eNOS/NO,单侧输尿管梗阻 z-bo 2020-11-06 391

　　OBJECTIVE: To investigate the effects of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) in microvascular lesions in mice with unilateral ureteral obstruction (UUO) renal interstitial fibrosis The role and mechanism.

　　Method: 64 KM mice were randomly divided into two groups: sham operation group n=32; unilateral ureteral obstruction UUO group n=32. Observation for 4 weeks, weekly detection of BUN, Scr and nitric oxide in each group of mice, flow cytometric count of peripheral blood CD133+/VEGFR+ endothelial progenitor cells (EPCs), Masson staining to observe the morphological changes of kidney tissue, immunology The expression of CD34+ in the renal interstitium was detected by histochemical method and the microvessel density was counted. The expression of eNOS and VEGF mRNA in the renal cortex was detected by real-time quantitative PCR.

　　Results: The blood nitric oxide, endothelial progenitor cell count, renal interstitial microvessel density, eNOS, VEGF mRNA expression levels continued to decline in the UUO group, and the differences were statistically significant in the second, third, and fourth weeks from the control group. Nitric oxide level was positively correlated with renal interstitial microvessel density (r=0.715, P<0.05); eNOS mRNA expression level was correlated with renal interstitial microvessel density (r=0.624, P<0.05), endothelial progenitor cell count (r=0.375) , P<0.05), 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 influence on vasodilation, mediating the expression of vascular and renal factor VEGF mRNA and mobilizing endothelial progenitor cells.