scholarly journals Adiponectin protects against lung ischemia-reperfusion injury in rats with type 2 diabetes mellitus

2018 ◽  
Author(s):  
Di Li ◽  
Lin‑Lin Song ◽  
Juan Wang ◽  
Chao Meng ◽  
Xiao‑Guang Cui
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

Expression profiles of long noncoding RNAs in type 2 diabetes mellitus rat associated with the progression of ischemia-reperfursion injury

2020 ◽  
Author(s):  
Wenhao Song ◽  
Yao Gong ◽  
Pei Tu ◽  
Lin Zhang ◽  
Zhili Jin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Expression Profiles ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Myocardial Ischemia Reperfusion

Abstract Background The aim of this study was to analyze the expressions of long noncoding RNA(lncRNA) in rat with type 2 diabetes mellitus(T2DM) complicated with acute myocardial ischemia reperfusion injury(IRI). Methods Type 2 diabetic rats were induced by high calorie diet combined with streptozotocin. IRI rats models were established by the ligation and release of left anterior descending coronary artery(LAD). The expression levels of lncRNA and mRNA in myocardial tissues of rats were detected via high-throughput sequencing technology, and Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis were performed. Result Transcriptome analyses were performed to show expression profiles of mRNAs and lncRNAs in myocardial tissues of diabetic rats with IRI. A total of 2,476 lncRNAs and 710 mRNAs were differentially expressed between operation group and sham operation group. Then, an mRNA-lncRNA coexpression network was constructed. Finally, the present study verified that TCONS_00036439、TCONS_00151548、TCONS_00153276、TCONS_00344188、TCONS_00277692、TCONS_00236469、TCONS_00236468、TCONS_00153290、TCONS_00360941、TCONS_00142622 were associated with the initiation and development of ischemia reperfusion injury. Then, an lncRNA-mRNA coexpression network was constructed. Conclusion There is differential expression of lncRNAs in myocardial IRI tissues of diabetic rats. Building gene regulation networks to find the nodal gene and lncRNA is useful for understanding the pathogenesis of type 2 diabetes mellitus complicated with acute myocardial ischemia reperfusion injury and providing new therapy target.

Abstract 111: Paradoxical Exacerbation of Arrhythmias by the Cardioprotective Mitochondrial K-ATP Channel Agonist Diazoxide in Type 2 Diabetes Mellitus

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Chaoqin Xie ◽  
Basil S Karam ◽  
Fadi G Akar
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Anion Channel ◽  
Sprague Dawley ◽  
Control Groups ◽  
And Control

Type 2 diabetes mellitus (T2DM) is a major risk factor for cardiovascular complications including ischemia reperfusion injury (IR). Activation of mitochondrial KATP channels by Diazoxide (DZX) promotes beta cell rest and suppresses glucose production in patients. We hypothesized that DZX prevents IR arrhythmias in T2DM owing to its dual cardioprotective & antidiabetic property. Methods: Obese Zucker Diabetic Fatty (ZDF) rats (n=17) with established T2DM were studied. Control groups consisted of lean ZDF (n=6) and normal Sprague Dawley (n=10) rats. High resolution optical action potential (AP) mapping was performed in hearts before and after challenge with no flow ischemia for 12min followed by reperfusion. Results: Basal properties including rate dependence of conduction velocity (CV) and AP duration (APD) were not significantly (p=NS) altered in T2DM. Remarkably, ischemia uncovered major differences between groups as APD in T2DM failed to adapt to the ischemic challenge. Unlike APD, CV was reduced in all groups. DZX paradoxically promoted arrhythmias as all DZX (30uM) treated T2DM hearts exhibited ischemia related VT. In contrast, untreated T2DM (0/5) and control (0/9) hearts did not exhibit VT during ischemia. Underlying arrhythmic vulnerability of DZX treated T2DM hearts was a pronounced reduction (by 75% p<0.01) of the cardiac wavelength (WL) caused by accelerated APD shortening in response to ischemia. Upon reperfusion, T2DM and control groups exhibited a high (60% T2DM vs 44% control, p=NS) rate of VT, although the VT cycle length in T2DM was significantly longer (72 vs 44ms, p<0.01) suggesting a more adverse substrate modification by IR injury. Blocking the inner membrane anion channel (IMAC) fully abrogated reperfusion VT in T2DM. Conclusion: Ischemia uncovers a paradoxical resistance of T2DM hearts to APD adaptation. DZX reverses this property resulting in accelerated APD & WL shortening. This promotes reentrant VT during ischemia. Therefore, the anti-diabetic agent DZX should be avoided in T2DM patients at risk of ischemic events. Instead IMAC is an effective antiarrhythmic target for these patients.

scholarly journals Hydrogen sulfide preconditions the db/db diabetic mouse heart against ischemia-reperfusion injury by activating Nrf2 signaling in an Erk-dependent manner

2013 ◽  
Vol 304 (9) ◽  
pp. H1215-H1224 ◽  
Author(s):  
Bridgette F. Peake ◽  
Chad K. Nicholson ◽  
Jonathan P. Lambert ◽  
Rebecca L. Hood ◽  
Hena Amin ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Hydrogen Sulfide ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Myocardial Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Heme Oxygenase 1 ◽  
Dependent Manner

