Dataset Information

Etomidate alleviates cardiac dysfunction, fibrosis and oxidative stress in rats with myocardial ischemic reperfusion injury.

ABSTRACT:

Background

Etomidate has been shown to reduce ischemia/reperfusion (I/R) injury in several tissues. Here we aimed to investigate the protective effects of etomidate on I/R injury in Sprague-Dawley (SD) rats.

Methods

Thirty rats were randomly divided into 5 groups and pretreated with saline or 0.5/1/2 mg/kg etomidate. I/R injury was induced in all groups except the sham control group. After administration with saline or 0.5/1/2 mg/kg etomidate daily for another 27 days, rats were sacrificed and the effects of etomidate were analyzed.

Results

Treatment with etomidate dose dependently improved echocardiography indexes, ameliorated myocardial histological alterations and reduced serum creatine kinase isoenzyme (CK-MB), myoglobin (Mb) and troponin I (cTnl) levels. Fibrosis markers transforming growth factor beta (TGF-β), alpha-smooth muscle actin (α-SMA) and fibronectin was decreased with etomidate treatment. Etomidate also decreased oxidative stress and inflammation in rats, indicated by increased superoxide dismutase (SOD) and glutathione (GSH), and reduced malondialdehyde (MDA) in myocardial tissues, as well as decreased inducible NO synthase (iNOS) and increased interleukin (IL)-10 in both serum and myocardial tissues.

Conclusions

Altogether, we showed that etomidate alleviated I/R injury in rats through reduced cardiac dysfunction, fibrosis and oxidative stress. These results supported the protective role of etomidate to myocardial I/R injury.

SUBMITTER: Xie D

PROVIDER: S-EPMC7576070 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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Publications

Etomidate alleviates cardiac dysfunction, fibrosis and oxidative stress in rats with myocardial ischemic reperfusion injury.

Xie Dili D Li Min M Yu Kang K Lu Hua H Chen Yong Y

Annals of translational medicine 20200901 18

<h4>Background</h4>Etomidate has been shown to reduce ischemia/reperfusion (I/R) injury in several tissues. Here we aimed to investigate the protective effects of etomidate on I/R injury in Sprague-Dawley (SD) rats.<h4>Methods</h4>Thirty rats were randomly divided into 5 groups and pretreated with saline or 0.5/1/2 mg/kg etomidate. I/R injury was induced in all groups except the sham control group. After administration with saline or 0.5/1/2 mg/kg etomidate daily for another 27 days, rats were s ...[more]

PMID: 33241030

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Project description:Diabetes mellitus promotes accelerated cardiovascular aging and inflammation, which in turn facilitate the development of cardiomyopathy/heart failure. High glucose-induced oxidative/nitrative stress, activation of various pro-inflammatory, and cell death pathways are critical in the initiation and progression of the changes culminating in diabetic cardiomyopathy. Cannabinoid 2 receptor (CB2R) activation in inflammatory cells and activated endothelium attenuates the pathological changes associated with atherosclerosis, myocardial infarction, stroke, and hepatic cardiomyopathy. In this study, we explored the role of CB2R signaling in myocardial dysfunction, oxidative/nitrative stress, inflammation, cell death, remodeling, and fibrosis associated with diabetic cardiomyopathy in type 1 diabetic mice. Control human heart left ventricles and atrial appendages, similarly to mouse hearts, had negligible CB2R expression determine by RNA sequencing or real-time RT-PCR. Diabetic cardiomyopathy was characterized by impaired diastolic and systolic cardiac function, enhanced myocardial CB2R expression, oxidative/nitrative stress, and pro-inflammatory response (tumor necrosis factor-α, interleukin-1β, intracellular adhesion molecule 1, macrophage inflammatory protein-1, monocyte chemoattractant protein-1), macrophage infiltration, fibrosis, and cell death. Pharmacological activation of CB2R with a selective agonist attenuated diabetes-induced inflammation, oxidative/nitrative stress, fibrosis and cell demise, and consequent cardiac dysfunction without affecting hyperglycemia. In contrast, genetic deletion of CB2R aggravated myocardial pathology. Thus, selective activation of CB2R ameliorates diabetes-induced myocardial tissue injury and preserves the functional contractile capacity of the myocardium in the diabetic milieu. This is particularly encouraging, since unlike CB1R agonists, CB2R agonists do not elicit psychoactive activity and cardiovascular side effects and are potential clinical candidates in the treatment of diabetic cardiovascular and other complications.

Dataset Information

Etomidate alleviates cardiac dysfunction, fibrosis and oxidative stress in rats with myocardial ischemic reperfusion injury.

Background

Methods

Results

Conclusions

Publications

Etomidate alleviates cardiac dysfunction, fibrosis and oxidative stress in rats with myocardial ischemic reperfusion injury.

Similar Datasets

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