scholarly journals Effects of Pinocembrin Pretreatment on Connexin 43 (Cx43) Protein Expression After Rat Myocardial Ischemia-Reperfusion and Cardiac Arrhythmia

2018 ◽  
Vol 24 ◽  
pp. 5008-5014 ◽  
Author(s):  
Peng Zhang ◽  
Jin Xu ◽  
Wei Hu ◽  
Dong Yu ◽  
Xiaolu Bai
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Cardiac Arrhythmia ◽  
Connexin 43 ◽  
Ischemia Reperfusion ◽  
Cx43 Protein ◽  
Myocardial Ischemia Reperfusion

scholarly journals Total saponins from Trillium Tschonoskii Maxim alleviate myocardial ischemia reperfusion injury in rat

2020 ◽  
Author(s):  
Xiujing Zhang ◽  
Wei Wang ◽  
Jie Tang ◽  
Qin Xie ◽  
Di Ma
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pathological Changes ◽  
Apoptosis Protein ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Trillium Tschonoskii

Abstract BackgroundTo investigate the effect and possible mechanisms of total saponins from Trillium Tschonoskii Maxim. (TST) on myocardial ischemia reperfusion injury in rat.Methods and ResultsRats were pre-treated with TST in 100 and 200 mg/kg, respectively. After 14 days intragastric administration, the model of myocardial ischemia-reperfusion injury was established by ligation of the left anterior descending coronary artery for 30 min and then releasing the ligated artery for 120 min. The hemodynamic indexes, anti-oxidation index, and the anti-inflammation factors were detected. Pathological changes in myocardia tissue were observed by H&E staining. Apoptosis protein expression of caspase 3, 9, 12, AMPK, phosphorylation AMPK (p-AMPK) and Sirt1 was detected by Western blot. Pretreating the rats with TST dramatically decreased the levels of MDA, TNF-α, IL-6 and IL-1β, increased the levels of SOD and GSH-Px, and the apoptosis protein expression were all significantly decreased. In addition, the protein expression of p-AMPK and Sirt1 were markedly increased in TST pre-treated group. Furthermore, TST pre-treatment also improved the histopathological changes.ConclusionTST protect the myocardium by reducing the levels of inflammation factors, peroxides and cell apoptosis, increasing the anti-oxidase, and improving the pathological changes. The possible mechanism maybe through the activating of the AMPK/Sirt1 signaling pathway.

scholarly journals The expression and role of β3AR protein in myocardial ischemia/reperfusion in rats

2021 ◽  
Author(s):  
Zi-Long Wang ◽  
Xiao-Chen Sun ◽  
Rong Luo ◽  
Dong-Ye Li ◽  
Hao-Chen Xuan
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Caspase 3 ◽  
Sham Group ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Sd Rats ◽  
Group I ◽  
Myocardial Ischemia Reperfusion

IntroductionTo explore serum norepinephrine (NE) concentration and β3-adrenoceptor (β3AR) protein expression at different times during myocardial ischemia/reperfusion (I/R) and examine the role of β3AR in I/R.Material and methods28 Sprague-Dawley (SD) rats were randomly divided into one sham group and six I/R groups. The rats in the I/R groups were subjected to ischemia for 45 minutes. After reperfusion, the serum NE concentration and the β3AR protein expression in the myocardial tissue of the left ventricular injury region were detected. Another 18 SD rats were randomly divided into a sham group, I/R groups, and I/R + BRL37344 group.ResultsCompared with the sham group, the serum NE concentration of rats in the I/R groups significantly increased at 6 hours (P < 0.001). The serum NE concentration and myocardial β3AR protein expression were both highest at 72 hours. Compared with the sham group, the expressions of the pro-apoptotic proteins Bax and cleaved caspase-3 after I/R were significantly increased (P < 0.01, P < 0.001, respectively), and the expression of anti-apoptotic protein Bcl-2 was significantly decreased (P < 0.01). Compared with I/R groups, the expressions of Bax and cleaved caspase-3 in the I/R + BRL37344 group were significantly decreased (P < 0.05, P < 0.01, respectively).ConclusionsWith the prolongation of myocardial I/R in rats, serum NE concentration and β3AR protein expression showed a significant increase trend and reached a peak at 72 hours. Specific β3AR agonist BRL37344 can reduce myocardial I/R injury in vivo in rats, alleviate apoptosis, reduce infarct size, and improve cardiac function.

