Modulatory effects of carvacrol against cadmium-induced hepatotoxicity and nephrotoxicity by molecular targeting regulation.

AIM

Cadmium (Cd) is a toxic heavy metal that causes severe toxic effects on different tissues including liver and kidney. Therefore the research for alternatives to reduce the damage caused by Cd has substantial importance. This study was performed to examine the possible modulatory effects of carvacrol (CRV) against Cd-induced hepatorenal toxicities and the possible mechanisms underlying these effects.

MATERIALS AND METHODS

In the present study, 35 male Wistar rats were randomly divided into 5 groups. The rats were treated with Cd (25 mg/kg) and treated with CRV (25 and 50 mg/kg body weight) for 7 consecutive days.

KEY FINDINGS

CRV could modulate Cd-induced elevations of ALT, ALP, AST, urea, creatinine, MDA and enhance antioxidant enzymes' activities such as SOD, CAT, and GPx, and GSH's level. CRV also reversed the changes in levels of inflammatory biomarker and apoptotic genes that include NF-κB, Bcl-3, MAPK-14, iNOS, COX-2, MPO, PGE2, Bax, Bcl-2, P53, Caspase-9, Caspase-6 and Caspase-3 in both tissues. The levels of 8-OHdG in the Cd-induced liver and kidney tissues were modulated after CRV treatment. Furthermore, CRV treatment considerably lowered Cd, Na, Fe, and Zn content while increased K, Ca, Mg and Cu contents in both tissues as compared to the Cd-exposed rats.

SIGNIFICANCE

The results of the present study revealed that CRV supplementation could be a promising strategy to protect the liver and kidney tissues against Cd-induced oxidative damage, inflammation and apoptosis.