The Effect of Vernonia amygdalina on Chloroquine-induced Cardiotoxicity in Adult Wistar Rats

Background: Cardiotoxicity could result from chemotherapeutic drugs or other medications used in disease control such as antimalarial drugs.

Chloroquine (C.Q), an antimalarial agent has also been used in the treatment of rheumatoid arthritis, giardiasis, extra-intestinal amebiasis and lupus erythematous. However, its cardiotoxic roles have been documented.

Vernonia amygdalina del. (V.A) has been reported to exhibit antioxidant and cytoprotective activities. These ameliorative and protect effects have been attributed to the presence of flavonoids. There is a paucity of data to support the cardioprotective potentials of this important neutraceutical. We aimed to evaluate the possible effects of Vernonia amygdalina on Chloroquine-induced cardiotoxicity in Wistar models.

Materials and Methods: Twenty-four male adult Wistar rats were randomized into four groups of six rats each: I, Control: given normal feed and water ad libitum for 28 days; II, administered 30 mg/kg body weight chloroquine orally for 28 days; III, administered 30 mg/kg body weight of chloroquine orally for 28 days and with 400mg/kg bodyweight of Vernonia amygdalina for another 14 days; VI, administered Vernonia amygdalina 400mg/kg body weight for 28 days. Antioxidant parameters [malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD)], and histology of rat cardiac muscles were examined in the different groups.

Results: There was a significantly (p<0.0.05) increase in MDA level, reduced GSH level, increased SOD activity, and altered microanatomy of the rat cardiac muscle in the positive control group when compared with those of the negative control group. The changes in MDA and GSH concentration and SOD activity parameters were significantly (p<0.0.05) mitigated in rats co-treated with V.A when compared with the positive control rats. Similarly, co-administration of V.A with C.Q inhibited chloroquine induced-cardiotoxicity by reducing the altered microanatomy of the cardiac muscle of the rat.

Conclusion: It was concluded that V.A ameliorated chloroquine-induced cardiotoxicity in rats via its antioxidant property.