Protective effects of tanshinone I against cisplatin-induced nephrotoxicity in mice
نویسندگان
1 Department of Pharmacy, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People’s Hospital, Yichang 443003, P.R. China
2 School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, P.R. China
3 School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, P.R. China
4 Department of Pharmacy, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People’s Hospital, Yichang 443003, P.R. China
5 Department of Pharmacy, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People’s Hospital, Yichang 443003, P.R. China
6 Department of Pharmacy, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People’s Hospital, Yichang 443003, P.R. China
7 School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, P.R. China
8 School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, P.R. China
9 Department of Nephrology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People’s Hospital, Yichang 443003, P.R. China
10 Department of Pharmacy, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People’s Hospital, Yichang 443003, P.R. China
11 Department of Pharmacy, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People’s Hospital, Yichang 443003, P.R. China
doi
10.22038/ijbms.2022.58959.13102چکیده
Objective(s): Cisplatin (CDDP) is a highly effective chemotherapeutic agent, but its clinical application has been limited by nephrotoxicity. Tanshinone Ⅰ (T-I), a phenanthrenequinone compound extracted from the Chinese herb Danshen, has been used to improve circulation and treat cardiovascular diseases. The aim of this study was to investigate the protective effect of T-I on CDDP-induced nephrotoxicity in mice.Materials and Methods: The BALB/c mouse models of nephrotoxicity were established by a single intraperitoneal injection of 20 mg/kg CDDP on the first day of the experiment. Three hours prior to CDDP administration, the mice were dosed with 10 mg/kg and 30 mg/kg T-I for 3 consecutive days intraperitoneally to explore nephroprotection of T-I.Results: Treatment with T-I significantly reduced blood urea nitrogen and creatinine levels in serum observed in CDDP-administered mice, especially at a dose of 30 mg/kg. T-I at 30 mg/kg significantly decreased malondialdehyde levels and increased glutathione levels and the enzymatic activity of catalase in kidney tissue compared to CDDP. Additionally, T-I (30 mg/kg) significantly reversed the CDDP-decreased expression level of superoxide dismutase 2 protein in renal tissue. Histopathological evaluation of the kidneys further confirmed the protective effect of T-I. Conclusion: The findings of this study demonstrate that T-I can protect against CDDP-induced nephrotoxicity through suppression of oxidative stress.
