Cardiotoxicity leading to cardiovascular dysfunction and ultimately
cardiac failure remains a major global health issue irrespective of race, age and country. Several factors including lipotoxicity, oxidative imbalance, exacerbated
angiotensin-converting enzyme (ACE) activity and altered bioenergetics have been implicated in the pathophysiology of
cardiovascular diseases. Turbina oblongata (E. Mey. ex Choisy) A. Meeuse is among the medicinal plants commonly used traditionally in the treatment and management of various ailments including cardiovascular dysfunctions in South Africa. In the present study, T. oblongata was investigated for its cardioprotective mechanism on oxidative-mediated
cardiotoxicity by determining its effect on redox imbalance, purinergic and
cholinergic dysfunction, and ACE activity as well as
lipid dysmetabolism and pathways in
iron-induced oxidative cardiac injury. Oxidative injury was induced ex vivo in freshly isolated heart by incubating with 0.1 mM FeSO4. Treatment was done by co-incubating with T. oblongata extract or
gallic acid which served as the standard
antioxidant. Induction of oxidative cardiac injury led to significant depleted levels of
glutathione,
triglyceride, HDL-
cholesterol,
superoxide,
catalase and ENTPDase activities, with concomitant elevated levels of
malondialdehyde,
cholesterol, LDL-
cholesterol, ACE,
acetylcholinesterase,
ATPase and
lipase activities. These levels and activities were significantly reversed following treatment with T. oblongata. Induction of oxidative injury also caused alterations in
lipid metabolites, with concomitant activation of beta oxidation of very long chain
fatty acids,
plasmalogen synthesis and mitochondrial beta-oxidation of long chain
saturated fatty acids pathways. Some of the altered metabolites were restored following treatment with T. oblongata, with concomitant inactivation of beta oxidation of very long chain
fatty acid pathway. These results indicate the cardioprotective effect of T. oblongata against oxidative-mediated
cardiotoxicity. This is evidenced by its ability to mitigate lipotoxicity and modulate dysregulated cardiometabolic activities as portrayed by its antioxidative activity and suppressive effects on ACE,
acetylcholinesterase and
lipase activities, while modulating cardiac
lipid dysmetabolism.