Attenuation of KCN-induced Neurotoxicity by Solvent Fractions of Antiaris africana Leaf

Adewunmi, Rofiat and Ilesanmi, Omotayo and Crown, Olamide and Komolafe, Kayode and Akinmoladun, Afolabi and Olaleye, Tolulope and Akindahunsi, Akintunde (2018) Attenuation of KCN-induced Neurotoxicity by Solvent Fractions of Antiaris africana Leaf. European Journal of Medicinal Plants, 23 (2). pp. 1-11. ISSN 22310894

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Abstract

Antiaris africana belongs to the family Moraceae, it is commonly called “False Iroko” tree and one of the medicinal plants used in treatment of mental and nervous disorders in Nigeria. We have previously established the neuroprotective properties of crude extract of A. africana. The present study was thus designed to investigate the neuroprotective effect of different solvent fractions of A. africana against cyanide neurotoxicity in vitro. Cyanide induced a significant (P<0.01) inhibition of NADH succinate dehydrogenase, a key enzyme in mitochondria function as well as significant increase in oxidative stress as observed in the high level of malonedialdehyde (MDA), protein carbonyl (PC) and activity of monoamine oxidase (MAO) and decreased concentration of reduced glutathione (GSH) as compared to the control. Co-administration with different solvent fractions of A. africana (hexane fraction [HFA], dichloromethane fraction [DFA] and methanolic fraction [MFA]) significantly ameliorated the toxic effect of KCN as compared to the induced, untreated group (P<0.05). The results in this study showed that HFA (79.04% reversal of NSD inhibitory activity of KCN), DFA (63.68% and 72.6% activity against KCN induced LPO and PC respectively). However, MFA showed the best activity against GSH depletion caused by KCN (12.21%) and inhibition of MAO activity induced by KCN (94.63%). In conclusion, all the fractions possess neuroprotective activities at varying degrees against mitochondria damage by KCN. This result further substantiated the ethnomedicinal usage of A. africana and can provide novel compounds in the treatment of mitochondria-related neurodegenerative diseases.

Item Type: Article
Subjects: OA Library Press > Medical Science
Depositing User: Unnamed user with email support@oalibrarypress.com
Date Deposited: 10 May 2023 06:59
Last Modified: 25 Jul 2024 07:48
URI: http://archive.submissionwrite.com/id/eprint/678

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