Buddleja saligna Willd (Loganiaceae) Inhibits Angiotensin‐Converting Enzyme Activity in Oxidative Cardiopathy with Concomitant Modulation of Nucleotide Hydrolyzing Enzymatic Activities and Dysregulated Lipid Metabolic Pathways

Abstract

Buddleja saligna Willd (Loganiaceae), mostly indigenous to South Africa is traditionally used in the treatment cardio‐dysfunctional related ailments amongst other diseases. The cardio‐protective effect of B. saligna was investigated in ferric‐induced oxidative cardiopathy. Hearts harvested from healthy male SD rats were incubated with 0.1 mM FeSO4 to induce oxidative damage and co‐incubated with B. saligna extract. Reaction mixtures without the extract served as negative control, while tissues without the extract or standard antioxidant (gallic acid) and pro‐oxidant served as the normal control. The tissues were analyzed for levels of glutathione, malondialdehyde, and nitric oxide as well as cholinergic, angiotensin‐converting enzyme (ACE), lipase, and purinergic enzymes activities, lipid profiles, fatty acid metabolic pathways and metabolites. Induction of oxidative damage significantly (p<0.05) depleted the levels of GSH, SOD, catalase, and ENTPDase activities, while concomitantly elevating the levels of MDA, NO, ACE, acetylcholinesterase, lipase and ATPase activities. These levels and activities were significantly reversed on treatment with B. saligna. Treatment with B. saligna also led to depletion of cardiac cholesterol and LDL‐c levels, while elevating triglyceride and HDL‐c level. It also depleted oxidative‐induced lipid metabolites with concomitant generation of thirteen other metabolites. B. saligna also inactivated oxidative‐induced pathways for beta oxidation of very long chain fatty acids, glycerolipid metabolism, and fatty acid elongation in mitochondria. These results suggest that B. saligna protects against ferric‐induced oxidative cardiopathy by mitigating oxidative stress, while concomitantly inhibiting ACE, acetylcholinesterase and lipase activities, and modulating lipid spectrum and dysregulated metabolic pathways.Support or Funding InformationThis work was supported by research funding from the National Research Foundation; and the Department of Science and Innovation (DSI) through the IKS‐Based Technology Innovations, Pretoria, South Africa