姜黄素对草酸钙诱导肾小管上皮细胞损伤的保护机制研究-现代医学

姜黄素对草酸钙诱导肾小管上皮细胞损伤的保护机制研究

单位：1. 开封市中心医院泌尿外科, 河南开封 475000;
2. 玉溪市人民医院泌尿外科, 云南玉溪 653100;
3. 昆明医科大学第一临床医学院, 云南昆明 650500

分类号：Q291

出版年·卷·期（页码）：2025·53·第十一期（1732-1739）

摘要：

目的：探索姜黄素对草酸钙诱导的大鼠肾小管上皮细胞损伤的保护机制。方法：将NRK-52E细胞分为3组：对照组(不做处理)，实验组一(使用15 mmol·L^-1草酸钙对细胞处理24 h)，实验组二(加入20 μmol·L^-1姜黄素预处理1 h，再加入15 mmol·L^-1的草酸钙共培养24 h)。各组细胞培养相应时间后使用CCK-8实验进行细胞活性的检测；使用乳酸脱氢酶(LDH)法检测细胞的损伤程度；使用丙二醛(MDA)检测细胞的脂质损伤程度；使用Western blotting实验检测细胞相关蛋白(p-p65/p65、IκBα)表达，使用TRizol法抽提细胞中总RNA，设计引物后分析各组细胞中炎症因子(MCP-1、IL-6)相对表达水平。结果：实验组一细胞活力较对照组降低，而LDH、MDA、MCP-1、IL-6水平高于对照组(均P＜0.01)。实验组二细胞活力较实验组一升高，而LDH、MDA、MCP-1、IL-6水平降低(均P＜0.05)。与对照组相比，实验组一总IκBα表达量显著降低，p-p65/p65相对表达量显著增加(均P＜0.01)；与实验组一相比，实验组二总IκBα蛋白表达量显著升高，p-p65/p65相对表达量显著降低(均P＜0.01)。结论：草酸钙可诱导NRK-52E细胞损伤，姜黄素抑制草酸钙诱导的NRK-52E细胞炎症反应的加剧，可能是通过升高IκBα、降低p-p65/p65的表达抑制NF-κB信号通路，从而减轻肾组织细胞损伤。

Objective: To explore the protective mechanism of curcumin against calcium oxalate-induced renal tubular epithelial cell injury in rats. Methods: NRK-52E cells were assigned into three groups: control group(without treatment),experimental group 1(NRK-52E cells treated with 15 mmol·L^-1 calcium oxalate for 24 h) and experimental group 2(NRK-52E cells pretreated with 20 μmol·L^-1 curcumin for 1 h, and then co-cultured with 15 mmol·L^-1 calcium oxalate for 24 h). Cell counting kit(CCK)-8 assay was used to detect the cell viability after the corresponding time of cell culture in each group. Lactate dehydrogenase(LDH) assay was used to detect the degree of cell injury. The degree of lipid damage was detected by malondialdehyde(MDA). Western blotting was used to detect the expression of cell-related proteins(p-p65/p65, IκBα). Total RNA was extracted by TRizol method, and the relative expression levels of inflammatory factors [monocyte chemotactic protein-1(MCP-1), interleukin-6(IL-6)] in each group were analyzed after designing primers. Results: The cell viability of the experimental group 1 was lower than that of the control group, and the levels of LDH, MDA, MCP-1 and IL-6 in the cells were significantly higher(all P<0.01). The cell viability of the experimental group 2 was significantly higher than that of the experimental group 1, and the levels of LDH, MDA, MCP-1 and IL-6 were decreased(all P<0.05). Compared with the control group, the expression of total I-kappa-B-alpha(IκBα) was significantly decreased, while the relative expression of p-p65/p65 was significantly increased(all P<0.01). Compared with the experimental group 1, the expression of total IκBα in the experimental group 2 was significantly increased, and the relative expression of p-p65/p65 was significantly decreased(all P<0.01). Conclusion: Calcium oxalate can induce NRK-52E cell injury. Curcumin can inhibit the aggravation of the inflammatory response in NRK-52E cells induced by calcium oxalate, by increasing IκBα and decreasing the expression of p-p65/p65 to inhibit NF-κB signaling pathway, so as to reduce renal cell injury.

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