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PHYTOCHEMICAL SCREENING AND EVALUATION OF THE ANTI-INFLAMMATORY EFFECT OF FLAVONOID-RICH SEED EXTRACT OF BUCHHOLZIA CORIACEA IN RATS

Enechi O. C., Okeke E. S*., Nwankwo N. E., Abonyi, C. U.,Ugwu L., Eze P., Agbo. N. C. and Enwerem U. C

Background: The increasing discovery of more medicinal plants have screening of their bioactivity in order to provide data that will help physicians and patients make wise decision before using them. Objective: This study was designed to elucidate comparative phytochemical screening and anti-inflammatory properties flavonoid-rich seed extracts of Buchholzia coriacea.Materials and Methods: Flavonoid-rich seed extracts of Buchholzia coriacea were used for this study. In vivo anti-inflammatory studies was done using the paw oedema method while the in vitro anti-inflammatory studies were performed for the extract using phospholipase A2 inhibition andcalcium chloride-induce platelet aggregation assays. Results: The analysis of the phytochemical content of the hydro-ethanol seed extracts of Buchholzia coriacea revealed the presence of different secondary metabolites in varying proportions. In the systemic oedema of the rat paw, scalar doses of the extract significantly (p < 0.05) suppressed the development of paw oedema induced by egg albumin. This compares well with a standard anti–inflammatory drug indomethacin (10 mg/kg b.w) which at 5 hours inhibited egg albumin induced rat paw oedema. Varying doses of the extract significantly (p< 0.05) inhibited phospholipase A2 activity in a concentration-related manner provoking inhibition comparable to that of prednisolone, a standard anti-inflammatory drug. Similarly, the extract significantly (p < 0.05) inhibited CaCl2-Induced platelet aggregation in a dose and time dependent manner. Conclusion: These results indicate that the extract produced good anti-inflammatory activity which could be as a result of the rich phytochemical constituents and the mechanisms ofaction of this anti-inflammatory effect could be as a result of th may be due to the inhibition of phospholipase A2 and platelet aggregation. Key words: Inflammation; Phospholipase A2; Platelet aggregation; prednisolone; Indomethacin.

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