Inhibitory effect of Cordyceps sinensis on rat allograft vasculopathy / 中华器官移植杂志

ABSTRACT

Objective To investigate the effects and mechanism of Cordyceps sinensis on transplant arteriosclerosis in a rat model Methods Brown Norway aortic allografts were transplanted into Lewis recipient rats,and the recipient rats were randomly divided into four groupsgroup A,isograft control group,Lewis-Lewis (n =10); group B,allograft control group,BN-Lewis (n =10); groups C and D,allograft experimental groups,BN-Lewis (n =10).Rats were given normal saline via intragastric injection,once every day for 60 days in groups A and group B,and received different doses (1.5 and 3 g·kg-1 ·d 1) of Cordyceps sinensis in groups C and group D respectively.Grafts were harvested on the day 60 after transplantation. Intimal thickness was detected by HE staining.Protein was extracted from the abdominal aortas for Western blotting.Cellular localization was assessed by histology and immunohistochemistry.The serum was analyzed by an enzyme-linked immunosorbent assay (ELISA). Results Transplanted arteries were normal in group A.Transplanted arteries in group A had allograft vasculopathy,and intimal thickness was significantly increased.Transplanted arteries in allograft experimental groups had endometritis changes,and intimal thickness was significantly decreased as compared with that in group B (P ＜ 0.05).Immunohistochemistry and Western blotting revealed that the expression levels of VEGF and PDGF-BB proteins in group A were significantly higher than in group B,and those in groups C and D were significantly reduced as compared with group B (P＜0.05).ELISA showed that serum VEGF and PDGF BB concentrations in group B were significantly increased as compared with group A (P＜0.05).Serum VEGF and PDGF-BB concentrations were significantly reduced in groups C and D as compared with group B (P＜0.05).Conclusion Cordyceps sinensis could significantly inhibit the intimal hyperplasia,and delayed transplant arteriosclerosis caused by chronic rejection,which may be related to the down-regulated expression of VEGF and PDGF-BB.