目的 探讨血管紧张素II-2受体（AT2R）激动剂复合物21（C21）对高级糖基化终末产物牛血清白蛋白（AGE-BSA）刺激下NRK-52E细胞细胞因子水平的影响及作用机制。方法 将NRK-52E细胞分为对照组以及AGE-BSA组（25、50、100、200）mg/L，培养48小时，通过实时定量PCR和ELISA检测白细胞介素-6（IL-6）和肿瘤坏死因子α（TNF-α）的mRNA和蛋白表达水平。然后对以AGE-BSA（25 mg/L）刺激48小时的NRK-52E细胞进行（0.01、0.05、0.1）mmol/L C21处理24小时，通过qRT-PCR和Western blot分析检测蛋白激酶C（PKC）、核因子κB p65（NF-κB p65）和转化生长因子β1（TGF-β1）的mRNA和蛋白表达水平。结果 IL-6和TNF-α的mRNA表达水平在不同剂量的AGE-BSA诱导下NRK-52E细胞中均显著增加，其中25 mg/L AGE-BSA组的增加最大。AGE-BSA刺激导致的NRK-52E细胞中PKC、NF-κB p65和TGF-β1的mRNA和蛋白表达水平明显降低（0.01、0.05、0.1）mmol/L C21。结论 AGE-BSA促进NRK-52E细胞中IL-6、TNF-α、PKC、NF-κB p65和TGF-β1的表达，而C21抑制AGE-BSA在NRK-52E细胞中的作用。

Objective To investigate the effect and mechanism of compound 21(C21), an agonist of angiotensin II-2 receptor (AT2R) on the cytokine levels of NRK-52E cells stimulated by advanced glycation end products bovine serum albumin (AGE-BSA). Methods NRK-52E cells were divided into control and (25, 50, 100, 200)mg/L AGE-BSA groups and cultured for 48 hours. The mRNA and protein expression levels of leukin-6 (IL-6) and tumor necrosis factor α (TNF-α) were detected by real-time quantitative PCR and ELISA. The NRK-52E cells stimulated by AGE-BSA(25 mg/L) for 48 hours were then treated with (0.01, 0.05, 0.1)mmol/L C21 for 24 hours. The mRNA and protein expression levels of protein kinase C (PKC), nuclear factor κB p65 (NF-κB p65) and transforming growth factor β1 (TGF-β1) were detected by qRT-PCR and Western blot analysis. Results The mRNA expression levels of IL-6 and TNF-α significantly increased in NRK-52E cells stimulated by AGE-BSA at different doses, with the greatest increase in the 25 mg/L AGE-BSA group. The mRNA and protein expression levels of PKC, NF-κB p65 and TGF-β1 in AGE-BSA-induced NRK-52E cells significantly decreased by (0.01, 0.05, 0.1)mmol/L C21. Conclusion AGE-BSA promotes the expression of IL-6, TNF-α, PKC, NF-κB p65 and TGF-β1 in NRK-52E cells, while C21 inhibits the effect of AGE-BSA on NRK-52E cells.