CAJ | 학술논문

目的：探讨丹酚酸 B 对高糖诱导肾小管上皮细胞分化的影响及可能机制。方法：体外培养大鼠肾小管上皮细胞 NRK52E 随机分为正常糖（NG）组、高渗（HM）组、高糖（HG）组和高糖＋Sal B（HB）组，分别培养24 h；采用免疫酶细胞化学染色对 NRK52E 细胞进行鉴定，MMT 法检测丹酚酸 B 对细胞生长活性的影响，免疫荧光细胞化学和 Western blotting 检测各组 TGF-β1、E-caderin、α-SMA 和 Col-Ⅳ蛋白的表达。结果：与 NG 组相比较，HG 组肾小管上皮细胞中 TGF-β1、α-SMA 和 Col-Ⅳ蛋白表达增多（P ＜0．05），而 E-cadherin 蛋白表达降低（P＜0．05）；与 HG 组比较，HB 组肾小管上皮细胞中 TGF-β1、α-SMA 和 Col-Ⅳ蛋白表达减少（P ＜0．05），而 E-cad-herin 蛋白表达增多（P ＜0．05）。结论：丹酚酸 B 对高糖诱导肾小管上皮细胞的上皮－间充质转化（EMT）有明显抑制作用，其机制可能是通过抑制 TGF-β1的表达，改善了肾小管纤维化病变的发生发展。
목적：탐토단분산 B 대고당유도신소관상피세포분화적영향급가능궤제。방법：체외배양대서신소관상피세포 NRK52E 수궤분위정상당（NG）조、고삼（HM）조、고당（HG）조화고당＋Sal B（HB）조，분별배양24 h；채용면역매세포화학염색대 NRK52E 세포진행감정，MMT 법검측단분산 B 대세포생장활성적영향，면역형광세포화학화 Western blotting 검측각조 TGF-β1、E-caderin、α-SMA 화 Col-Ⅳ단백적표체。결과：여 NG 조상비교，HG 조신소관상피세포중 TGF-β1、α-SMA 화 Col-Ⅳ단백표체증다（P ＜0．05），이 E-cadherin 단백표체강저（P＜0．05）；여 HG 조비교，HB 조신소관상피세포중 TGF-β1、α-SMA 화 Col-Ⅳ단백표체감소（P ＜0．05），이 E-cad-herin 단백표체증다（P ＜0．05）。결론：단분산 B 대고당유도신소관상피세포적상피－간충질전화（EMT）유명현억제작용，기궤제가능시통과억제 TGF-β1적표체，개선료신소관섬유화병변적발생발전。
Objective:To investigate the effect of Salvianolic acid B (Sal B)on the high-glucose in-duced epithelial-mesenchymal transition (EMT)in renal tubule epithelial cells and the possible mech-anism.Methods:NRK52E cells,the rat renal tubular epithelial cells,were cultured in vitro.The cells were randomly divided into normal glucose group (group NG),high mannitol group (group HM),high glucose group (group HG)and high glucose and Sal B group (group HB),and each group was cultured for 24 h.Immunocytochemistry was used to identify the renal tubule epithelial cells.MTT was adopted to the effect of Salvianolic acid B on cell growth activity.Immunofluorescence cytochemistry staining was used to assess the protein expression of E-cadherin and α-SMA.Western blotting was used to detect the protein expression of TGF-β1,E-caderin,α-SMA and Col-Ⅳ under different conditions.Results:Compared with group NG,the protein expression of TGF-β1,α-SMA and Col-Ⅳ increased significantly(P <0.05 )while the expression of E-cadherin significantly de-creased (P <0.05)in renal tubular epithelium after treated with high glucose for 24 h.Compared with group HG,in group HB,Sal B decreased the expression of TGF-β1,α-SMA and Col-Ⅳ (P <0.05) and upregulated E-cadherin protein expression in renal tubular epithelium cells after treated with Sal B <br> for 24 h (P <0.05 ).Conclusion:Sal B can significantly inhibit HG-induced expression of EMT through reducing the expression of TGF-β1,which may ameliorate occurrence and development of re-nal tubule fibrosis lesion.