Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 142, Issue -, Pages -Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2021.111995
Keywords
Nephrotoxicity; Danshensu; Cisplatin; Oxidative stress; Inflammation
Funding
- National Natural Science Foundation of China [81903697, 8180131467]
- Programs for Science and Technology Development and Plan of Yantai [2015YD012]
- Medicine and Health Technology Development Plan of Shandong Province [2018WS562]
- Traditional Chinese Medicine Plan-ning Project of Shandong Province [2017-225]
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Danshensu has protective effects against cisplatin-induced nephrotoxicity by improving kidney damage, attenuating abnormal renal function indicators and oxidative stress, activating Nrf2/HO-1, and inhibiting the NF-kappa B pathway.
The clinical application of cisplatin was mainly limited by severe nephrotoxicity. Danshensu was the main pharmacological active diterpenoids which extracted from the roots of Salvia milthiorriza Bunge. This study is aimed to investigate the protective effects and potential mechanisms of Danshensu against cisplatin-induced nephrotoxicity. After fasting for 12 h, all mice groups except the control group were administered a single intraperitoneal injection of 25 mg/kg cisplatin. 1 h later, cisplatin (25 mg/kg) + Danshensu (15 mg/kg, 30 mg/ kg, 60 mg/kg) groups were treated with corresponding doses of Danshensu once a day for 7 consecutive days. Blood urea nitrogen (BUN), creatinine, reactive oxygen species (ROS), superoxide dismutase (SOD), Glutathione peroxidase (GPx), Catalase (CAT) and malondialdehyde (MDA) were assayed in this study. The expression of inflammatory cytokines TNF-alpha, IL-6 and IL-1 beta were examined by ELISA. The results showed that Danshensu could improve kidney damage, attenuate serum BUN, creatinine, cytokines and oxidative stress markers. Further studies showed that Danshensu can induce Nrf2/HO-1 activation and inhibition of NF-kappa B pathway. In conclusion, Danshensu exerts the protective effects on cisplatin-induced nephrotoxicity, which may be related to the activation of Nrf2/HO-1 and inhibition of NF-kappa B pathway.
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