冬虫夏草制剂对自发性高血压大鼠肾组织ICAM-1和VCAM-1表达的影响

目的:观察自发性高血压大鼠(SHR)肾组织中细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)表达及冬虫夏草制剂对其影响.方法:清洁级雄性SHR 22只、WKY大鼠6只(W组),SHR随机分为非干预组(S组)、冬虫夏草制剂组(C组)、福辛普利组(F组)、冬虫夏草制剂加福辛普利组(FC组),后3组以冬虫夏草制剂4 g/(kg·d)和/或福辛普利10 mg/(kg·d)灌胃,S组及W组以等量清水灌胃,测血压,8周末测尿蛋白、血肌酐,取肾组织做HE,Masson染色,免疫组织化学及RT-PCR方法检测ICAM-1,VCAM-1蛋白及mRNA表达情况.结果:与WKY大鼠比较,SHR尿蛋白排泄量增高,肾组织ICAM-1,VCAM-1蛋白及mRNA表达增强.与S组比较,福辛普利使大鼠血压下降,而冬虫夏草制剂无明显降压作用.但C,F,FC组均有尿蛋白排泄量、血肌酐水平下降;肾组织ICAM-1,VCAM-1蛋白及mRNA表达下调.结论:高血压造成肾脏损害时可出现肾组织ICAM-1和VCAM-1的异常表达,冬虫夏草制剂可有效改善二者的异常表达,具有良好的肾保护作用.

Effect of Cordceps Sinensis on the expression of ICAM-1 and VCAM-1 in the kidney of spontaneously hypertensive rats

Objective To observe the effect of Cordceps Sinensis (CS) on the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in the kidney of spontaneously hypertensive rats(SHR), and to investigate the mechanism of CS. Methods Male SHRs (23 week old) were randomly divided into 4 groups: a group without any treatment (Group S), a group treated with Cordceps sinensis at 4 F), and a group received daily intragastric administration of CS at 4 male WKY rats were used as normals controls. At the end of 8 weeks, all rats were sacrificed. Serum creatinine(Scr), 24 h urinary protein count, and the expression of ICAM-1 and VCAM-1 were examined by immunohistochemical technique and RT-PCR. Results Compared with the WKY rats, blood pressure, 24 h urinary protein count, Scr,and the expression of ICAM-1 andVCAM-1 in the kidney of SHR significantly increased (P＜0.05).Compared with Group S, blood pressure decreased after treatment by fosinopril (P＜0.05). Compared with Group S, the levels of Scr, 24 h urinary protein count, and glomerular lesion were significantly reduced in the CS and/or fosinopril treatment group. The expression of ICAM-1 and VCAM-1 was significantly decreased in these groups (P＜0.05).Conclusion CS may play a role in the protection and anti-fibrosis in the process of renal injury in SHR through reducing the expression of ICAM-1 and VCAM-1.