scholarly journals The Protective Effect of Cx43 Protein-Mediated Phosphocreatine on Myocardial Ischemia/Reperfusion Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Chen-xi Wang ◽  
Jun-jun Guo ◽  
An-jie Di ◽  
Yu Zhu ◽  
Wei-min Han ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Ischemia ◽  
Protective Effect ◽  
Coronary Blood Flow ◽  
Ischemia Reperfusion ◽  
Sham Operation ◽  
Free Oxygen Radicals ◽  
Cx43 Expression ◽  
Cx43 Protein ◽  
Myocardial Ischemia Reperfusion

Objectives. To verify the protective effect of phosphocreatine on myocardium in an ischemic model and the possible mechanism of action. Methods. The model of myocardial ischemia/reperfusion (I/R) was established by the ligation balloon method. 30 SD rats were randomly divided into three groups, n = 10 in each group. Sham operation group: the coronary artery was not blocked and observed for 120 minutes. The ischemia/reperfusion (I/R) group was given ischemia for 30 minutes and ischemia reperfusion for 90 minutes. Phosphocreatine (PCr) group: after 30 minutes of ischemia, the rats were intraperitoneally injected with PCr (200 mg/kg) for 90 minutes. The animal groups of myocardial ischemia/reperfusion model in vitro were the same as those in vivo. The heart was removed by thoracotomy and washed immediately in H-K buffer solution. Then, the heart was installed on the Langendorff instrument. The concentration of PCr perfusion fluid in the PCr group was 10 mmol/L. The changes in coronary blood flow in isolated myocardium were recorded. The heart rate and electrocardiogram were recorded by RM6240BT. At the end of the experiment, myocardial pathological sections and Cx43 immunofluorescence staining were made, and the contents of malondialdehyde (MDA) in myocardial tissue were detected. Results. Phosphocreatinine treatment improved the myocardial ischemia model, performance in electrocardiogram (ECG) changes (ST segment apparent), and histological changes (decrease in necrotic myocardial cells, inflammatory cell infiltration, and a reduction in myocardial edema). At the same time, MDA decreased, while coronary blood flow and Cx43 expression significantly improved. Conclusions. Phosphocreatine can improve the electrocardiogram and restore histologic changes in ischemic myocardium and coronary blood flow. The postulated mechanism is by inhibiting the generation of free oxygen radicals and restoring the expression of Cx43 protein.

Abstract 18247: Inhibition of PKCβ2 Attenuates Myocardial Ischemia Reperfusion Injury in Diabetic Rat Through Cavolin-3-dependant Akt Activation

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yanan Liu ◽  
Jiqin Jin ◽  
Haobo Li ◽  
Huansen Huang ◽  
Michael G Irwin ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
High Glucose ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Coronary Artery Ligation ◽  
Myocardial Infarct Size ◽  
Hypoxic Cell ◽  
Myocardial Ischemia Reperfusion

