Gallic Acid Reduces Experimental Colitis in Rats by Downregulation of Cathepsin and Oxidative Stress

Abstract

Objective: Ulcerative colitis (UC) is an idiopathic inflammatory bowel disease (IBD) with common, repetitive inflammation of the colon and rectum, which is highly defined by loss of blood on colon mucosa, ulceration and acute inflammation. The present study aimed to investigate the potential protective effects of gallic acid (GA) through a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis rat model, using biochemical and histopathological parameters. Materials and Methods: The study consisted of four groups, each including seven rats, namely control group, colitis group, colitis-GA 50 mg/kg group and colitis-GA 100 mg/kg group. Colon tissue samples were analyzed for malondialdehyde (MDA), myeloperoxidase (MPO), cathepsin B and cathepsin L values. Results: Tissue MDA, MPO, cathepsin L and cathepsin B values increased significantly in colitis group (p=0.028, p=0.038, p=0.024, p=0.019, respectively). However, MDA, MPO, cathepsin L and cathepsin B values showed a significant decrease in animals with GA (at a dose of 100 mg/kg) administration in TNBS-induced colitis in rats (p=0.021, p=0.026, p=0.019, p=0.031, respectively). Colitis group was defined by the severe detriment of surface epithelium, submucosal edema and inflammatory cell infiltration. Treatment with GA significantly decreased inflammatory cell infiltration. Conclusion: GA can be used as an effective agent in the treatment of colitis due to its inhibitory properties in multiple pathways and its potent antioxidant effects.

Keywords

• cathepsin
• colitis
• gallic acid
• myleperoxidase
• oxidative stress.