Alireza Moradi1, Mahdieh Abolfathi2, Mahsa Javadian3, Esfandiar Heidarian2, Hoshang Roshanmehr4, Mansoor Khaledi5, Ali Nouri6. 1. Department of Physiology, Iran University of Medical Sciences, Tehran, Iran. 2. Clinical Biochemistry Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran. 3. Medical Plant Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran. 4. Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. 5. Department of Medical Microbiology, Faculty of Medicine, Shahed University of Medical Science, Tehran, Iran. 6. Clinical Biochemistry Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran; Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: Ali.Noori1371@gmail.com.
Abstract
BACKGROUND/AIM: Diclofenac (DIC) is a Nonsteroidal anti-inflammatory drug (NSAID) and consumption of this drug creates side effects such as renal injury. The purpose of this work was to assess the influences of gallic acid (GA) on DIC-induced renal injury in rats. MATERIAL AND METHODS: Rats were segregated into five groups. Group 1, control group; Group 2 received DIC-only (50 mg/kg bw, i.p.) for 7 consecutive days; Groups 3, received GA-only (100 mg/kg bw, po) for 7 consecutive days; group 4 received DIC (50 mg/kg bw, i.p.) plus GA (50 mg/kg, po) for 7 consecutive days and group 5 received DIC (50 mg/kg bw, i.p.) plus GA (100 mg/kg, po) for 7 consecutive days. RESULTS: The data indicated that the levels of the serum protein carbonyl, sGOT, sGPT, urea, creatinine, uric acid, nitrite content, MDA, serum IL-1β, and the renal IL-1β gene expression were remarkably increased in DIC-only treated animals compared to control group. In the other hand, treatment with gallic acid led to significant improvements in abnormalities of DIC-induced oxidative stress and serum biochemical parameters. Histological changes were also ameliorated by GA oral administration. CONCLUSION: The results indicated that oral injection of GA could alleviate the noxious effects of DIC on the antioxidant defense system and renal tissue.
BACKGROUND/AIM: Diclofenac (DIC) is a Nonsteroidal anti-inflammatory drug (NSAID) and consumption of this drug creates side effects such as renal injury. The purpose of this work was to assess the influences of gallic acid (GA) on DIC-induced renal injury in rats. MATERIAL AND METHODS:Rats were segregated into five groups. Group 1, control group; Group 2 received DIC-only (50 mg/kg bw, i.p.) for 7 consecutive days; Groups 3, received GA-only (100 mg/kg bw, po) for 7 consecutive days; group 4 received DIC (50 mg/kg bw, i.p.) plus GA (50 mg/kg, po) for 7 consecutive days and group 5 received DIC (50 mg/kg bw, i.p.) plus GA (100 mg/kg, po) for 7 consecutive days. RESULTS: The data indicated that the levels of the serum protein carbonyl, sGOT, sGPT, urea, creatinine, uric acid, nitrite content, MDA, serum IL-1β, and the renal IL-1β gene expression were remarkably increased in DIC-only treated animals compared to control group. In the other hand, treatment with gallic acid led to significant improvements in abnormalities of DIC-induced oxidative stress and serum biochemical parameters. Histological changes were also ameliorated by GA oral administration. CONCLUSION: The results indicated that oral injection of GA could alleviate the noxious effects of DIC on the antioxidant defense system and renal tissue.