Background: Activation of PKCβ has been shown to play a critical role in myocardial ischemia/reperfusion (MI/R) injury in hearts from non-diabetic rodents. Our recent studies showed that PKCβ2 is overexpressed in the myocardium of diabetic rats that were associated with more severe post-ischemic MI/R injury relative to non-diabetic rats. We hypothesized that myocardial PKCβ overexpression is a major contributor responsible for the exacerbation of MI/R injury in diabetes and that PKCβ inhibition can attenuate MI/R injury in diabetes. Methods and results: Five-week streptozotocin-induced diabetic rats were treated with the selective PKCβ inhibitor ruboxistaurin (RBX, 1 mg/kg/day delivered via oral gavage) for 4 weeks, starting from 1 week after diabetes induction, before inducing MI/R achieved by 30 min of left descending coronary artery ligation followed by 2 hours of reperfusion. Cardiac function was measured using pressure-volume conductance system. In in vitro study, cardiac H9C2 cells were exposed to high glucose (30 mM/L) and subjected to 4 hours hypoxia followed by 4 hours reoxygenation (H/R) in the with or without selective PKCβ2 inhibitor CGP53353 (1 mol/L), siRNAs of PKCβ2 or Caveolin (Cav)-3. Cell apoptosis and mitochondrial transmembrane potential were respectively assessed by TUNEL and JC-1 staining. At the end of reperfusion, RBX significantly decreased myocardial infarct size (% of area at risk, 35±5% vs. 49±3% in control, P <0.05) and attenuated cardiac dysfunction, and increased cardiac protein expression of Cav-3 and phosphorylated/activated Akt (p-Akt) in diabetic rats (All P <0.05 vs. control). H/R significantly increased H9C2 cell injury under high glucose condition evidenced as increased TUNEL-positive and JC-1 monomeric cells (All P <0.05 vs. control), which was associated with increased PKCβ2 phosphorylation and decreased Cav-3 protein expression. Either CGP53353 or PKCβ2 siRNA significantly attenuated all these changes and enhanced p-Akt. Cav-3 gene knockdown significantly reduced p-Akt and increased post-hypoxic cell injury despite of concomitant reduction in PKCβ2 phosphorylation. Conclusions: PKCβ2 inhibition with RBX protects diabetic hearts from MI/R injury through Cav-3-dependent activation of Akt.

The Protective Effects of Preconditioning With Dioscin on Myocardial Ischemia/Reperfusion-Induced Ventricular Arrhythmias by Increasing Connexin 43 Expression in Rats

2018 ◽  
Vol 24 (3) ◽  
pp. 262-268 ◽  
Author(s):  
Jin Cheng ◽  
Chuang Sun ◽  
Jingyu Zhang ◽  
Qing Zou ◽  
Qimeng Hao ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ventricular Arrhythmias ◽  
Connexin 43 ◽  
Ischemia Reperfusion ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Protective Effects ◽  
Arterial Blood ◽  
Myocardial Ischemia Reperfusion

Myocardial ischemia–reperfusion (IR) injury is associated with high disability and mortality worldwide. This study was to explore the roles of dioscin in the myocardial IR rats and discover the related molecular mechanisms. Rats were divided into 5 groups: sham, IR, IR + 15 mg/kg dioscin, IR + 30 mg/kg dioscin, and IR + 60 mg/kg dioscin. Heart rate (HR), mean arterial blood pressure (MAP), and rate pressure product (RPP) were evaluated at 10 minutes before ischemia, immediately after ischemia, and at the beginning, middle, and end of reperfusion. Arrhythmia score and myocardial infarct size were examined in rats of all groups. The serum creatine kinase-muscle/brain (CKMB) and cardiac troponin I (cTnI) levels were analyzed via enzyme-linked immunosorbent assay. Protein amount of total connexin 43 (T-Cx43) and phosphorylated connexin 43 (P-Cx43) was evaluated by Western blot. Ischemia reperfusion significantly decreased HR, MAP, and RPP of rats compared to the sham group. However, dioscin significantly attenuated the above phenomena in a dose-dependent manner. Dioscin markedly inhibited IR-induced increase in arrhythmias score, infarct size, and serum CKMB and cTnI levels. In addition, dioscin strikingly induced IR-repressed expression of T-Cx43 and P-Cx43. Our results suggested that dioscin pretreatment exhibited protective effects against myocardial IR injury. Moreover, we found that dioscin attenuated myocardial IR-induced ventricular arrhythmias via upregulating Cx43 expression and activation.

scholarly journals Tetrandrine Ameliorates Myocardial Ischemia Reperfusion Injury through miR-202-5p/TRPV2

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Wei Zhao ◽  
Youyang Wu ◽  
Fanhao Ye ◽  
Shiwei Huang ◽  
Hao Chen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Protein Expression ◽  
Western Blot ◽  
Ischemia Reperfusion ◽  
Cardiomyocyte Apoptosis ◽  
H9c2 Cells ◽  
Group I ◽  
Myocardial Ischemia Reperfusion ◽  
Myocardial Infarction Size

