Salvianolic Acid C Protects against Cisplatin-Induced Acute Kidney Injury through Attenuation of Inflammation, Oxidative Stress and Apoptotic Effects and Activation of the CaMKK-AMPK-Sirt1-Associated Signaling Pathway in Mouse Models

doi:10.3390/antiox10101620

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Title:	Salvianolic Acid C Protects against Cisplatin-Induced Acute Kidney Injury through Attenuation of Inflammation, Oxidative Stress and Apoptotic Effects and Activation of the CaMKK-AMPK-Sirt1-Associated Signaling Pathway in Mouse Models
Authors:	Chien, Liang-Hsuan Wu, Chien-Ta Deng, Jeng-Shyan Jiang, Wen-Ping Huang, Wen-Chin Huang, Guan-Jhong
Contributors:	China Med Univ, Coll Chinese Med, Dept Chinese Pharmaceut Sci & Chinese Med Resourc Kaohsiung Med Univ, Coll Pharm, Fac Pharm Asia Univ, Dept Hlth & Nutr Biotechnol Chia Nan Univ Pharm & Sci, Dept Pharm China Med Univ, Grad Inst Biomed Sci, Sch Med China Med Univ, Sch Med, Int Masters Program Biomed Sci
Keywords:	salvianolic acid C cisplatin acute kidney injury anti-inflammation oxidative stress apoptosis CaMKK-AMPK-Sirt1 pathway
Date:	2021
Issue Date:	2023-11-11 11:45:23 (UTC+8)
Publisher:	MDPI
Abstract:	Acute kidney injury (AKI) is a sudden reduction in kidney activity and has a high mortality rate. Salvianolic acid C (SAC), one of the main polyphenolic components of Salvia miltiorrhiza, displays significant pharmacologically active effects. An animal model of cisplatin-induced kidney injury was used to study the potential of SAC to improve AKI. First, SAC was administered intraperitoneally in mice for 10 consecutive days, and then cisplatin was administered intraperitoneally on day 7 to establish a nephrotoxicity mouse model. SAC mitigated renal histological changes, blood creatinine (CRE) and blood urea nitrogen (BUN) production and the levels of inflammatory mediators in the cisplatin-induced AKI. Furthermore, malondialdehyde (MDA) levels were reduced and glutathione (GSH) was increased after intraperitoneal injection (i.p.) administration of SAC. In addition, based on Western blot data, SAC reduced the expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor kappa B (NF-kappa B) and mitogen-activated protein kinase (MAPK) activation in mouse renal tissues. Finally, SAC diminished the level of TLR-4 expression and enhanced the production of several antioxidative enzymes (superoxidase dismutase (SOD1), glutathione peroxidase (GPx3), catalase, nuclear-factor-erythroid-2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1)), Sirtuin 1 (Sirt1), p-AMP-activated protein kinase (AMPK) and p-Ca2+/calmodulin-dependent protein kinase kinase (CaMKK). In addition, Sirt1 inhibition (EX 527) inverted the effect of SAC against cisplatin-induced nephrotoxicity. Collectively, SAC provides a therapeutic target with promising clinical potential after cisplatin treatment by attenuating oxidative stress and inflammation.
Relation:	ANTIOXIDANTS-BASEL, v.10, n.10, pp.1620
Appears in Collections:	[Dept. of Pharmacy] Periodical Articles

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