L.carnitine can attenuate cadmium induced hepatotoxicity in rat: emphasis on TLR4-NFκB axis

Document Type : Original research articles

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Department of Pharmacology, Egyptian Drug Authority, EDA, Formerly NODCAR, Giza, Egypt

Abstract

Cadmium (Cd), an environmental health hazard, is a causative agent of many pathological conditions especially liver diseases. The possible ameliorative role of L. Carnitine on cadmium- provoked liver injury was discussed in this study. Twenty-four male rats were daily challenged for 30 days with CdCl2 (cadmium chloride) 5mg/kg/day and/or L. Carnitine 100 mg/kg/day. L. Carnitine administration halted the alteration of liver function biomarkers induced by cadmium which appeared as decreased AST, ALT and ALP levels . L. Carnitine prohibited CdCl2-generated oxidative stress via Nrf2/HO.1 pathway by increasing TAC and decreasing MDA and NO. L. Carnitine also restrained inflammatory insult created by CdCl2 by suppressing TLR4/NFκB pathway through reducing the inflammatory mediators including TNF-α, IL-1β and IL-18. Finally, our biochemical data were confirmed by the improvement of the liver histology by L. Carnitine . These results revealed that TLR4/NFκB axis implicated in L. Carnitine protection against CdCl2-triggered hepatotoxicity accompanied by inhibition of oxidative stress and this may provide new ideas in order to treat cadmium-related diseases

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Azhar International Journal of Pharmaceutical and Medical Sciences
Volume 4, Issue 2
June 2024
Pages 141-153

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