Antilipoperoxidative and membrane stabilizing effect of diosgenin, in experimentally induced myocardial infarction

Abstract

Altered membrane integrity has been suggested as a major factor in the development of cellular injury during myocardial necrosis. The present study was designed to investigate the effect of diosgenin on lysosomal hydrolases, membrane-bound enzymes, and electrolytes during isoproterenol (ISO)-induced myocardial necrosis in rats. Animals were pretreated with DIOS (80 mg/kg) for a period of 35 days. Myocardial infarction was experimentally induced with ISO (85 mg/kg) twice at 24 h interval. Experimental myocardial infarction was evidenced with marked elevation of creatine kinase-MB (CK-MB) in serum with concomitant increase in lipid peroxidation (plasma thiobarbituric acid reactive substances (TBARS) and hydroperoxides (HP)). Activity of lysosomal hydrolases (beta-glucuronidase, beta-N-acetyl glucosaminidase, beta-D-galactosidase, cathepsin D, and acid phosphatase) was found to be increased in serum and heart tissue of ISO-alone treated animals. DIOS (80 mg/kg) pretreated groups showed significant decrease in CK-MB, lipid peroxidation, and lysosomal hydrolases activity. The membrane-bound enzymes such as Ca2+-ATPase and Mg2+-ATPase activity was increased and Na+/K+-ATPase activity was decreased in the heart tissues of ISO-alone treated animals. These enzyme alterations lead to the change in the electrolytes content such as sodium, potassium, and calcium in the heart tissue. However, DIOS (80 mg/kg) pretreatment reversed the membrane-bound enzymes activity and thereby maintained the normal electrolyte concentration. These results suggest the protective action of diosgenin in ISO-induced myocardial infarction. The salubrious effect observed in this study might be due to the antioxidant and membrane stabilizing potential of diosgenin.

UPLC-QTOF-MS identification of metabolites in rat biosamples after oral administration of Dioscorea saponins: A comparative study

“…As diosgenin is the main aglycone of hydrolyzed DNTS, DPTS and DZTS (Tang et al, 2013;Yi et al, 2014b), and in particular, diosgenin have been reported for the anti-myocardial ischemia activity (Jayachandran et al, 2009), we hypothesize that diosgenin, as a metabolite, can be found due to oral administration of these three total saponins; this could constitute part of evidence supporting similarity in efficacy of these three herbs. (2) Are there significant differences in the metabolic profiles and metabolite levels of rat groups administered with saponins from these herbs?…”

Cardio Protective Effect of Vitamin A against Isoproterenol-Induced Myocardial Infarction

“…The present study showed decreased activities of Na -ATPase which may be attributed to the direct antioxidant activity and antioxidant enzyme-stimulatory effect of vitamin A which thereby protects the -SH group from oxidative damage (33).…”

Mitochondrial ATP-sensitive K+ channels mediate the antioxidative influence of diosgenin on myocardial reperfusion injury in rat hearts

“…Dioscin also increased SOD activity and decreased intracellular ROS and MDA levels (Qin et al 2014). Similarly, cardioprotective effect of diosgenin was observed in isoproterenol-induced myocardial infarction; groups treated with diosgenin had lower levels of CK-MB, lipid peroxidation and lysosomal hydrolysis activity (Jayachandran et al 2009). On the other hand, diosgenin reduced the apoptosis level induced by H 2 O 2 in human vein endothelial cells by increasing SOD, GPX and NOS activity and by reducing free radicals levels (Gong et al 2010).…”

“…In traditional medicine diosgenin is used as an anti-hypercholestrolemic, antihypertriacylglycerolemic, anti-diabetic and anti-hyperglycemic agent (Jnarez-Oropeza et al 1987;McAnuff et al 2005;Son et al 2007). Cardioprotective effects of diosgenin were observed in myocardial infarction induced by isoproterenol to its antioxidant and membrane-stabilizing effects (Jayachandran et al 2009). In previous study, we found that this agent reduces the myocardial reperfusion injury through its capacity to inhibit the production of inflammatory cytokines in rat (Ebrahimi et al 2014).…”