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CRP, IL-6 and TNF-α in the pathogenesis of allograft arteriosclerosis in rats
- SHI Ping,SUN Wen-yu,YANG Min
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JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES). 2008, 46(3):
258-262.
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Abstract
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To study the role of serum inflammatory factors and allograft adventitial inflammation in the pathogenesis of allograft arteriosclerosis in rats. Methods Thirty-six allograft rats and 16 within strain control rats were randomly divided into 4 groups (9 experimental rats and 4 controls): group A, sacrificed at the first postoperative week; group B, sacrificed at the second postoperative week; group C, sacrificed at the third postoperative week; and group D, sacrificed at the fourth postoperative week. Blood samples were collected before the transplantation operations and at the time of sacrifice. The method of Enzyme Linked Immunosorbent Assay was used for serum inflammatory factors (CRP, IL-6 and TNF-α), HE staining for pathologic changes of aortic allograft and immunohistochemical method for adventitial inflammatory cell infiltration, α-actin, CDK1 and PCNA. The inflammatory factors and other observation results were compared between groups and the pre-operative groups. ResultsCRP level significantly increased in all control groups and experimental groups (P＜0.01) and of B, C and D experimental groups were higher than the controls (P＜0.01). IL-6 level increased in the experimental group B (P＜0.05) and significantly increased in groups A, C and D (P＜0.01) and in the control groups A, B and C (P＜0.05), but it was significant higher in the experimental groups than in the control groups (P＜0.01). TNF-α level had no difference between the controls and the preoperative basal levels, all experimental groups had higher levels than the preoperative and control groups (P＜0.01). Adventitial inflammatory cell infiltration was found in the allograft groups 7 days after the transplantation, mild adventitial collagen fiber proliferation accompanied by inflammatory infiltration was found in the allograft groups 14 days after the transplantation, and significantly adventitial proliferation with smooth muscle cells, collagen fiber and inflammatory cells, intimal fibrous degeneration and smooth muscle cell proliferation were found in the allograft groups 28 days after the transplantation. In allograft adventitial smooth muscle cells, the expressions of α-actin, PCNA and CDK1 were increased (P＜0.05) and preceded the expressions in intimal smooth muscle cells. ConclusionThe serum inflammatory factor levels in thoracic aorta transplantation rats gradually increase, indicating that increased inflammatory factors and allograft adventitial inflammation resulting from immune or nonimmune factors and adventitial SMC proliferation are both involved in the pathogenesis of early allograft arteriosclerosis.
