Kalpaamruthaa modulates oxidative stress in cardiovascular complication associated with type 2 diabetes mellitus through PKC-β/Akt signaling

被引:9
作者
Latha, Raja [1 ]
Shanthi, Palanivelu [2 ]
Sachdanandam, Panchanadham [1 ]
机构
[1] Univ Madras, Dept Med Biochem, Dr ALM Postgrad Inst Basic Med Sci, Madras 600113, Tamil Nadu, India
[2] Univ Madras, Dept Pathol, Dr ALM Postgrad Inst Basic Med Sci, Madras 600113, Tamil Nadu, India
关键词
type 2 diabetes mellitus; cardiovascular damage; Kalpaamruthaa; oxidative stress; protein kinase C; PROTEIN-KINASE-C; OCCURRING BIFLAVONOID DERIVATIVES; SMOOTH-MUSCLE-CELLS; SEMECARPUS-ANACARDIUM; PHOSPHOINOSITIDE; 3-KINASE; GLUTATHIONE-REDUCTASE; BODY-WEIGHT; INSULIN; ACTIVATION; LIVER;
D O I
10.1139/cjpp-2012-0443
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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-beta (PKC-beta)/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-beta 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-beta and the p-Akt signaling pathway.
引用
收藏
页码:901 / 912
页数:12
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