金丝桃苷通过NOX4抑制膀胱尿路上皮癌细胞的增殖OA
Inhibitory Effect of Hyperoside on Prodiferation of Bladder Urothelial Carcinoma Cells via NOX4
目的 分析金丝桃苷对膀胱尿路上皮癌(bladder urothelial carcinoma,BLCA)细胞增殖的抑制作用和机制.方法 CCK-8 和克隆形成实验检测金丝桃苷对BLCA增殖的影响;蛋白质印迹检测不同浓度和时间金丝桃苷干预下细胞中烟酰胺腺嘌呤二核苷酸磷酸氧化酶4(NOX4)表达水平;检测金丝桃苷靶向抑制NOX4 对细胞增殖以及mTOR、AKT、S6、NOX4 蛋白表达的影响.结果 金丝桃苷组细胞增殖能力、细胞克隆数、移植瘤组织体积和质量、Ki67 蛋白表达水平均明显降低(P<0.05).金丝桃苷作用时间越长或浓度越高,NOX4 的表达水平下降越明显(P<0.05).与对照组比较,金丝桃苷组p-mTOR、p-S6、p-AKT和NOX4 表达和克隆细胞数明显下降,NOX4 过表达组和金丝桃苷+NOX4 过表达组上述指标均明显升高(P<0.05).结论 金丝桃苷通过抑制NOX4 表达抑制BLCA增殖.
Objective To analyze the inhibitory effect of hyperoside on inhibiting the prolifera-tion of bladder urothelial carcinoma(BLCA)cells and the mechanism.Methods Cell prolifera-tion was detected by CCK-8 and colony formation assays.The expression level of nicotinamide ade-nine dinucleotide phosphate oxidase 4(NOX4)in cells under different concentration of hyperoside and intervention time,and the expression levels of mTOR,AKT,S6 cells and NOX4 proteins were detected by Western blotting.Results The proliferation ability of cells,number of cell colonies,volume and mass of transplanted tumor tissues,and expression level of Ki67 protein were signifi-cantly decreased in the hyperoside group(P<0.05).The expression level of NOX4 was significant-ly decreased with the increase of the treatment time and concentration of hyperoside(P<0.05).Compared with those in the control group,the expression levels of p-mTOR,p-S6,p-Akt and NOX4,and number of colonies were significantly decreased in the hyperoside group,while the a-bove indexes were significantly increased in the NOX4 overexpression group and the hyperoside+NOX4overexpression group(P<0.05).Conclusion Hyperoside can inhibit BLCA proliferation by supressing the expression of NOX4.
高慧林;王海临;梦琪
巴彦淖尔市医院泌尿外科 内蒙古自治区巴彦淖尔市,015000巴彦淖尔市医院泌尿外科 内蒙古自治区巴彦淖尔市,015000巴彦淖尔市医院泌尿外科 内蒙古自治区巴彦淖尔市,015000
医药卫生
金丝桃苷膀胱尿路上皮癌NOX4 蛋白
hyperosidebladder urothelial carcinomaNOX4 protein
《医学分子生物学杂志》 2026 (1)
43-50,8
内蒙古自治区自然科学基金(No.2020MS08060) This work was supported by a grant from the Natural Science Foundation Project of Inner Mongolia Autonomous Region(No.2020MS08060)
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