- Author:
Sheng-zhang LIN
1
;
Hong-fei TONG
;
Kang-jie CHEN
;
He JING
;
Xiao YANG
;
Shu-sen ZHENG
Author Information
- Publication Type:Journal Article
- MeSH: Acute Disease; Animals; Apoptosis; drug effects; Cytokines; blood; Drug Evaluation, Preclinical; Emodin; pharmacology; therapeutic use; Graft Rejection; prevention & control; Immunosuppressive Agents; pharmacology; therapeutic use; Liver; drug effects; pathology; ultrastructure; Liver Transplantation; immunology; rehabilitation; Rats; Rats, Inbred BN; Rats, Inbred Lew; T-Lymphocyte Subsets; immunology; pathology; Transplantation, Homologous
- From: Chinese journal of integrative medicine 2010;16(2):151-156
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the mechanism of action of emodin for suppressing acute allograft rejection in a rat model of liver transplantation.
METHODSBrown 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.
RESULTSCompared 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 (AI) of 35.83+/-2.32, and elevated plasma levels of interleukin-2 (IL-2), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-alpha), CD4(+) and CD4 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-alpha, CD4(+) and CD4(+)/CD8(+) ratio, but elevated levels of IL-10 as compared with the allograft group.
CONCLUSIONPost-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.