Cardioprotective effects of anisodamine against myocardial ischemia/reperfusion injury through the inhibition of oxidative stress, inflammation and apoptosis

被引：43
作者：
Yao, Bao-Ju [1 ]
He, Xiao-Qing [2 ]
Lin, Yu-Hui [2 ]
Dai, Wen-Jun [2 ]
机构：
[1] First Peoples Hosp Huainan, Dept Cardiol, Huainan 232007, Anhui, Peoples R China
[2] Guangzhou Med Univ, Dept Cardiol, Affiliated Hosp 3, 63 Duobao Rd, Guangzhou 510150, Guangdong, Peoples R China
来源：
MOLECULAR MEDICINE REPORTS | 2018年 / 17卷 / 01期
关键词：
anisodamine; myocardial ischemia; reperfusion; oxidative stress; inflammation; apoptosis; RANDOMIZED CLINICAL-TRIAL; FEMORAL-HEAD; ALLERGIC-ASTHMA; ADIPOGENIC DIFFERENTIATION; MURINE MODEL; OSTEONECROSIS; CELLS; BONE; POPULATION; EXPRESSION;
D O I：
10.3892/mmr.2017.8009
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
The aim of the present study was to investigate the cardioprotective effects of anisodamine against myocardial ischemia/reperfusion (I/R) injury and the molecular mechanisms involved. The present results demonstrated that anisodamine attenuated myocardial infarct sizes, decreased the levels of creatine kinase and lactate dehydrogenase, whereas it increased the left ventricular (LV) systolic pressure, the LV end-diastolic pressure, and the LV pressure maximum rising and falling rates in a myocardial I/R rat model. In addition, anisodamine was revealed to suppress oxidative stress, inflammatory factor production and myocardial cell apoptosis, as demonstrated by the downregulation of caspase-3 and apoptosis regulator BAX protein expression. The production of reactive oxygen species was decreased and the protein expression of inducible nitric oxide synthase (iNOS) was downregulated, whereas the expression of endothelial NOS was enhanced. In addition, the activity of nicotinamide-adenine dinucleotide phosphate oxidase (Nox) was suppressed and the expression of Nox4 was downregulated in rats with myocardial I/R injury. In conclusion, the results of the present study suggested that anisodamine exerted a cardioprotective effect against myocardial I/R injury in rats, through the inhibition of oxidative stress, the suppression of inflammatory processes and the inhibition of myocardial cell apoptosis.
引用
收藏
页码：1253 / 1260
页数：8
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