The interplay of neutrophils, platelets, and cytokines in the healing process of acetic acid-induced stomach ulcer on trivalent chromium-exposed mice

Abstract
Background: The trace element trivalent chromium has been reported for its beneficial role in experimental colitis and normal gastrointestinal tissues. This study aimed to investigate the effect of trivalent chromium on the injured stomach in mice.
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 reduced significantly compared to the control. The platelets increased dramatically in 10- and 100 ppm compared to control on day 1. There were decreasing neutrophils in the test groups compared to 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 14 respectively. Superoxide dismutase increased, (p = 0.0372, 0.0441, and 0.0421 on days 3, 7, and 14, respectively) in the chromium groups compared to the control. Myeloperoxidase decreased significantly, p = 0.0466, and 0.0383 on days 3 and 7 in the chromium groups compared to 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