| Objective To investigate the effect of hyperuricemia(HUA)and the protective effect of Triptolide(TP)intervention on podocytes.To establish a rat model of hyperuricemia nephropathy,observe the pathological pathology of the kidney and the expression of podocyte marker protein nephrin and IL-1β in renal tissues,and to preliminarily explore the molecular mechanism and mechanism of renal damage in hyperuricemia rats The protective effect of triptolide on hyperuricemia nephropathy.Methods Thirty-two male SD rats of clean grade were randomly divided into normal control group(NC),model group(MG),triptolide intervention group(TP)and allopurinol group(ALLO),with 8 rats in each group.Rats in the NC group were fed with normal diet and intragastrically with sodium hydroxymethyl cellulose solution;the model group,triptolide intervention group,and allopurinol group were fed with yeast feed,and adenine solution potassium oxonate emulsion suspension was administered by gavage every morning;in addition,TP group was given triptolide solution by gavage and ALLO group was given allopurinol plus distilled water by gavage every afternoon.8 consecutive weeks.and rats were regularly tested for serum Uric Acid(s UA),Serum creatinine(Scr),Blood Urea Nitrogen(BUN)And 24 h Urine Protein(24 h UPT)level,light microscope,electron microscope to observe renal histopathology and podocyte pathology,immunohistochemistry,Real time PCR and Western-Blot technology to detect podocyte nephrin and renal tissue IL-1β expression.Results After 4 and 8 weeks of modeling,the s UA,Scr,BUN and 24 h UPT of the model group were significantly higher than those of the control group(P<0.01),after 8weeks of modeling,the model group rats The expression of IL-1β in the kidney increased and the expression of nephrin decreased,which was significantly different from the control group(P<0.01).Electron microscopy observed irregularly thickened glomerular basement membrane,epithelial cell swelling,foot process fusion,and renal interstitial inflammatory cell infiltration.After the intervention of triptolide,the expression of IL-1β in the kidney of rats was down-regulated,and the expression of nephrin was increased.Compared with the model group,the difference was significant(P<0.01).The levels of s UA,Scr,BUN and 24 h UPT decreased,as mentioned above in podocytes The pathological changes were significantly alleviated.Conclusion The abnormal expression of podocyte-related protein nephrin and renal IL-1β may be involved in the occurrence and development of HUA renal damage.Triptolide may improve the renal function damage of patients with HUA nephropathy by inhibiting inflammation and protecting podocytes. |