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.