

Publisher: Govi-Verlag
ISSN: 0031-7144
Source: Die Pharmazie - An International Journal of Pharmaceutical Sciences, Vol.70, Iss.11, 2015-11, pp. : 740-744
Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.
Abstract
The aim of this study was to investigate the protective effects of notoginsenoside R1 (R1) in the rat model ofmyocardial ischemia reperfusion injury and the possible mechanisms. Myocardial ischemia/reperfusion injury (MIRI) was induced by ischemia for 30 min and reperfusion for 60 min. Fifty male SD rats (250-300 g), were randomly divided into 5 groups: sham, model, R1 (20 mg/kg, 40 mg/kg, 60 mg/kg). The activities of serum lactate dehydrogenase (LDH), creatine kinase (CK), myeloperoxidase (MPO), total superoxide dismutase (T-SOD), and malondialdehyde (MDA)were determined after 60 min of reperfusion. Interleukin-1β (IL-1β), interleukin-8 (IL-8) and tumor necrosis factor (TNF)-α were evaluated by enzyme-linked immunosorbent assay (ELISA), VitaminD3 Upregulated Protein 1 (VDUP1), IκB α, P-IκB α, NF-κBP65, pNF-κBP65 were measured by western blotting. Our study demonstrated that R1 can ameliorate the impaired mitochondrial morphology and oxidation system; IL-1 , IL-8 and TNF- were recovered. Western blotting studies demonstrated that R1 substantially inhibited p-IκBα, NF-κBP65, p- NF-κBP65 protein levels and increased VDUP1 protein level. These findings suggest that R1 may effectively ameliorate the progression of 1/R injury and could be used as a therapy for patients with myocardial ischemia/reperfusion injury.
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