乳酸脱氢酶
丙二醛
髓过氧化物酶
再灌注损伤
肌酸激酶
超氧化物歧化酶
缺血
医学
药理学
肿瘤坏死因子α
下调和上调
肌酸
内分泌学
化学
内科学
氧化应激
生物化学
炎症
酶
基因
作者
Kun‐Peng Xia,Hua-Ming Ca,Changzhong Shao
出处
期刊:PubMed
日期:2015-11-01
卷期号:70 (11): 740-4
被引量:27
摘要
The aim of this study was to investigate the protective effects of notoginsenoside R1 (R1) in the rat model of myocardial 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), Vitamin D3 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 β, IL-8 and TNF-α 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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