CAJ | 학술논문

目的：：观察雷公藤内酯醇( TP)对IgA肾病( IgAN)大鼠尿蛋白和足细胞nephrin、podocin蛋白及mRNA表达的影响。方法：采用牛血清白蛋白+四氯化碳+脂多糖的方法建立IgAN大鼠模型。将60只大鼠随机分为正常组、模型组、洛丁新组、TP剂量组、TP中剂量组、TP高剂量组,每组10只。于0,10,14周收集血尿标本,并处死大鼠留取肾组织标本。检测24 h尿蛋白定量,血生化指标,分别采用实时定量PCR及ELISA法检测肾组织nephrin、podocin mRNA和蛋白表达。结果：(1)实验前各组大鼠尿蛋白差异无统计学意义(P>0.05),第10周末各造模组蛋白尿均明显高于正常组(P<0.01),第14周末TP各剂量组及洛丁新组蛋白尿均较模型组明显减少(P<0.01),TP高剂量组Alt值高于其余各组(P<0.05)；(2)与正常组相比,模型组nephrin、podocin蛋白、mRNA表达明显降低(P<0.01)；TP各剂量组及洛丁新组nephrin、podocin蛋白、mRNA表达均较模型组明显增高(P<0.05)；TP中、高剂量组较洛丁新组nephrin、podocin蛋白浓度显著增高(P<0.05)；TP各剂量组与洛丁新组及TP各剂量组间nephrin、podocin mRNA表达均差异无统计学意义(P>0.05)。结论：TP能够明显减轻IgAN大鼠的蛋白尿,且能明显提高肾组织nephrin、podocin mRNA及蛋白的表达。提示TP能调节IgAN足细胞相关分子nephrin、podocin基因及蛋白的表达,减少足细胞损害,减少尿蛋白。
목적：：관찰뢰공등내지순( TP)대IgA신병( IgAN)대서뇨단백화족세포nephrin、podocin단백급mRNA표체적영향。방법：채용우혈청백단백+사록화탄+지다당적방법건립IgAN대서모형。장60지대서수궤분위정상조、모형조、락정신조、TP제량조、TP중제량조、TP고제량조,매조10지。우0,10,14주수집혈뇨표본,병처사대서류취신조직표본。검측24 h뇨단백정량,혈생화지표,분별채용실시정량PCR급ELISA법검측신조직nephrin、podocin mRNA화단백표체。결과：(1)실험전각조대서뇨단백차이무통계학의의(P>0.05),제10주말각조모조단백뇨균명현고우정상조(P<0.01),제14주말TP각제량조급락정신조단백뇨균교모형조명현감소(P<0.01),TP고제량조Alt치고우기여각조(P<0.05)；(2)여정상조상비,모형조nephrin、podocin단백、mRNA표체명현강저(P<0.01)；TP각제량조급락정신조nephrin、podocin단백、mRNA표체균교모형조명현증고(P<0.05)；TP중、고제량조교락정신조nephrin、podocin단백농도현저증고(P<0.05)；TP각제량조여락정신조급TP각제량조간nephrin、podocin mRNA표체균차이무통계학의의(P>0.05)。결론：TP능구명현감경IgAN대서적단백뇨,차능명현제고신조직nephrin、podocin mRNA급단백적표체。제시TP능조절IgAN족세포상관분자nephrin、podocin기인급단백적표체,감소족세포손해,감소뇨단백。
Objective:To observe the effects of triptolide(TP) on proteinuria, the expression of proteins and mRNA of nephrin and podocin in rats with IgAN. Methods:IgAN model was established by intravenous injection of bovine serum albumin, car-bon tetrachloride and lipopolysaccharide. 60 rats were randomly divided into normal group, model group, benazepril group, TP low dose group, TP medium dose group, TP high dose group. At each time point, the blood and urine samples were collected, and renal tissues were processed after killed. The 24 h urinary protein excretion and blood biochemistry parameters were measured by routine methods. The levels of nephrin, podocin mRNA and nephrin, podocin protein expression were determined using real-time PCR and ELISA. Results:(1)The proteinuria of each group had no difference at baseline (P>0. 05). At the 10 th week, the proteinuria in model group was significantly higher than the normal group (P<0. 01), while in the 14 th weekend, the proteinuria of TP group of each dose and benazepril group were significantly weaker than that in the model group (P<0. 01). ALT in TP high dose group was significantly higher than the other groups (P<0. 05). (2)The protein and mRNA expressions of nephrin and podocin in the model group all became significantly lower compared with the normal group (P<0. 01); their expression in TP group in each dose and benazepril group were stronger than that in the model group (P<0. 05); The protein expression in TP medium dose group and TP high dose group were stronger than that in benazepril group (P<0. 05); However, there was no significant difference among TP groups and benazepril group in the expression of nephrin mRNA or podocin mRNA (P>0. 05). Conclusion:TP can obviously de-crease proteinuria and raise the expression of nephrin, podocin mRNA and protein in rats. This suggested that TP can raise the ex-pression of nephrin and podocinto reduce the injury of podocyte and recover the damage of glomerular filtration membrane barrier, and the protective effects of TP on nephrin and podocin may be better than benazepril.