Hydrogen sulfide (H2S) therapy protects nondiabetic animals in various models of myocardial injury, including acute myocardial infarction and heart failure. Here, we sought to examine whether H2S therapy provides cardioprotection in the setting of type 2 diabetes. H2S therapy in the form of sodium sulfide (Na2S) beginning 24 h or 7 days before myocardial ischemia significantly decreased myocardial injury in db/db diabetic mice (12 wk of age). In an effort to evaluate the signaling mechanism responsible for the observed cardioprotection, we focused on the role of nuclear factor E2-related factor (Nrf2) signaling. Our results indicate that diabetes does not alter the ability of H2S to increase the nuclear localization of Nrf2, but does impair aspects of Nrf2 signaling. Specifically, the expression of NADPH quinine oxidoreductase 1 was increased after the acute treatment, whereas the expression of heme-oxygenase-1 (HO-1) was only increased after 7 days of treatment. This discrepancy was found to be the result of an increased nuclear expression of Bach1, a known repressor of HO-1 transcription, which blocked the binding of Nrf2 to the HO-1 promoter. Further analysis revealed that 7 days of Na2S treatment overcame this impairment by removing Bach1 from the nucleus in an Erk1/2-dependent manner. Our findings demonstrate for the first time that exogenous administration of Na2S attenuates myocardial ischemia-reperfusion injury in db/db mice, suggesting the potential therapeutic effects of H2S in treating a heart attack in the setting of type 2 diabetes.

scholarly journals Adiponectin improves coronary no-reflow injury by protecting the endothelium in rats with type 2 diabetes mellitus

2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Xue Han ◽  
Ye Wu ◽  
Xin Liu ◽  
Lu Ma ◽  
Tingting Lv ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Ischemia Reperfusion ◽  
No Reflow ◽  
Cell Adhesion Molecule 1

To determine the effect of adiponectin (APN) on the coronary no-reflow (NR) injury in rats with Type 2 diabetes mellitus (T2DM), 80 male Sprague–Dawley rats were fed with a high-sugar–high-fat diet to build a T2DM model. Rats received vehicle or APN in the last week and then were subjected to myocardial ischemia reperfusion (MI/R) injury. Endothelium-dependent vasorelaxation of the thoracic aorta was significantly decreased and serum levels of endothelin-1 (ET-1), intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were noticably increased in T2DM rats compared with rats without T2DM. Serum APN was positively correlated with the endothelium-dependent vasorelaxation, but negatively correlated with the serum level of ET-1. Treatment with APN improved T2DM-induced endothelium-dependent vasorelaxation, recovered cardiac function, and decreased both NR size and the levels of ET-1, ICAM-1 and VCAM-1. Hypoadiponectinemia was associated with the aggravation of coronary NR in T2DM rats. APN could alleviate coronary NR injury in T2DM rats by protecting the endothelium and improving microcirculation.

scholarly journals Adiponectin-Transfected Endothelial Progenitor Cells Have Protective Effects After 2-Hour Middle-Cerebral Artery Occlusion in Rats With Type 2 Diabetes Mellitus

2021 ◽  
Vol 12 ◽  
Author(s):  
Meiyao Wang ◽  
Yan Li ◽  
Renwei Zhang ◽  
Shuaimei Zhang ◽  
Hongliang Feng ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Protective Effects ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Cerebral Artery Occlusion

Objectives: This present study aimed to examine the effects of adiponectin-transfected endothelial progenitor cells (LV-APN-EPCs) on cerebral ischemia–reperfusion injury in rats with type 2 diabetes mellitus (T2DM) and to explore the underlying mechanisms.Methods: Seventy male Sprague–Dawley rats with T2DM were randomly divided into sham, phosphate-buffered saline (PBS), LV-APN-EPCs, LV-EPCs, and EPCs groups. Transient middle cerebral artery occlusion (MCAO) was induced by the intraluminal suture method. After 1 h of reperfusion, the five interventions were performed by tail-vein injections. The modified neurological severity score (mNSS) was used to assess neurological function before and on days 1, 7, and 14 after MCAO. After 14 days, magnetic resonance imaging scanning, hematoxylin and eosin staining, terminal dUTP nick-end labeling staining, Western blotting analysis, cluster of differentiation (CD) 31 immunofluorescence, and enzyme-linked immunosorbent assay were used to evaluate infarct rate, morphological damage, cell apoptosis, and microvessel density.Results: Compared with PBS, LV-EPCs, and EPCs groups, the LV-APN-EPCs group showed significantly lower mNSS score, lower infarct rate, and less morphological damage (all P &lt; 0.05). In addition, compared with other groups, the LV-APN-EPCs group had significantly increased levels of B cell lymphoma/leukemia-2 (Bcl-2) protein, CD31+ microvessels, endothelial nitric oxide synthase, and vascular endothelial growth factor, and decreased levels of Bcl-2-associated X protein and neuronal apoptosis in the peri-infarct cortex (all P &lt; 0.05).Conclusion: These results suggest that LV-APN-EPCs exert protective effects against cerebral ischemia–reperfusion injury in T2DM rats by increasing angiogenesis.

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