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      저자 : Lingshi Meng (검색결과 1 건)
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        Protective Effect of Andrographolide on Alleviating Chronic Alcoholic Liver Disease in Mice by Inhibiting Nuclear Factor Kappa B and Tumor Necrosis Factor Alpha Activation

        Yuan Song,Xiangqun Wu,Di Yang,Fang Fang,Lingshi Meng,Ya Liu,Weiwei Cui 한국식품영양과학회 2020 Journal of medicinal food Vol.23 No.4

        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.

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