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ORIGINAL ARTICLE
Year : 2015  |  Volume : 11  |  Issue : 42  |  Page : 209-216

Protective role of Kalpaamruthaa in type II diabetes mellitus-induced cardiovascular disease through the modulation of protease-activated receptor-1


1 Department of Medical Biochemistry, Dr. A.L.M. Post-Graduate Institute of Basic Medical Sciences, University of Madras, Chennai, Tamil Nadu, India
2 Department of Pathology, Dr. A.L.M. Post-Graduate Institute of Basic Medical Sciences, University of Madras, Chennai, Tamil Nadu, India

Correspondence Address:
Prof. Panchanadham Sachdanandam
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
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1296.157739

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Background: Kalpaamruthaa (KA) is a formulatory herbal preparation has beneficial antioxidant, anti-apoptotic and anti-inflammatory properties against cardiovascular damage (CVD). Objective: The present study was undertaken to investigate the protective role of KA in type II diabetes mellitus-induced CVD through the modulation of protease-activated receptor-1 (PAR1). Materials and Methods: CVD was developed in 8 weeks after type II diabetes mellitus induction with high fat diet (2 weeks) and low dose of streptozotocin (2 × 35 mg/kg b.w. i.p. in 24 h interval). CVD-induced rats treated with KA (200 mg/kg b.w. in 0.5 ml of olive oil) orally for 4 weeks. Results: KA increased the activities of enzymatic antioxidants and the levels of non-enzymatic antioxidants in pancreas of CVD-induced rats. KA effectively reduced the lipid peroxides and carbonyl content in the pancreas of CVD-induced rats. KA reduced cellular damage by ameliorating the activities of marker enzymes in plasma, heart and liver. The protective nature of KA was further evidenced by histological observation in pancreas. Further, KA reduced CVD by decreasing the expression of PAR1 in heart. Conclusion: This study exhibits the defending role of KA in type II diabetes mellitus-induced CVD through altering PAR1.


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