Wang Yan, Zhang Yun-Hui, Tang Yin-Ru, Lan Jie, Huang Zhi-Ying, Tian Wei, Huang Qian, Peng Yan, Gao Yuan, Hu Yue-Qin, Zhang Xue-Nong
Department of Pharmacy, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang 443003, P.R. China.
School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, P.R. China.
Iran J Basic Med Sci. 2022 Mar;25(3):414-418. doi: 10.22038/IJBMS.2022.58959.13102.
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.
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.
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.
The findings of this study demonstrate that T-I can protect against CDDP-induced nephrotoxicity through suppression of oxidative stress.
顺铂（CDDP）是一种高效的化疗药物，但其临床应用受到肾毒性的限制。丹参酮Ⅰ（T-I）是从中药丹参中提取的菲醌类化合物，已被用于改善血液循环和治疗心血管疾病。本研究旨在探讨T-I对CDDP诱导的小鼠肾毒性的保护作用。
在实验第一天通过单次腹腔注射20mg/kg CDDP建立肾毒性BALB/c小鼠模型。在给予CDDP前3小时，给小鼠腹腔注射10mg/kg和30mg/kg的T-I，连续3天，以探讨T-I的肾保护作用。
T-I治疗显著降低了给予CDDP的小鼠血清中的血尿素氮和肌酐水平，尤其是在剂量为30mg/kg时。与CDDP相比，30mg/kg的T-I显著降低了肾组织中的丙二醛水平，提高了谷胱甘肽水平和过氧化氢酶的酶活性。此外，T-I（30mg/kg）显著逆转了CDDP降低的肾组织中超氧化物歧化酶2蛋白的表达水平。肾脏的组织病理学评估进一步证实了T-I的保护作用。
本研究结果表明，T-I可通过抑制氧化应激来预防CDDP诱导的肾毒性。
