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mitochondrial, drp, diabetic, group, myocardial, sevp, rats, injury, fission, article, myocardium, google, scholar, groups, cell, cardioprotective, effect, cas, oxidative, normal, mdivi, apoptosis, expression, diabetes, sevoflurane, stress, dsev, fig, protein, study, inhibition, min, mda, size, sod, activity, levels, dir, subjected, ischemiareperfusion, postconditioning, role, increased, mitochondria, data, effects, reperfusion, infarct, china, production,

Topics {✒️}

impairing nrf2/brg1/ho-1 signaling dynamin-related protein 1 enzyme-linked immunosorbent assay drp1-related mitochondrial fission article  google scholar diabetes-weakening cardioprotection induced diabetes-induced deleterious effects drp1-mediated mitochondrial fission drp1-dependent mechanism involved cardiac enzymes ck-mb article download pdf rat β-actin forward mitochondrial fission dependent age-matched control group myocardial ischemia–reperfusion injury myocardial ischemia-reperfusion injury myocardial ischemia/reperfusion injury normal ischemia/reperfusion group diabetic ischemia/reperfusion group reactive oxygen species mitochondrial fission mediated mitochondrial outer membrane reactive oxide species institutional animal care privacy choices/manage cookies shanxi medical university reactive oxygen production excessive oxidative stress full access scavenges reactive oxygen diabetes mellitus creatine kinase-mb sprague-dawley stz effectively reduce myocardial controls oxidative stress excessive mitochondrial fission related subjects myocardial infarct size increased oxidative stress fission protein drp1 research laboratory center mitochondrial fission acts inhibiting mitochondrial fission mitochondrial fission played reduce mitochondrial fission infarct size expressed upstream signalling molecule increased mitochondrial fission oxidative stress level improved mitochondrial morphology

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         headline:Diabetes impairs the protective effects of sevoflurane postconditioning in the myocardium subjected to ischemia/ reperfusion injury in rats: important role of Drp1
         description:Sevoflurane postconditioning (SevP) effectively relieves myocardial ischemia/reperfusion (I/R) injury but performs poorly in the diabetic myocardium. Previous studies have revealed the important role of increased oxidative stress in diabetic tissues. Notably, mitochondrial fission mediated by dynamin-related protein 1 (Drp1) is an upstream pathway of reactive oxygen production. Whether the ineffectiveness of SevP in the diabetic myocardium is related to Drp1-dependent mitochondrial fission remains unknown. This study aimed to explore the important role of Drp1 in the diabetic myocardium and investigate whether Drp1 inhibition could restore the cardioprotective effect of SevP. In the first part of the study, adult male Sprague-Dawley rats were divided into 6 groups. Rats in the diabetic groups were fed with high-fat and high-sugar diets for 8 weeks and injected intraperitoneally with streptozotocin (35 mg/kg). Myocardial I/R was induced by 30 min of occlusion of the left anterior descending branch of the coronary artery followed by 120 min of reperfusion. SevP was applied by continuous inhalation of 2.5 % sevoflurane 1 min before reperfusion, which lasted for 10 min. In the second part of the study, we applied mdivi-1 to investigate whether Drp1 inhibition could restore the cardioprotective effect of SevP in the diabetic myocardium. The myocardial infarct size, mitochondrial ultrastructure, apoptosis index, SOD activity, MDA content, and Drp1 expression were detected. TTC staining and TUNEL results showed that the myocardial infarct size and apoptosis index were increased in the diabetic myocardium. However, SevP significantly alleviated myocardial I/R injury in the normal myocardium but not in the diabetic myocardium. Additionally, we found an elevation in Drp1 expression, accompanied by more severe fission-induced structural damage and oxidative stress in the diabetic myocardium. Interestingly, we discovered that the beneficial effect of SevP was restored by mdivi-1, which significantly suppressed mitochondrial fission and oxidative stress. Our study demonstrates the crucial role of mitochondrial fission dependent on Drp1 in the diabetic myocardium subjected to I/R, and strongly indicates that Drp1 inhibition may restore the cardioprotective effect of SevP in diabetic rats.
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            Mitochondrial fission
            Diabetes mellitus
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      headline:Diabetes impairs the protective effects of sevoflurane postconditioning in the myocardium subjected to ischemia/ reperfusion injury in rats: important role of Drp1
      description:Sevoflurane postconditioning (SevP) effectively relieves myocardial ischemia/reperfusion (I/R) injury but performs poorly in the diabetic myocardium. Previous studies have revealed the important role of increased oxidative stress in diabetic tissues. Notably, mitochondrial fission mediated by dynamin-related protein 1 (Drp1) is an upstream pathway of reactive oxygen production. Whether the ineffectiveness of SevP in the diabetic myocardium is related to Drp1-dependent mitochondrial fission remains unknown. This study aimed to explore the important role of Drp1 in the diabetic myocardium and investigate whether Drp1 inhibition could restore the cardioprotective effect of SevP. In the first part of the study, adult male Sprague-Dawley rats were divided into 6 groups. Rats in the diabetic groups were fed with high-fat and high-sugar diets for 8 weeks and injected intraperitoneally with streptozotocin (35 mg/kg). Myocardial I/R was induced by 30 min of occlusion of the left anterior descending branch of the coronary artery followed by 120 min of reperfusion. SevP was applied by continuous inhalation of 2.5 % sevoflurane 1 min before reperfusion, which lasted for 10 min. In the second part of the study, we applied mdivi-1 to investigate whether Drp1 inhibition could restore the cardioprotective effect of SevP in the diabetic myocardium. The myocardial infarct size, mitochondrial ultrastructure, apoptosis index, SOD activity, MDA content, and Drp1 expression were detected. TTC staining and TUNEL results showed that the myocardial infarct size and apoptosis index were increased in the diabetic myocardium. However, SevP significantly alleviated myocardial I/R injury in the normal myocardium but not in the diabetic myocardium. Additionally, we found an elevation in Drp1 expression, accompanied by more severe fission-induced structural damage and oxidative stress in the diabetic myocardium. Interestingly, we discovered that the beneficial effect of SevP was restored by mdivi-1, which significantly suppressed mitochondrial fission and oxidative stress. Our study demonstrates the crucial role of mitochondrial fission dependent on Drp1 in the diabetic myocardium subjected to I/R, and strongly indicates that Drp1 inhibition may restore the cardioprotective effect of SevP in diabetic rats.
      datePublished:2021-02-16T00:00:00Z
      dateModified:2021-02-16T00:00:00Z
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         Dynamin‐related protein 1
         Mitochondrial fission
         Diabetes mellitus
         Sevoflurane postconditioning
         Myocardial ischemia reperfusion injury
         Cardiology
         Cardiac Surgery
         Angiology
         Blood Transfusion Medicine
         Internal Medicine
         Medicine/Public Health
         general
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