Histopathology and Immunohistochemistry Evidence of Protective Effects of <i>Arachis hypogaea</i> Seed on 1, 2- Dimethylhydrazine-Induced Carcinogenesis in Male and Female Rat Colon
DOI:
https://doi.org/10.26538/tjpps/v3i9.5Keywords:
Cytokeratin 20, Histopathology, Colon carcinogenesis, 1, 2- dimethylhydrazine (DMH), Arachis hypogaeaAbstract
The study investigated the potential of a peanut-supplemented diet to reverse 1, 2- dimethyl hydrazine (DMH)-induced carcinogenesis linked tissue morphology and biomolecular alterations in rats’ colon. Fifty-six healthy Wistar rats of both sexes used for this study were divided into seven (7) groups of 4 rats each. Group A (control) rats were maintained on normal rat feeds. Groups B and C were maintained on normal rat feed and administered DMH (25 mg/kg body weight per week subcutaneously) for 12 and 24 weeks, respectively. After 12 weeks of DMH administration, a peanut-supplemented diet was provided for the remaining 12 weeks for Group D rats. Group E rats received DMH and a peanut-supplemented diet concomitantly for 24 weeks. Group F rats were on a peanut-supplemented diet for 12 weeks, followed by DMH administration for the remaining 12 weeks. Group G rats were maintained on a peanut-supplemented diet only for 24 weeks without DMH administration. At the end of the treatment period (24 weeks), the rats were sacrificed under mild anaesthesia, and portions of the colon were collected and fixed for histopathological and immunohistochemical examination. Colon histology revealed that DMH treatment without peanut supplementation caused severe histoarchitectural changes that were ameliorated by a peanut-supplemented diet. Immunohistochemistry of the colons showed that rats administered DMH only were positive for cytokeratin 20, indicating cancerous cells, and those exposed to DMH and peanut-supplemented diet were cytokeratin 20 negative. These results suggest that Arachis hypogaea seeds via peanut-supplemented diet protected rats’ colons against 1, 2-dimethylhydrazine-induced colon carcinogenesis.
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