Protective effects of Ginsenoside Rg1 against carbon tetrachloride-induced liver injury in mice through suppression of inflammation

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• 作者：Yao Xin^a ; ¹ ; Jiang Wei^b ; ¹ ; Ma Chunhua^c ; Yu Danhong^d ; Zhu Jianguo^a ; Cheng Zongqi^a ; ^{Chengzqsuzhou@163.com" class="auth_mail" title="E-mail the corresponding author} ; Bao Jian-an^a ; ^{Baojasuzhou@126.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：CCl4-induced hepatotoxicity ; Ginsenoside Rg1 ; Inflammation
• 刊名：Phytomedicine
• 出版年：2016
• 出版时间：1 June 2016
• 年：2016
• 卷：23
• 期：6
• 页码：583-588
• 全文大小：2180 K

文摘

AMP-activated protein kinase (AMPK) is one of the principal cellular energy sensors participating in maintenance of energy balance but recent evidences also suggested that AMPK might be involved in the regulation of inflammation.

Study design/methods

Ginsenoside Rg1 (Rg1) was used to investigate the potential roles of AMPK in carbon tetrachloride (CCl₄)-induced hepato-toxicity. The experimental data indicated that treatment with Rg1 significantly decreased the elevation of plasma aminotransferases and alleviated hepatic histological abnormalities in CCl₄-exposed mice. Treatment with Rg1 also inhibited the increase of myeloperoxidase (MPO) and malondialdehyde (MDA), the induction of TNF-α, IL-6, inducible nitric oxide synthase (iNOS), nitric oxide and the upregulation of matrix metalloproteinase 2 (MMP-2), MMP-3 and MMP-9 in mice exposed to CCl₄. These effects were associated with suppressed nuclear accumulation of NF-κB p65.

Conclusion

These results indicated that Rg1 effectively suppressed the inflammatory responses and alleviated liver damage induced by CCl₄, implying that AMPK activation might be beneficial for ameliorating inflammation-based liver damage.