scholarly journals Nicorandil inhibits cardiomyocyte apoptosis and improves cardiac function by suppressing the HtrA2/XIAP/PARP signaling after coronary microembolization in rats

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Jing Zheng ◽  
Manyun Long ◽  
Zhenbai Qin ◽  
Fen Wang ◽  
Zhiqing Chen ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Cardiomyocyte Apoptosis ◽  
Coronary Microembolization

Resveratrol Attenuates Cardiomyocyte Apoptosis in Rats Induced by Coronary Microembolization Through SIRT1-Mediated Deacetylation of p53

2019 ◽  
Vol 24 (6) ◽  
pp. 551-558 ◽  
Author(s):  
Qing Mao ◽  
Xiulin Liang ◽  
Yufu Wu ◽  
Yongxiang Lu
Keyword(s):  
Cardiac Function ◽  
Caspase 3 ◽  
Troponin I ◽  
Myocardial Dysfunction ◽  
Picric Acid ◽  
Protective Role ◽  
Apoptotic Index ◽  
Cardiomyocyte Apoptosis ◽  
Sirtuin 1 ◽  
Coronary Microembolization

Objective: Coronary microembolization (CME)-induced cardiomyocyte apoptosis is the primary factor in causing cardiac dysfunction. Resveratrol (RES) is known to play a protective role in a variety of cardiovascular diseases, yet it is not known whether RES has a protective role in CME. Therefore, the effect of RES on cardiomyocyte apoptosis and cardiac function damage which are induced by CME in rats was investigated in this study. Methods: Fifty Sprague-Dawley rats were separated into 5 groups randomly (10 rats were included in each): sham group, CME group, RES+CME group, RES+CME+Sirtuin-1 (SIRT-1) inhibitor EX527 (RES+CME+EX) group, and CME+EX group. Cardiac function, serum c-troponin I (cTnI) level, apoptotic index, and microinfarct were measured by cardiac ultrasound, myocardial enzyme assessment, TdT-mediated dUTP Nick-end labeling and hematoxylin-basic fuchsin-picric acid staining. The levels of p53, p53 acetylation, SIRT-1, Bax, Bcl-2, and cleaved caspase-3 were detected by Western blot. Results: Myocardial dysfunction, enhanced apoptotic index as well as cTnI were caused after the operation of CME. Coronary microembolization induced increased expression of p53 acetylation and cleaved caspase-3, while the SIRT-1 and Bcl-2/Bax ratio was reduced. The CME effect was reversed by RES while EX527 attenuated this protective effect. Conclusions: Resveratrol can improve cardiac function, in the sense that it attenuates CME-induced cardiomyocyte apoptosis, which is perhaps associated with its inhibition pro-apoptotic pathway of p53 which is transcription-independent.

Coronary Microembolization Induces Cardiomyocyte Apoptosis in Swine by Activating the LOX-1-Dependent Mitochondrial Pathway and Caspase-8-Dependent Pathway

2015 ◽  
Vol 21 (2) ◽  
pp. 209-218 ◽  
Author(s):  
Tao Liu ◽  
You Zhou ◽  
Jiang-You Wang ◽  
Qiang Su ◽  
Zhong-Li Tang ◽  
...  
Keyword(s):  
Mitochondrial Pathway ◽  
Cardiomyocyte Apoptosis ◽  
Caspase 8 ◽  
Coronary Microembolization ◽  
Dependent Pathway

scholarly journals Effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure by regulating TGF-β1/Smad3 signaling pathway

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Chun Xie ◽  
Huaxin Qi ◽  
Lei Huan ◽  
Yan Yang
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Cardiomyocyte Apoptosis ◽  
Luciferase Reporter ◽  
Rat Cardiomyocytes ◽  
Smad 3 ◽  
Tgf Β1

Abstract Purpose: The present study set out to investigate the effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure (HF) and its mechanism. Methods: HF rat model and hypoxia/reoxygenation (H/R) cardiomyocyte model were established. miR-195-5p expression and transforming growth factor-β1 (TGF-β1)/signal transduction protein (Smad)3 signaling pathway in HF rats and H/R cardiomyocytes were interfered. miR-195-5p expression was tested by Rt-PCR, TGF-β1/Smad3 signaling pathway related proteins were detected by Western Blot, apoptosis of HF rat cardiomyocytes was tested by TUNEL, and apoptosis of cardiomyocytes induced by H/R was checked by flow cytometry. Results: miR-195-5p was lowly expressed in myocardium of HF rats, while TGF-β1 and Smad3 proteins were high-expressed. Up-regulating miR-195-5p expression could obviously inhibit cardiomyocyte apoptosis of HF rats, improve their cardiac function, and inhibit activation of TGF-β1/Smad3 signaling pathway. Up-regulation of miR-195-5p expression or inhibition of TGF-β1/Smad3 signaling pathway could obviously inhibit H/R-induced cardiomyocyte apoptosis. Dual-luciferase reporter enzyme verified the targeted relationship between miR-195-5p and Smad3. Conclusion: miR-195-5p can inhibit cardiomyocyte apoptosis and improve cardiac function in HF rats by regulating TGF-β1/Smad3 signaling pathway, which may be a potential target for HF therapy.

