文献类型：期刊文献

英文题名：Icariin synergizes therapeutic effect of dexamethasone on adriamycin-induced nephrotic syndrome

作者：Lv, Juan[1,3];Xue, Guozhong[2];Zhang, Yunxia[3];Wang, Xinbin[1];Dai, Enlai[1]

第一作者：Lv, Juan

通信作者：Dai, EL[1]

机构：[1]Gansu Univ Chinese Med, Dept Integrated Tradit Chinese & Western Med, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Univ Chinese Med, Dept Nephrol, Affiliated Hosp, Lanzhou, Gansu, Peoples R China;[3]Gansu Prov Hosp TCM, Dept Neurol, Lanzhou, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Dept Integrated Tradit Chinese & Western Med, Lanzhou 730000, Gansu, Peoples R China.|[10735]甘肃中医药大学;

年份：2023

卷号：28

期号：1

外文期刊名：EUROPEAN JOURNAL OF MEDICAL RESEARCH

收录：;Scopus(收录号：2-s2.0-85146850279);WOS:【SCI-EXPANDED(收录号:WOS:000920993800004)】；

基金：This research was supported by Regional Science Foundation Project (81760799).

语种：英文

外文关键词：Adriamycin; Autophagy; Podocyte injury; Nephrotic syndrome

摘要：BackgroundGlomerular damage is a common clinical indicator of nephrotic syndrome. High-dose hormone treatment often leads to hormone resistance in patients. How to avoid resistance and improve the efficiency of hormone therapy draws much attention to clinicians.MethodsAdriamycin (ADR) was used to induce nephropathy model in SD rats. The rats were treated with dexamethasone (DEX), icariin (ICA), and DEX + ICA combination therapy. The changes in urinary protein (UP), urea nitrogen (BUN), and serum creatinine (SCR) contents in rats were detected by enzyme-linked immunosorbent assay (ELISA), and the degree of pathological injury and the expression level of podocin were detected by HE staining and immunohistochemistry, to test the success of the model and the therapeutic effects of three different ways. The effect of treatments on podocytes autophagy was evaluated via transfection of mRFP-GFP-LC3 tandem adenovirus in vitro.ResultsThe contents of UP, SCR, and BUN were significantly increased, the glomerulus was seriously damaged, and the expression of Nephrosis2 (NPHS2) was significantly decreased in the ADR-induced nephrotic syndrome rat model compared to that of the control group. DEX, ICA, and the DEX + ICA combined treatment significantly alleviated these above changes induced by ADR. The combined treatment of DEX + ICA exhibited better outcome than single treatment. The combined treatment also restored the podocyte autophagy, increased the expression of microtubule-associated protein light-chain 3II (LC3II), and reduced the expression of p62 in vitro. The combined treatment protects podocytes by mediating the PI3K/AKT/mTOR (rapamycin complex) signaling pathway.ConclusionICA enhances the therapeutic effect of DEX on the nephrotic syndrome.