动物造模 z-bio 2022-04-26 411

　　Objective: To investigate the role and mechanism of endothelial nitric oxide synthase and nitric oxide in microvascular disease in mice with unilateral ureteral obstruction and renal interstitial fibrosis.

　　METHODS: 64 KM mice were randomly divided into two groups: sham-operated group n=32; unilateral ureteral obstruction UUO group n=32. After 4 weeks of observation, the blood BUN, Scr and nitric oxide of the mice in each group were detected every week. Histochemical method was used to detect the expression of CD34+ in the renal interstitium and count the microvessel density, and real-time quantitative PCR was used to detect the expression of eNOS and VEGF mRNA in the renal cortex.

　　Results: The blood nitric oxide, endothelial progenitor cell count, renal interstitial microvessel density, eNOS, and VEGF mRNA expression levels in the UUO group continued to decrease, and the differences were statistically significant at the 2nd, 3rd, and 4th weeks compared with the control group. The level of nitric oxide was positively correlated with renal interstitial microvessel density (r=0.715, P<0.05); eNOS mRNA expression level was positively correlated with renal interstitial microvessel density (r=0.624, P<0.05), endothelial progenitor cell count (r=0.375) , P<0.05) and VEGF mRNA (r=0.351, P<0.05) were positively correlated.

　　Conclusion: The eNOS/NO pathway is involved in the regulation of renal interstitial microvessels in UUO mice, and its regulation involves the effects on vasodilation, mediating the expression of pro-vascular renal factor VEGF mRNA, and mobilizing endothelial progenitor cells.