The Interplay of Neutrophils, Platelets, and Cytokines in the Healing Process of Acetic Acid-Induced Stomach Ulcer on Trivalent Chromium-Exposed Mice

Abstract

Background: Trivalent chromium is a trace element effective in treating experimental colitis and normal gastrointestinal tissues. We aimed to investigate the effect of trivalent chromium on the injured stomach inmice.Methods: Sixty male slc:ddY mice were used. The animals were randomized into three groups of 20 mice (the control, 10ppm, and 100ppm). Five mice each of twenty were sacrificed on days 0 (for the cytokine study), 3, 7, and 14 and examined. Following anesthesia, the ulcer was induced with acetic acid via laparotomy and through the intraluminal route post-chromium exposure. The blood was obtained from cardiac puncture, and the stomach tissue was scored and excised for myeloperoxidase, catalase, superoxide dismutase, malondialdehyde, total nitrite, cytokines assays, and histology.Results: Ulcer scores of the chromium-exposed group were reduced significantly compared to those of the control group. The platelets increased dramatically in 10- and 100 ppm compared to the control on day 1. There were decreasing neutrophils in the test groups compared with the control across the days of investigation. The malondialdehyde values (nmol/mg protein) significantly reduced in the 10ppm (6.42±0.24+; 3.70±0.42+) and 100ppm (5.22±0.47+; 2.95±0.31+) groups compared to the control (8.35±0.43; 4.53±0.48) on days 7 and 14respectively. Superoxide dismutase increased, (P=0.0372, 0.0441, and 0.0421) on days 3, 7, and 14, respectively in the chromium groups compared with the control. Myeloperoxidase decreased significantly, P=0.0466, and 0.0383 on days 3 and 7 in the chromium groups compared with the control group, respectively. There was no significant change with Catalase and Nitrates assessed. IL-1α, TNF-α, and interferon-γ reduced while IL-10 increased in the mRNA chromium exposed.Conclusion: Chromium exposure to mice upgrades the restoration of gastric ulcers in mice by inhibiting reactive oxygen radicals while promoting endogenous antioxidants