›› 2006, Vol. 5 ›› Issue (8): 433-436.

• 基础研究 • Previous Articles     Next Articles

  

  • Received:1900-01-01 Revised:1900-01-01 Online:2006-08-12 Published:2006-08-12

Abstract: Objective To study the role of tumor necrosis factor-α(TNF-α) and platelet deviced growth factor-BB (PDGF-BB) in the pathogenesis of adriamycin-induced nephropathy and the effects and moxonidine or monopril on them. Method Rats were received twice-intravenous injection of adriamycin and divided into nephropathy group(NEP)、moxonidine treatment group (for a dose of 1.5 mg/(kg·d) and monopril treatment group [10 mg/(kg·d)];10 healthy rats were as control group. At the end of the experiment,the proteinuria and nonepinephrine (NE)、angiotensin Ⅱ(AngⅡ) and TNF-α in blood were detected.Kidey damage were evaluated by quantitative histology.The protein expression of TNF-α and PDGF-BB were determined by immunohistochemical staining. Results Compared with control group,proteinuria and the levels of NE、AngⅡ and TNF-α in the blood were increased(P<0.01),the expression of TNF-α and PDGF-BB in renal tissue were all significantly up-regulated(P<0.01) in adrianycin induced nephropathy rats.After the treatment of moxonidine and monopril, related parameters were all inhibited(P<0.01). Conclusion Increased expression of TNF-α and PDGF-BB protein may play an important role in the progression of kidney disease,moxonidine and monopril can protect kidney by down-regulating the expression of TNF-αand PDGF-BB.

Key words: Platelet deviced growth factor-BB(PDGF-BB), Moxonidine, Monopril

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