Objective. This study is aimed at investigating the therapeutic effects of tetrandrine (Tet) on myocardial ischemia reperfusion (I/R) injury and probe into underlying molecular mechanism. Methods. H9C2 cells were divided into hypoxia/oxygenation (H/R) group, H/R+Tet group, H/R+Tet+negative control (NC) group, and H/R+Tet+miR-202-5p inhibitor group. RT-qPCR was utilized to monitor miR-202-5p and TRPV2 expression, and TRPV2 protein expression was detected via western blot and immunohistochemistry in H9C2 cells. Cardiomyocyte apoptosis was evaluated through detection of apoptosis-related markers and flow cytometry. Furthermore, myocardial enzyme levels were detected by ELISA. Rats were randomly separated into sham operation group, I/R group, I/R+Tet group (50 mg/kg), I/R+Tet+NC group, and I/R+Tet+miR-202-5p inhibitor group. miR-202-5p and TRPV2 mRNA expression was assessed by RT-qPCR. TRPV2 protein expression was detected through western blot and immunohistochemistry in myocardial tissues. Apoptotic levels were assessed via apoptosis-related proteins and TUNEL. Pathological changes were observed by H&E staining. Myocardial infarction size was examined by Evans blue-TCC staining. Results. Abnormally expressed miR-202-5p as well as TRPV2 was found in H/R H9C2 cells and myocardial tissues of I/R rats, which was ameliorated following Tet treatment. Tet treatment significantly suppressed H/R- or I/R-induced cardiomyocyte apoptosis. ELISA results showed that CK-MB and LDH levels were lowered by Tet treatment in H/R H9C2 cells and serum of I/R rats. H&E staining indicated that Tet reduced myocardial injury in I/R rats. Also, myocardial infarction size was lowered by Tet treatment. The treatment effects of Tet were altered following cotreatment with miR-202-5p inhibitor. Conclusion. Our findings revealed that Tet may ameliorate myocardial I/R damage via targeting the miR-202-5p/TRPV2 axis.

scholarly journals Paeonol Protects Against Myocardial Ischemia/Reperfusion-Induced Injury by Mediating Apoptosis and Autophagy Crosstalk

2021 ◽  
Vol 11 ◽  
Author(s):  
Chin-Feng Tsai ◽  
Hsing-Hui Su ◽  
Ke‐Min Chen ◽  
Jiuan-Miaw Liao ◽  
Yi-Ting Yao ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Molecular Mechanisms ◽  
Troponin I ◽  
Ischemia Reperfusion ◽  
Beclin 1 ◽  
Root Bark ◽  
Injured Myocardium ◽  
Vehicle Treatment ◽  
Myocardial Ischemia Reperfusion

Many studies have shown that crosstalk exists between apoptosis and autophagy, despite differences in mechanisms between these processes. Paeonol, a major phenolic compound isolated from Moutan Cortex Radicis, the root bark of Paeonia × suffruticosa Andrews (Paeoniaceae), is widely used in traditional Chinese medicine as an antipyretic, analgesic and anti-inflammatory agent. In this study, we investigated the detailed molecular mechanisms of the crosstalk between apoptosis and autophagy underlying the cardioprotective effects of paeonol in rats subjected to myocardial ischemia/reperfusion (I/R) injury. Myocardial I/R injury was induced by occlusion of the left anterior descending coronary artery (LAD) for 1 h followed by 3 h of reperfusion. Paeonol was intravenously administered 15 min before LAD ligation. We found that paeonol significantly improved cardiac function after myocardial I/R injury and significantly decreased myocardial I/R-induced arrhythmia and mortality. Paeonol also significantly decreased myocardial infarction and plasma LDH activity and Troponin-I levels in carotid blood after I/R. Compared with vehicle treatment, paeonol significantly upregulated Bcl-2 protein expression and significantly downregulated the cleaved forms of caspase-8, caspase-9, caspase-3 and PARP protein expression in the I/R injured myocardium. Myocardial I/R-induced autophagy, including the increase of Beclin-1, p62, LC3-I, and LC3-II protein expression in the myocardium was significantly reversed by paeonol treatment. Paeonol also significantly increased the Bcl-2/Bax and Bcl-2/Beclin-1 ratios in the myocardium after I/R injury. The cardioprotective role of paeonol during I/R injury may be due to its mediation of crosstalk between apoptotic and autophagic signaling pathways, which inhibits apoptosis and autophagic cell death.

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