title: Kalpaamruthaa modulates oxidative stress in cardiovascular complication associated with type 2 diabetes mellitus through PKC-β/Akt signaling.
abstract: This study aimed at investigating the efficacy of Kalpaamruthaa (KA) on cardiovascular damage (CVD) associated with type 2 diabetes mellitus in experimental rats by reducing oxidative stress and the modulation of the protein kinase C-β (PKC-β)/Akt signaling pathway. CVD-induced rats were treated with KA (200 mg·(kg body mass)(-1)·(day)(-1)) orally for 4 weeks. KA effectively reduced insulin resistance with alterations in blood glucose, hemoglobin, and glycosylated hemoglobin in CVD-induced rats. Elevated levels of lipids in CVD-induced rats were decreased upon KA administration. In CVD-induced rats the levels of lipoproteins were returned to normal by KA treatment. KA effectively reduced the lipid peroxidative product and protein carbonyl content in liver of CVD-induced rats. KA increased the activities and (or) levels of enzymatic and nonenzymatic antioxidants in liver of CVD-induced rats. KA treatment reduced the fatty inclusion and mast cell infiltration in liver of CVD-induced rats. Further, treatment with KA reduced the chromatin condensation and marginization in myocardium of CVD-induced rats. KA alters insulin signaling by decreasing PKC-β and increasing p-Akt and GLUT4 expressions in heart of CVD-induced rats. The above findings suggest that KA renders protection against CVD induced by type 2 diabetes mellitus by augmenting the cellular antioxidant defense capacity and modulating PKC-β and the p-Akt signaling pathway.
authors.affiliation: a Department of Medical Biochemistry, Dr. A.L.M. Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600 113, Tamil Nadu, India.
authors.forename: Raja
authors.initials: R
authors.lastname: Latha
authors.forename: Palanivelu
authors.initials: P
authors.lastname: Shanthi
authors.forename: Panchanadham
authors.initials: P
authors.lastname: Sachdanandam
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D015153:Blotting, Western; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D058065:Diabetic Cardiomyopathies / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D007150:Immunohistochemistry; D050356:Lipid Metabolism / Q000187:drug effects; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008407:Mast Cells / Q000187:drug effects; D046529:Microscopy, Electron, Transmission; D009206:Myocardium / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects*; D010936:Plant Extracts / Q000494:pharmacology*; D050050:Protein Carbonylation / Q000187:drug effects; D064546:Protein Kinase C beta / Q000378:metabolism / Q000502:physiology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D001786:Blood Glucose; D051275:Glucose Transporter Type 4; C510231:Kalpaamruthaa; D008055:Lipids; D008074:Lipoproteins; D010936:Plant Extracts; C495694:Slc2a4 protein, rat; D051057:Proto-Oncogene Proteins c-akt; D064546:Protein Kinase C beta