Abstract

Abstract: Objective: To investigate the effect of tripterine on Notch signaling pathway in renal tissue of IgA nephropathy rats. Methods: SD male rats were divided into the control group, IgAN nephropathy model group, benazepril group, 1mg/kg/d tripterine intervention group and 10mg/kg/d tripterine intervention group according to the random number table method, with 10 rats in each group. The urinary sediment and 24-hour urinary protein quantity were detected by conventional methods. The expressions of Notch1, Jagged1, Hes1 and Hey1 in renal tissue of rats were detected by real-time fluorescent quantitative PCR. Results: IgA nephropathy model was successfully established. The hematuria and proteinuria in model group were higher than those of control group (P<0.05). The expressions of Notch1, Jagged1, Hes1 and hey1 in kidney tissue of IgA nephropathy rats were significantly increased (P<0.05). Compared with the model group, hematuria and proteinuria in tripterine intervention group were alleviated. The expressions of Notch1, Jagged1, Hes1 and Hey1 in rat renal tissue were decreased (P<0.05). Moreover, the expressions of Notch1, Jagged1, Hes1 and Hey1 in renal tissue of rats in 10mg/kg/d tripterine intervention group were decreased (P<0.05). Conclusion: Tripterine can decrease the levels of hematuria and proteinuria in IgA nephropathy rats. The expression of Notch signaling pathway in IgA nephropathy rats is increased by the down-regulation of tripterine, suggesting that tripterine has a certain therapeutic effect on IgA nephropathy rat. And its role may be realized through this signal pathway so as to provide the new mentality for the diagnosis and treatment of IgA nephropathy.

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