Effects of HGF in Celsior solution on levels of INF-γ. IL-4 and IL-10 in a rat liver transplantation model
10.3760/cma.j.issn.1007-8118.2010.07.013
- VernacularTitle:Celsior液中HGF对大鼠肝移植后INF-γ、IL-4与IL-10水平的影响
- Author:
Tao LI
;
Huamei TANG
;
Xing SUN
;
Guoqiang QIU
;
Zhihai PENG
- Publication Type:Journal Article
- Keywords:
Liver transplantation;
Celsior;
HGF;
Non-heart-beating donor;
INF-γ;
IL-4;
IL-10
- From:
Chinese Journal of Hepatobiliary Surgery
2010;16(7):524-526
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the impact of recombinant human hepatocyte growth factor (rhHGF) in Celsior (CS) solution on the expression of INF-γ, IL-4 and IL-10 in a rat liver transplan-tation model. Methods After flushed with CS solution with addition of rhHGF (experimental group) or saline (control group), NHBD livers were stored at 4℃; for 16 h.then they were transplanted using the two-cuff technique with arterial reconstruction. The serum levels of INF-γ, IL-4 and IL-10 at lh after reperfusion were detected using ELISA. The INF-γ, IL-4 and IL-10 mRNA in the corresponding liver tissue were determined by RT-PCR. The 7-day survival rate was calculated and the histopatho-logical examination results were analyzed by hematoxylin and eosin staining. Results Compared with the control group, the experimental group showed lower INF-γ level and higher IL-4 and IL-10 levels in serum at 1 h after reperfusion (P<0. 05). The level of INF-γ mRNA in liver tissue was significant decreased at 1 h after reperfusion (P<0. 05) , and the level of IL-4 and IL-10 mRNA was significantly increased in the experimental group (P<0. 05). In experimental group, recipients got a better survival rate and histopathological examination showed a well-preserved hepatic architecture without hepatocyte necrosis, milder sinusoidal and portal congestion. Conclusion Adding exogenous rhHGF in CS solu-tion can protect NHBD livers from ischemia-reperfusion injury and prolong the survival in rats, which might be due to down-regulation of TNF-γ and up-regulation of IL-4 and IL-10.
