曲美他嗪（TMZ）是一种对肾脏病理有潜力的新兴治疗环戊二腈衍生物。然而，TMZ对重金属诱导的肾脏毒性的保护机制尚不清楚。因此，本研究旨在探讨TMZ是否可以减轻汞诱导的大鼠肾毒性。大鼠被注射TMZ（3mg/kg bw）和/或氯化汞（HgCl2）（4mg/kg bw）4天（每组n=6只大鼠）。血液分析结果显示，与对照组相比，HgCl2组中肌酐、尿素和尿酸水平显著增加。与对照组相比，HgCl2引起肾脏超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx）活性明显降低，并导致丙二醛（MDA）、白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、半胱氨酸蛋白酶-3和半胱氨酸蛋白酶-9水平显著增加。与对照组相比，抗炎细胞因子白细胞介素-4（IL-4）和白细胞介素-10（IL-10）的肾脏水平显著降低。相反，在接受TMZ + HgCl2的大鼠中，与HgCl2组相比，肾脏标志物MDA、TNF-α、IL-6和半胱氨酸蛋白酶-3/-9明显降低。肾脏SOD、CAT、GPx、IL-4和IL-10显著升高，病理学损伤得到改善。总体而言，TMZ可能通过抑制氧化炎症和凋亡来重新应用于阻断HgCl2的肾毒性作用。

Trimetazidine (TMZ) is a promising emerging therapeutic piperazine derivative for renal pathologies. However, the nephroprotective mechanism of TMZ against heavy metal-induced toxicity is unknown. This study, therefore, aimed to explore whether TMZ could mitigate mercury-induced nephrotoxicity in rats. Rats were injected TMZ (3 mg/kg bw) and/or mercury chloride (HgCl2) (4 mg/kg bw) for 4 days (n = 6 rats per group). The blood analysis revealed marked increases in creatinine, urea and uric acid levels in HgCl2 group compared to the control. HgCl2 induced prominent decreases in renal superoxide dismutase (SOD), catalase (CAT), glutathione peroxide (GPx) activities compared to the control followed by marked increases in the levels of malondialdehyde (MDA), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), caspase-3 and caspase-9. Whereas the renal levels of anti-inflammatory cytokines interleukin-4 (IL-4) and interleukin-10 (IL-10) reduced considerably compared to the control. Contrarily, it was found that in the rats administered TMZ + HgCl2, levels of renal markers, MDA, TNF-α, IL-6 and caspases-3/-9 were prominently reduced compared to the HgCl2 group. The renal SOD, CAT, GPx, IL-4, and IL-10 were markedly elevated along with ameliorated histopathological lesions. On the whole, therefore, TMZ could be repurposed for blocking HgCl2 nephrotoxicity via inhibition of oxidative inflammation and apoptosis in rats.