动物实验,单侧输尿管梗阻小鼠肾间质微血管病变 z-bio 2021-01-21 389

　　Objective: To investigate the effects of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) on renal matrix fibrosis in mice with unilateral urinary tract obstruction and their mechanisms.

　　 Method: 64 KM mice were randomly divided into two groups: 32 in the sham operation group; 32 in the UUO group with unilateral urinary tract obstruction. 4 weeks of observation, weekly detection of BUN, Scr and nitric oxide in each group of mice, peripheral blood CD133 +/VEGFR + endothelial precursor cells (endothelial precursor cells, EPC) flow cytometry counts, kidney tissue Morphological Masson staining was used to observe the physiological changes, immunohistochemical renal matrix CD34+ expression count microvessel density, renal cortex eNOS, real-time quantitative PCR to detect VEGF mRNA expression.

　　 Results: The blood nitric oxide, endothelial precursor cell number, renal interstitial microvessel density, eNOS, and VEGF mRNA expression levels continued to decrease in the UUO group. There were statistical differences in the control group at 2, 3 and 4 weeks. This is very important. Nitric oxide level was positively correlated with renal matrix microvessel density (r = 0.715, P\u003c0.05). The expression level of eNOS mRNA is the density of renal interstitial microvessels (r = 0.624, P\u003c0.05), the number of endothelial precursor cells (r = 0.375, P\u003c0.05), and VEGF mRNA (r = 0.351, P\u003c0. 05). ) Is positively correlated.

　　 Conclusion: The eNOS/NO pathway is involved in the regulation of renal interstitial microvasculature in UUO mice, involving vasodilation, mediation of vascular and renal factor VEGF mRNA expression, and endothelial precursor cells.