| Objective To explore the activin A expression in rat experimental kidney fibrosis induced by UUO and analyze its role in the pathogenesis of kidney fibrosis. rh-Fs treatment experiment proved futher the result that ACT A involved in the kidney fibrosis.Methods (1) 40 male Wistar rats were randomly divided into the sham operation group(n=8),3 day after UUO group(n=8), 7 day after UUO group(n=8), 14 day after UUO group(n=8), 21 day after UUO group(n=8). Kidney fibrosis was induced by UUO(unilateral ureteral obstruction). At the different time point, rats were killed. ACT A expression was detected in the every group by immunohistochemistry. The ACT A messenger RNA transcription was assessed by semi-quantity reverse transcription polymerase chain reaction(RT-PCR). (2) The 16 kidney fibrosis rats were randomly divided into rh-Fs (recombinant human follistatin) treatment group (n=8) and saline solution control group (n=8). rh-Fs was infused via penis vein. After 24 hours, the rats were killed. PCNA and ACT A expression were measured.Results (1) The expression of ACT A was not detected in sham operation and contralateral kidneys. In contrast, the expression level of ACT A was significantly increased at 3d after UUO operation and thereafter. The expression of ACT A was restricted to tubular cells and was not observed in glomeruli or interstitium of the kidney with UUO. (2) In follistatin-treated rats, PCNA expression was significantly reduced than that in control rats. Two groups had no difference on ACT A expression.Conclusion ACT A expression is enhanced in kidney fibrosis, and maybe involved in the pathogenesis of kidney fibrosis.
|
PDF Full Text Request