ABSTRACT
We investigated the effect of apigenin, a dietary flavonoid, on isoproterenol hydrochloride (ISO)-induced apoptotic signaling in cardiomyoblast H9C2 cells. The results showed that apigenin treatment (10 µM) prevented ISO (31.25 µM)-induced lipid peroxidative levels and antioxidants status in H9C2 cells. Furthermore, apigenin inhibited expression of inflammatory markers in ISO-treated cells. In addition, apigenin prevented ISO-induced DNA damage and apoptotic signaling through modulating the expression of Bax, caspase-3, -8 and -9, cytochrome c, and Fas proteins in H9C2 cells. It is concluded that apigenin prevents ISO-induced antioxidants depletion, oxidative DNA damage, inflammatory, and apoptotic signaling in H9C2 cells. Thus, the present results demonstrated that apigenin has a cardioprotective effect on cardiomyoblasts cells.
Subject(s)
Antioxidants/pharmacology , Apigenin/pharmacology , Apoptosis/drug effects , Cardiotonic Agents/adverse effects , Isoproterenol/adverse effects , Myoblasts, Cardiac/drug effects , Oxidative Stress/drug effects , Animals , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Biomarkers/metabolism , Cardiotonic Agents/antagonists & inhibitors , Cell Line , DNA Damage/drug effects , Inflammation Mediators/agonists , Inflammation Mediators/antagonists & inhibitors , Inflammation Mediators/metabolism , Isoproterenol/antagonists & inhibitors , Lipid Peroxidation/drug effects , Membrane Potential, Mitochondrial , Mitochondria, Heart/drug effects , Mitochondria, Heart/immunology , Mitochondria, Heart/metabolism , Mitochondrial Membranes/drug effects , Mitochondrial Membranes/immunology , Mitochondrial Membranes/metabolism , Myoblasts, Cardiac/cytology , Myoblasts, Cardiac/immunology , Myoblasts, Cardiac/metabolism , Rats , bcl-2-Associated X Protein/agonists , bcl-2-Associated X Protein/antagonists & inhibitors , bcl-2-Associated X Protein/metabolism , fas Receptor/agonists , fas Receptor/antagonists & inhibitors , fas Receptor/metabolismABSTRACT
AIM: The objective of this study was to evaluate the probable mechanism of action of Biochanin A (BCA) on high-fat diet-induced insulin resistance mice. METHODS: Twenty-four male C57/BL/6J mice were divided into two and fed either control diet or a high fat-high diet (HFD). After 6 weeks, mice were grouped into: Control, Control + BCA, HFD and HFD + BCA (n = 6). Mice were made diabetic by feeding them an HFD. RESULTS: Body weight, plasma glucose, insulin, leptin levels and HOMA values were significantly lower in the BCA supplemented HFD group when related to the HFD group. Furthermore, BCA supplementation significantly increased Insulin receptor substrate 1 (IRS 1), PI3K, Akt and Glucose transporter type 4 (GLUT-4) protein abundance in skeletal muscle when equated with HFD. CONCLUSION: This study demonstrates that BCA can improve insulin sensitivity by activating insulin signalling, suggesting that it may possess antidiabetic activities.
Subject(s)
Diabetes Mellitus, Experimental , Insulin Resistance , Animals , Male , Mice , Diet, High-Fat , Genistein/pharmacology , Insulin , Mice, Inbred C57BLABSTRACT
Galangin (GA) is an active flavonoid of the rhizome of Alpinia galanga that belongs to the ginger family. GA exhibit potent anti-inflammatory properties. Therefore, we evaluated the preventive effects of GA against isoproterenol (ISO)-induced inflammation and myocardial fibrosis in male albino Wistar rats. We found that GA (1 mg/kg b.wt.) pretreatment attenuated the ISO-mediated (5 mg/kg b.wt. for 14 consecutive days) elevation of heart rate, activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase-MB (CKMB) in the rat serum. We also noticed that GA prevented the ISO-mediated cardiac markers i.e. cardiac troponin T and I (cTnT and cTnI) expression in the serum of rats. Further, GA pretreatment prevented ISO-mediated lipid peroxidation and diminished blood pressure and loss of antioxidants status in the heart tissue of ISO treated rats. In addition, GA treatment modulates ISO-induced alterations the expressions of tissue inhibitor of metalloproteinases-1 (TIMP-1), p-AKT, glycogen synthase kinase-3ß (p-GSK-3ß) and peroxisome proliferators-activated receptor-γ (PPAR-γ) in the heart tissue. Furthermore, molecular analysis (PCR array and western blot) revealed that GA pretreatment prevented inflammation and fibrosis related gene expression pattern in ISO-induced rats. Taken together, the results indicate the cardioprotective effect of GA against ISO-induced inflammation and fibrosis. The antioxidant and anti-inflammatory potential of GA could be considered for its cardioprotective effect in the ISO-treated rats.