金丝桃苷通过NOX4抑制膀胱尿路上皮癌细胞的增殖

doi:10.3870/j.issn.1672-8009.2026.01.006

摘要/Abstract

摘要： 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。

关键词: 金丝桃苷, 膀胱尿路上皮癌, NOX4蛋白

Abstract: Objective To analyze the inhibitory effect of hyperoside on inhibiting the proliferation of bladder urothelial carcinoma(BLCA)cells and the mechanism. Methods Cell proliferation was detected by CCK-8 and colony formation assays.The expression level of nicotinamide adenine 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 significantly decreased in the hyperoside group(P<0.05).The expression level of NOX4 was significantly 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 above 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.

Key words: hyperoside, bladder urothelial carcinoma, NOX4 protein

中图分类号:

高慧林, 王海临, 梦琪. 金丝桃苷通过NOX4抑制膀胱尿路上皮癌细胞的增殖[J]. 医学分子生物学杂志, 2026, 23(1): 43-50.

GAO Huilin, WANG Hailin, Meng Qi. Inhibitory Effect of Hyperoside on Prodiferation of Bladder Urothelial Carcinoma Cells via NOX4[J]. Journal of Medical Molecular Biology, 2026, 23(1): 43-50.

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