Sesquiterpenoids from the root of Panax Ginseng protect CCl4-induced acute liver injury by anti-inflammatory and anti-oxidative capabilities in mice.

肝损伤 医学 脂质过氧化 抗氧化剂 传统医学 炎症
作者
Weidong Wang,Shijie Wang,Jinping Liu,Enbo Cai,Hongyan Zhu,He Zhongmei,Yugang Gao,Pingya Li,Yan Zhao
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier]
卷期号:102: 412-419 被引量:26
标识
DOI:10.1016/j.biopha.2018.02.041
摘要

The oxidative stress and inflammatory response play an important role in carbon tetracholoride (CCl4)-induced acute liver injury. In this work, sesquiterpenoids from the root of Panax Ginseng (SPG) were prepared, and then the hepatoprotective effects of SPG against CCl4-induced acute liver injury were investigated and the underlying mechanism was explored in mice. All mice were divided into four groups: the control, CCl4 and SPG (2.5 and 10 mg/kg, dissolved in soybean oil, i.g.) groups. All mice were given continuous administration for 7 days, and injected with CCl4 (0.1 mL/10 g body weight 0.2% CCl4 solution in soybean oil, i.p.) 1 h after the end of the administration except the control group. Mice were sacrificed 24 h post-CCl4 injection. The results indicated that SPG significantly reduced the increasement of serum AST and ALT levels induced by CCl4-treatment. And the histopathological analysis revealed that SPG treated mice had normal liver architecture and no necrosis. The decreased activities of SOD, GSH and CAT, and increased MDA level were inhibited by SPG treatment. At the same time, the levels of TNF-α, IL-1β and IL-6 were significantly decreased by SPG treatment. SPG treatment also reduced the heptic protein expressions of NF-κB p65, COX-2, MAPK p38, ERK and JNK in the liver. These fingdings demonstrated that SPG exhibited strong hepatoprective effect on the CCl4-induced acute liver injury, which was related to anti-oxidantive and anti-inflammatory capabilities; and the anti-inflammatory effect of SPG might mediated by the NF-κB and MAPKs signaling pathways. Taken together, SPG might be a potential material for drug and functional food development against chemical hepatic injury.

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