scholarly journals Human trophoblast-derived exosomes attenuate doxorubicin-induced cardiac injury by regulating miR-200b and downstream Zeb1

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Jie Ni ◽  
Yihai Liu ◽  
Lina Kang ◽  
Lian Wang ◽  
Zhonglin Han ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Cardiac Fibrosis ◽  
Cardiac Injury ◽  
Cardiomyocyte Apoptosis ◽  
Luciferase Reporter ◽  
Human Trophoblast ◽  
Trophoblast Stem

AbstractHuman trophoblast stem cells (TSCs) have been confirmed to play a cardioprotective role in heart failure. However, whether trophoblast stem cell-derived exosomes (TSC-Exos) can protect cardiomyocytes from doxorubicin (Dox)-induced injury remains unclear. In the present study, TSC-Exos were isolated from the supernatants of human trophoblasts using the ultracentrifugation method and characterized by transmission electron microscopy and western blotting. In vitro, primary cardiomyocytes were subjected to Dox and treated with TSC-Exos, miR-200b mimic or miR-200b inhibitor. Cellular apoptosis was observed by flow cytometry and immunoblotting. In vivo, mice were intraperitoneally injected into Dox to establish a heart failure model. Then, different groups of mice were administered either PBS, adeno-associated virus (AAV)-vector, AAV-miR-200b-inhibitor or TSC-Exos via tail vein injection. Then, the cardiac function, cardiac fibrosis and cardiomyocyte apoptosis in each group were evaluated, and the downstream molecular mechanism was explored. TSC-Exos and miR-200b inhibitor both decreased primary cardiomyocyte apoptosis. Similarly, mice receiving TSC-Exos and AAV-miR-200b inhibitor exhibited improved cardiac function, accompanied by reduced apoptosis and inflammation. The bioinformatic prediction and luciferase reporter results confirmed that Zeb1 was a downstream target of miR-200b and had an antiapoptotic effect. TSC-Exos attenuated doxorubicin-induced cardiac injury by playing antiapoptotic and anti-inflammatory roles. The underlying mechanism could be an increase in Zeb1 expression by the inhibition of miR-200b expression. In summary, this study sheds new light on the application of TSC-Exos as a potential therapeutic tool for heart failure.

scholarly journals Extracellular vesicles from human cardiac progenitor cells inhibit cardiomyocyte apoptosis and improve cardiac function after myocardial infarction

2014 ◽  
Vol 103 (4) ◽  
pp. 530-541 ◽  
Author(s):  
L. Barile ◽  
V. Lionetti ◽  
E. Cervio ◽  
M. Matteucci ◽  
M. Gherghiceanu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Progenitor Cells ◽  
Extracellular Vesicles ◽  
Cardiomyocyte Apoptosis ◽  
Cardiac Progenitor Cells

scholarly journals Puerarin pretreatment attenuates cardiomyocyte apoptosis induced by coronary microembolization in rats by activating the PI3K/Akt/GSK-3β signaling pathway

2021 ◽  
Vol 25 (2) ◽  
pp. 147-157
Author(s):  
Zhi-Qing Chen ◽  
You Zhou ◽  
Jun-Wen Huang ◽  
Feng Chen ◽  
Jing Zheng ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cardiomyocyte Apoptosis ◽  
Coronary Microembolization ◽  
Gsk 3Β

scholarly journals The Effects of Ginsenoside Rg2 on Trastuzumab-Induced Cardiotoxicity

2021 ◽  
Vol 7 (3) ◽  
pp. 1-5
Author(s):  
Xiaoyong Qi ◽  
Keyword(s):  
Cardiac Function ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Cardiomyocyte Apoptosis ◽  
Caspase 9 ◽  
Cell Experiment

Ginsenoside Rg2 inhibited the deterioration of cardiac function in rats, ginsenoside Rg2 inhibited cardiomyocyte apoptosis, increased the expression of Caspase-3,Caspase-9 and BAX in cell experiment. Conclusions: Ginsenoside Rg2 could protect cardiomyocytes in TZM-induced toxicity and it might be via inhibiting cell apoptosis.

scholarly journals LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88

2021 ◽  
Author(s):  
Feng Gao ◽  
Xiaochen Wang ◽  
Tingting Fan ◽  
Zhidan Luo ◽  
Mengqin Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Primary Response ◽  
Cardiomyocyte Apoptosis ◽  
Non Coding Rna ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Abstract Objective Long non-coding RNA (lncRNA) play critically in myocardial ischemia-reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis. Methods Mice with I/R injury were injected with the vectors that altered miR-185-3p and LINC00461 expression. miR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury were measured, as well as cardiac function, hemodynamics, myocardial fibrosis, infarction area, oxidative stress, and cardiomyocyte apoptosis. Results Raised LINC00461 and Myd88 and suppressed miR-185-3p levels were measured in I/R mice. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial collagen hyperplasia, fibrosis and infarction, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. Conclusion Down-regulation of LINC00461 attenuates myocardial I/R injury via suppressing miR-185-3p-targeted Myd88 expression.

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