Protective effect of morin on cardiac mitochondrial function during isoproterenol-induced myocardial infarction in male Wistar rats

Abstract

Altered mitochondrial function and free radical-mediated tissue damage have been suggested as an important pathological event in isoproterenol (ISO)-induced cardiotoxicity. This study was undertaken to know the preventive effect of morin on mitochondrial damage in ISO-induced cardiotoxicity in male Wistar rats. Myocardial infarction (MI) in rats was induced by ISO (85 mg/kg) at an interval of 24 hours for 2 days. Morin was given to rats as pre-treatment for 30 days orally using an intragastric tube. ISO-treated rats showed a significant elevation of mitochondrial thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (HP) level and pre-treatment with morin significantly prevented the increase of TBARS and HP level to near normality. The level of enzymic and non-enzymic antioxidants was decreased significantly in ISO-treated rats and pre-treatment with morin significantly increased the levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase, and reduced glutathione to normality. The activities of mitochondrial enzymes such as isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase were decreased significantly in ISO-treated myocardial ischemic rats and upon pre-treatment with morin restored these enzymes activity to normality. In addition, the decreased activities of cytochrome-C oxidase and NADH-dehydrogenases were observed in ISO-treated rats and pre-treatment with morin prevented the activities of cytochrome-C oxidase and NADH-dehydrogenase to normality. Pre-treatment with morin favorably restored the biochemical and functional parameters to near normal indicating morin to be a significant protective effect on cardiac mitochondrial function against ISO-induced MI in rats.

Treatment with Rhus tripartita extract curtails isoproterenol-elicited cardiotoxicity and oxidative stress in rats

“…Mechanistically, the outcome of ISO treatment in rats comprises a myriad of biochemical alterations in the cardiac tissue [ 41 ]. ISO-elicited histopathological modifications are paralleled by oxidative and nitrosative stress resulting in the modification of redox enzymes such as superoxide dismutase, catalase and glutathione [ 42 ] as well as endogenous redox-sensitive mediators such as nitric oxide [ 43 ] and hydrogen sulfide. ISO-triggered generation of reactive oxygen species in cardiac tissue fosters enhanced apoptosis of cardiac cells [ 44 ] and is associated with increased cytosolic calcium, cAMP and mitochondrial depolarization [ 45 ].…”

Morin exerts neuroprotection via attenuation of ROS induced oxidative damage and neuroinflammation in experimental diabetic neuropathy

“…Morin is a natural bioflavonoid obtained from onion, sea weeds, Indian guava ( Psidium guajava ), Almond ( Prunus dulcis ), Fig ( Chlorophora tinctoria ), Red wine, Osage orange, and other members of Moraceae family . It possesses several pharmacological properties such as antioxidant, anti‐inflammatory, chemoprotective, and anticancer activities . Morin has been well studied for its antioxidant and mitochondrial protective effects.…”

Ursolic acid modulates MMPs, collagen-I, α-SMA, and TGF-β expression in isoproterenol-induced myocardial infarction in rats

“…35 In hypoxia condition, TCA cycle enzyme activities are expected to be low. 36 These enzymes are located in the inner mitochondrial membrane and affected by the excessive production of free radicals induced by ISO. The reduction in these enzymes proved the defect in aerobic oxidation of pyruvate, which might result in the low production of ATP molecules.…”