Cardioprotective effects of sinomenine in myocardial ischemia/reperfusion injury in a rat model

Lu, Chen; X, Guo; He, Xianghui; Yu, Chang Yeon; Zheng, Fa; Xu, Chenji; Zhang, Shuwen; Zhou, Yongqiang; Li, Junfang

doi:10.1016/j.jsps.2022.04.005

Cited by 7 publications

(2 citation statements)

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“…Since MIRI is the main cause of deterioration of cardiac function after coronary bypass or myocardial infarction, much attention has been paid to the search for effective drugs to treat this type of disease (Arslan et al, 2010). In previous work, SIN has shown ex vivo protection against arrhythmia, oxidative stress, and inflammation in a rat model of MIRI (Xie and Jin, 1993;Zhang et al, 2021;Lu et al, 2022). However, the isolated heart cannot fully represent the heart in vivo under normal physiological conditions because it is not regulated by the sympathetic nervous system, parasympathetic nervous system, and renin-angiotensin-aldosterone system (RAAS) (Papa, 2020;Martin et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

“…Although previous studies have confirmed the anti-oxidative stress and anti-inflammatory properties of SIN in MIRI ex vivo ( Xie and Jin, 1993 ; Lu et al, 2022 ), the in vivo function of SIN in MIRI has not yet been elucidated. We propose that administration of SIN may be able to prevent ischemia/reperfusion-induced cardiac injury by preventing oxidative stress, cellular apoptosis, and inflammation in vivo .…”

Section: Introductionmentioning

confidence: 95%

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Sinomenine Confers Protection Against Myocardial Ischemia Reperfusion Injury by Preventing Oxidative Stress, Cellular Apoptosis, and Inflammation

Xia

et al. 2022

Front. Pharmacol.

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Sinomenine (SIN), an alkaloid extracted from the root of S. acutum. sinomenine, has been shown to have antiarrhythmic, antioxidant, and anti-inflammatory effects in myocardial ischemia-reperfusion injury (MIRI) ex vivo. In this study, we investigated the cardioprotective effects of SIN in an in vivo mouse model of MIRI. Adult male C57BL/6J mice received SIN (80 mg/kg) for 5 days and underwent 30 min of percutaneous occlusion of the left anterior descending artery (LAD) followed by 24 h of reperfusion. Results showed that pretreatment with SIN significantly reduced myocardial infarct size and concentrations of markers of cardiac injury and improved left ventricular ejection fraction (EF) and shortening fraction (FS) in MIRI mice. The SIN pretreatment prevented the MIRI-induced decrease in the expression levels of Bcl-2, increase in the expression levels of caspase-3, caspase-9, and Bax, and increase in the number of TUNEL-positive cells in ischemic heart tissue. It was also found that pretreatment with SIN prevented the MIRI-induced oxidative stress imbalance in ischemic heart tissue, as shown by the increase in total antioxidant capacity (T-AOC) and glutathione (GSH) and the decrease in malondialdehyde (MDA), reactive oxygen species (ROS), and dihydroethidium (DHE) density. Further studies showed that the stimulus of cardiac ischemia/reperfusion caused a remarkable increase in the expression levels of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) mRNA in ischemic heart tissue, which was effectively prevented by pretreatment with SIN. These results demonstrate that SIN can attenuate MIRI-induced cardiac injury in vivo by preventing oxidative stress, inflammation, and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%