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Abstract
The carvacrol is thought to promote optimal health via its antioxidant and free radical scavenging effects. The aim of our present study was to investigate the efficacy of carvacrol on the development of kidney injury in acute pancreatitis model (AP) induced by cerulein and to explore the underlying mechanism. The rats were randomised into groups to receive (I) no therapy; (II.) 50 µg/kg cerulein at 1-h intervals by four intraperitonally injection (i.p.); (III) 50, 100 and 200 mg/kg carvacrol by one i.p.; and (IV) cerulein+carvacrol after 2 h of cerulein injection. 12 h later, serum was provided to assess the blood urea nitrogen (BUN), creatinine (CRE) and uric acid (UA) values. Also, renal tissues were obtained for histological and biochemical measurements. Kidney oxidative stress markers were evaluated by changes in the amount of lipid peroxides measured as malondialdehyde (MDA) and changes in tissue antioxidant enzyme levels, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-PX). Histopathological examination was performed using scoring systems. We found that the increasing doses of carvacrol decreased pancreatitis-induced MDA levels. Moreover, the renal SOD, CAT and GSH-Px activities in the AP+carvacrol group were higher than that of the rats in the AP group. In the treatment groups, the BUN, CRE and UA were reduced. Besides, necrosis, coagulation and inflammation in the kidney were alleviated (p < 0.05). Finally, the magnitude of the protective effect on kidney is certain, and 200 mg/kg carvacrol is an effective theraphy for oxidative stress caused by AP.