Effect of Emodin in Suppressing Acute Rejection Following Liver Allograft Transplantation in Rats

被引:0
作者
林胜璋 [1 ,2 ,3 ]
童洪飞 [4 ]
陈康杰 [1 ,5 ]
荆河 [3 ]
杨潇 [3 ]
郑树森 [1 ,6 ]
机构
[1] Department of Hepatobiliary Surgery,First Affiliated Hospital of Medical College,Zhejiang University
[2] Key Lab of Combined Multi-organ Transplantation,Ministry of Health
[3] Department of General Surgery,Second Affiliated Hospital of Wenzhou Medical College
[4] Department of General Surgery,Second Affiliated Hospital of Wenzhou Medical College,Wenzhou(),China
[5] Key Lab of Combined Multi-organ Transplanlation,Ministry of Health,Hangzhou
[6] Key Lab of Combined Multi-organ Transplanlation,Ministry of Health
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中图分类号
R285.5 [中药实验药理];
学科分类号
1008 ;
摘要
<正>Objective:To investigate the mechanism of action of emodin for suppressing acute allograft rejection in a rat model of liver transplantation.Methods:Brown Norway(BW) recipient rats of orthotopic liver transplantation(OLT) were divided into three groups,Group A receiving isografting(with BW rats as donor), Group B receiving allografting(with Lewis rats as donor),Group C receiving allografting and emodin treatment (50 mg/kg daily).They were sacrificed on day 7 of post-transplantation,and their hepatic histology,plasma cytokine levels,and T-cell subset expression were detected.Results:Compared with those in Group A,rats in Group B exhibited severe allograft rejection with a rejection activity index(RAI) of 7.67±0.98,extensive hepatocellular apoptosis with an apoptosis index(Al) of 35.83±2.32,and elevated plasma levels of interleukin-2 (IL-2),interleukin-10(IL-10),tumor necrosis factor-α(TNF-α),CD4+ and CD4+/CD8+ ratio.However,recipients in Group C showed a decrease in histological grade of rejection and hepatocellular apoptosis,as well as a decrease in plasma levels of IL-2,TNF-α,CD4+ and CD4+/CD8+ ratio,but elevated levels of IL-10 as compared with the allograft group.Conclusion:Post-OLT acute rejection could be attenuated by emodin,its mechanism of action may be associated with protecting hepatocytes from apoptosis,polarizing the Th 1 paradigm to Th2,and inhibiting the proliferation of CD4+ T cell in plasma.
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页码:151 / 156
页数:6
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