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

BaoJu Yao | Zendy; Xiaoqing He | Zendy; Yuhui Lin | Zendy; Wenjun Dai | Zendy

Open Access

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

Author(s) -

BaoJu Yao,

Xiaoqing He,

Yuhui Lin,

Wenjun Dai

Publication year - 2017

Publication title -

molecular medicine reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.727

H-Index - 56

eISSN - 1791-3004

pISSN - 1791-2997

DOI - 10.3892/mmr.2017.8009

Subject(s) - anisodamine , oxidative stress , nicotinamide adenine dinucleotide phosphate , pharmacology , nox4 , apoptosis , nitric oxide , lactate dehydrogenase , reactive oxygen species , medicine , nitric oxide synthase , creatine kinase , reperfusion injury , nadph oxidase , inflammation , ischemia , chemistry , endocrinology , biochemistry , oxidase test , enzyme

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.

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