Bitis arietans venom (BAV) is known to cause various pathophysiological disorders by altering the cellular inclusions and enzymatic activities of different organs. Moringa oleifera leaf has been reportedly used for treatment of snake envenoming but there is no information on its neutralizing potentials against Bitis arietans venom. This study investigated the antivenin activity of ethanol crude extract of M. oleifera leaf on B. arietans envenomed rats and its inhibitory effects on some biological activities of the venom. The lethal dose (LD 50 ) of BAV was estimated at 1.5 mg/kg −1 . BAV induced various toxic effects in the in vivo study however, treatment with M. oleifera leaf extract (MOLE) ameliorated BAV-induced hypernatraemia and hypercalcemia. Acute anemia observed in untreated envenomed rats was reversed after treatment with various concentrations of MOLE with a significant (p < 0.05) dose dependent increase in hematological indices. Liver damage in untreated envenomed rats as indicated by higher concentration of serum liver enzymes and higher concentration of antioxidant enzymes were significantly (p < 0.05) decreased in MOLE treated rats. Also, BAV exhibited hemorrhagic, hemolytic and coagulating activities which were inhibited in a dose dependent manner by MOLE. A mild DNA fragmentation noticed in tissues of the heart of untreated envenomed rats was ameliorated in the MOLE treated rats. Results obtained in this study indicated that M. oleifera leaf have antivenin activity against B. arietans venom induced toxicities and underscores its use in folk medicine for the treatment of snake bites.
Echis ocellatus snakebite causes more fatalities than all other African snake species combined. Moringa oleifera reportedly possesses an antivenom property. Therefore, we evaluated the effectiveness of M. oleifera ethanol extract (MOE) against E. ocellatus venom (EOV) toxicities. Thirty male rats were grouped as follows (n = 5): Group 1 (normal control received saline), groups 2 to 6 were administered intraperitoneally, 0.22 mg/kg (LD50) of EOV. Group 2 was left untreated while group 3 to 6 were treated post-envenoming with 0.2 mL of polyvalent antivenom, 200, 400, and 600 mg/kg of MOE respectively. MOE significantly (p<0.05) normalized the altered haematological indices and blood electrolytes profiles. MOE attenuated venom-induced cellular dysfunctions, characterized by a significant increase in NRF2, and concomitant downregulation of increased antioxidant enzymes (SOD and CAT) activities in the serum and heart of the treated rats. MOE normalized the elevated TNF-α and IL-1β in serum and heart tissues. Furthermore, the IgG titre value was significantly (p<0.5) higher in the envenomed untreated group compared to the MOE-treated groups. Hemorrhagic, hemolytic and coagulant activities of the venom were strongly inhibited by the MOE dose, dependently. Lesions noticed on tissues of vital organs of untreated rats were abolished by MOE. Our findings substantiate the effectiveness of MOE as a potential remedy against EOV toxicities.
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