AMELIORATIVE EFFECTS OF TANNIC ACID ON ETHANOL-INDUCED NEURODEGENERATION IN THE PREFRONTAL CORTEX

Background: High alcohol intake is a known cause of brain damage. Tannic acid (TA) poses as a potential treatment measure. Aim: To investigate the histomorphology changes in the microstructures of the prefrontal cortex of adult Wistar rats during treatment with tannic acid following ethanol-induced neurotoxicity. Methodology: Thirty-six (36) adult male Wistar rats (160g-240g) were assigned into six (6) groups (A to F) of 6 rats each. Group “A” (untreated negative control) received daily doses of distilled water at 6ml/kg/bwt while Group “B” (alcohol control group) received daily doses of 6g/kg/bwt of 40% ethanol only. Group “C, D and E” received daily doses of 6g/kg/bwt of 40% ethanol co-administrated with 200mg/kg/bwt, 100mg/kg/bwt and 50mg/kg/bwt of TA respectively. Group “F” (positive control group) received daily doses of 6g/kg/bwt of 40% ethanol co-administrated with 335mg/kg/bwt of Vitamin E. All treatments were oral and lasted 14 days. The animals were sacrificed under intraperitoneal ketamin/thiopental sodium as anaesthesia after 24 hours of fasting. Brain tissues were quickly but carefully removed and fixed in 10% formal saline. The prefrontal cortex was grossed and processed according to standard protocols, sectioned at 5μm thick for standard histological studies. Result: Histomorphological analysis demonstrates that high and medium doses of TA preserve neuronal integrity and mitigate the damaging effects of ethanol exposure. Treatment with vitamin E suggests that while antioxidant properties may aid in neuronal preservation, they do not fully address the inflammatory responses triggered by ethanol. Conclusion: Tannic acid exhibits comparatively better neuroprotective effects against ethanol-induced prefrontal cortex toxicity.