Article Publish Status: FREE
Abstract Title:

Carnosic Acid Attenuates Cadmium Induced Nephrotoxicity by Inhibiting Oxidative Stress, Promoting Nrf2/HO-1 Signalling and Impairing TGF-β1/Smad/Collagen IV Signalling.

Abstract Source:

Molecules. 2019 Nov 18 ;24(22). Epub 2019 Nov 18. PMID: 31752142

Abstract Author(s):

Sonjit Das, Saikat Dewanjee, Tarun K Dua, Swarnalata Joardar, Pratik Chakraborty, Shovonlal Bhowmick, Achintya Saha, Simanta Bhattacharjee, Vincenzo De Feo

Article Affiliation:

Sonjit Das


Cadmium (Cd) imparts nephrotoxicity via triggering oxidative stress and pathological signal transductions in renal cells. The present study was performed to explore the protective mechanism of carnosic acid (CA), a naturally occurring antioxidant compound, against cadmium chloride (CdCl)-provoked nephrotoxicity employing suitable in vitro and in vivo assays. CA (5µM) exhibited an anti-apoptotic effect against CdCl(40 µM) in normal kidney epithelial (NKE) cells evidenced from cell viability, image, and flow cytometry assays. In this study, CdCltreatment enhanced oxidative stress by triggering free radical production, suppressing the endogenous redox defence system, and inhibiting nuclear factor erythroid 2-related factor 2 (Nrf2) activation in NKE cells and mouse kidneys. Moreover, CdCltreatment significantly endorsed apoptosis and fibrosis via activation of apoptotic and transforming growth factor (TGF)-β1/mothers against decapentaplegic homolog (Smad)/collagen IV signalling pathways, respectively. In contrast, CA treatment significantly attenuated Cd-provoked nephrotoxicity via inhibiting free radicals, endorsing redox defence, suppressing apoptosis, and inhibiting fibrosis in renal cells in bothin vitro and in vivo systems. In addition, CA treatment significantly (<0.05-0.01) restored blood and urine parameters to near-normal levels in mice. Histological findings further confirmed the protective role of CA against Cd-mediated nephrotoxicity. Molecular docking predicted possible interactions between CA and Nrf2/TGF-β1/Smad/collagen IV. Hence, CA was found to be a potential therapeutic agent to treat Cd-mediated nephrotoxicity.

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