MSc. Second Military Medical University - Shanghai ChangZheng Hospital - Department of Organ Transplantation - Shanghai, China.
Acta Cir Bras. 2022 Jun 15;37(3):e370305. doi: 10.1590/acb370305. eCollection 2022.
To explore the mechanism and investigate the protective effect of hydroxysafflor yellow A (HSYA) on renal oxidative stress, which cyclosporine A (CsA) induces.
HK-2 cells were treated with CsA to get CsA-induced oxidative stress. The effects on oxidative stress and apoptosis of HK-2 cells were detected. The contents of SOD, MDA, GSH-Px, ROS, and CAT in serum were measured, and the expression of apoptosis-related proteins was detected by western blot. Then, established the renal oxidative stress injury rats to verify the efficacy of HSYA.
HSYA could reduce the ROS and MDA contents induced by CsA. Compared with the CsA group, the activities of SOD, CAT, and GSH-Px increased significantly when treated with HSYA. HSYA could inhibit CsA-induced apoptosis in HK-2 cells, and promote the protein of Bcl-2 and inhibit the expression of Bax. Animal experiments showed that HSYA could reduce CsA-induced renal cell injury by reducing glomerular cell vacuoles and inflammatory factors in tissues. It also decreased serum creatinine (Crea) and blood urea nitrogen, increased Crea clearance significantly.
HSYA could significantly improve the antioxidant capacity of the kidney cells and inhibit cell apoptosis, thereby effectively ameliorating CsA-induced oxidative stress in vitro and in vivo.
探讨羟基红花黄色素 A（HSYA）对环孢素 A（CsA）诱导的肾氧化应激的作用机制和保护作用。
用 CsA 处理 HK-2 细胞以获得 CsA 诱导的氧化应激。检测 HK-2 细胞氧化应激和凋亡的影响。测定血清中超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-Px）、活性氧（ROS）和过氧化氢酶（CAT）的含量，并用 Western blot 检测凋亡相关蛋白的表达。然后，建立肾氧化应激损伤大鼠模型，验证 HSYA 的疗效。
HSYA 可降低 CsA 诱导的 ROS 和 MDA 含量。与 CsA 组相比，用 HSYA 处理后 SOD、CAT 和 GSH-Px 的活性显著增加。HSYA 可抑制 CsA 诱导的 HK-2 细胞凋亡，并促进 Bcl-2 蛋白的表达，抑制 Bax 的表达。动物实验表明，HSYA 可通过减少肾小球细胞空泡和组织中的炎症因子来减轻 CsA 诱导的肾细胞损伤。它还降低了血清肌酐（Crea）和血尿素氮，显著增加了 Crea 清除率。
HSYA 可显著提高肾细胞的抗氧化能力并抑制细胞凋亡，从而有效改善体外和体内 CsA 诱导的氧化应激。
