Histopathological Evaluation of The Protective Effects of Resveratrol Against Gastrointestinal Tissue Damage Induced by Cisplatin in Rats
The Effects of Resveratrol Against Gastrointestinal Tissue Damage Induced by Cisplatin in Rats
Keywords:Cisplatin, Resveratrol, Histopathology, Small Intestine, Apoptosis
Background: The purpose of this study was to investigate the effects of differing doses of resveratrol (RES) against cisplatin (CP)-induced gastrointestinal injury in small intestinal tissue using histopathological and immunohistochemical methods.
Materials and Methods: Forty-eight healthy male Wistar albino rats aged 12-16 weeks were divided into eight groups, control RES-30, RES-60, RES-90, CP, CP+RES30, CP+RES60, and CP+RES90. Small intestine tissues were collected at the end of the experimental period and subjected to routine hematoxylin & eosin and Periodic Acid Schiff staining. Tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) were evaluated from immunohistochemically stained tissues. DNA fragmentation was evaluated using the TUNEL technique.
Results: Based on the histopathological findings, vacuolization and shedding were observed in the small intestine surface epithelium with notable fusion and shortening in the villus structure in the CP group. Significant decreases were observed in the CP+RES30, CP+RES60, and particularly CP+RES90 groups compared to the CP group in terms of apical surface epithelial degeneration, villous fusion, and inflammatory cell infiltration. The apoptotic index (AI) and TNF-α immunoreactivities were significantly higher in the CP group compared to the control group (p<0.05). AI and TNF-α immune intensity were significantly lower in the CP+RES30, CP+RES60, and CP+RES90 groups compared to the CP group (p<0.05). It has been determined that among the treatment groups, particularly the CP+RES30 group showed the lowest damage score values and immunoreactivity of TNF-α with AI compared to the CP group.
Conclusions: In conclusion, CP caused severe histological tissue injury, intestinal apoptosis, and proinflammatory cytokine release, while RES administered before CP treatment exhibited a dose-dependent protective effect (particularly at RES30 mg/kg) against CP-induced intestinal injury.
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