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Objective : To study hyperuricemia glomerular endothelial cells , vascular smooth muscle cell proliferation and to explore hyperuricemia mechanism of pathogenesis of renal injury . Methods: Clinical and animal experiments in terms of both ( a ) the normal group were detected by ELISA with hyperuricemia group , and high uric acid in the blood before and after intervention group reflect endothelial cell function index N0, indicators of endothelial dysfunction ET-1, PAI-1; reflect the proliferation of vascular smooth muscle indicators PDGF, MCP-1; , and IL-6, IL-18, TNF-α, COX2 and other inflammatory factors . ( 2 ) Light microscopy of renal pathology in each group without distinction ; observed by immunohistochemical NOS, PDGF and other factors in each group kidney tissues . Results: ( 1 ) biochemical detection : Hyperuricemia can make and rat plasma endothelial function indicators reflect NO significantly reduced (P lt; 0.05), endothelial cell dysfunction indicators ET-1, PAI-1 significantly higher (P lt; 0.05); reflect the proliferation of vascular smooth muscle indicators PDGF, MCP-1 was significantly higher (P lt; 0.05); IL-6, IL-18, TNF-α, COX2 other inflammatory factors also significantly higher (P lt; 0.05). Uric acid from the sky after the intervention COX2, IL-6, IL-18, PAI-1, ET-1, PDGF, TNF-α, MCP-1 and significantly lower (P lt; 0.05), NO was significantly higher (P lt; 0.05 ) . ( 2 ) renal pathology : light microscopy , it was observed hyperuricemia can make the renal vascular intimal hyperplasia , wall thickening , luminal narrowing slightly ; immunohistochemical staining can be seen hyperuricemia can make PDGF in the kidney tissues increased significantly, while the expression of NOS significantly reduced. Conclusion: Hyperuricemia can damage glomerular endothelial cell function, promote vascular smooth muscle cell proliferation , leading to kidney damage.
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