) model group (n = 10); (2) silymarin group (0.1 mg/g body weight [BW], n = 10); (3) AD (0.05 mg/g BW) group (n = 10); (4) AD (0.1 mg/g BW) group (n = 10); and (5) AD (0.2 mg/g BW) group (n = 10). Mice in AD groups were treated orally by gavage once per day. The experimental results show that serum aminotransferase, liver lipids, lipid peroxidation, and antioxidant capacities were significantly changed in the model group after alcohol treatment, and the liver tissue histological findings showed pathological changes. Compared with the model group, treatment with AD improved serum aminotransferase, liver function, lipid accumulation, and hepatic reactive oxygen species levels. And AD decreased the hepatic NF-κB and tumor necrosis factor alpha (TNF-α) protein expression of ALD mice. This research demonstrated that AD can alleviate liver pathological injury and oxidative stress in mice exposed to ethanol by decreasing the expression of NF-κB and TNF-α.
Keywords: NF-κB; TNF-α; alcoholic liver disease; andrographolide.