scholarly journals Liraglutide, a glucagon‑like peptide‑1 analog, inhibits high glucose‑induced oxidative stress and apoptosis in neonatal rat cardiomyocytes

2019 ◽  
Author(s):  
Lihui Zhang ◽  
Caige Li ◽  
Qiuxiao Zhu ◽  
Na Li ◽  
Hong Zhou
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Oxidative stress enhances phosphorylation of p53 in neonatal rat cardiomyocytes

2007 ◽  
Vol 303 (1-2) ◽  
pp. 167-174 ◽  
Author(s):  
Xilin Long ◽  
Michael J. Goldenthal ◽  
José Marín-García
Keyword(s):  
Oxidative Stress ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Propofol attenuates H2O2-induced oxidative stress and apoptosis via the mitochondria- and ER-medicated pathways in neonatal rat cardiomyocytes

APOPTOSIS ◽  
2017 ◽  
Vol 22 (5) ◽  
pp. 639-646 ◽  
Author(s):  
Xue-Ru Liu ◽  
Lu Cao ◽  
Tao Li ◽  
Lin-Lin Chen ◽  
Yi-Yan Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Abstract 72: Hydrogen Sulfide Prevents Myocardial Hypertrophy in a Klf5-dependent Manner

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Guoliang Meng ◽  
Liping Xie ◽  
Yong Ji
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Promoter Activity ◽  
Myocardial Hypertrophy ◽  
Neonatal Rat ◽  
Cardiomyocyte Hypertrophy ◽  
Dependent Manner ◽  
Ang Ii ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Rationale: H 2 S is a gasotransmitter that regulates multiple cardiovascular functions. Krüppel-like transcription factor (KLF) exerts diverse functions in the cardiovascular system. Objectives: The aim of present study was to investigate the effect of hydrogen sulfide (H 2 S) on myocardial hypertrophy. Methods and results: Myocardial samples of 22 patients with left ventricle hypertrophy were collected and underwent histological and molecular biological analysis. Spontaneously hypertensive rats (SHR) and neonatal rat cardiomyocytes were studied for functional and signaling response to GYY4137, a H 2 S-releasing compound. Expression of cystathionine -lyase (CSE), a main enzyme for H 2 S generation in human heart, decreased in human hypertrophic myocardium, while KLF5 expression increased. In SHR treated with GYY4137 for 4 weeks, myocardial hypertrophy was inhibited as evidenced by improvement in cardiac structural parameters, heart mass index, size of cardiac myocytes and expression of atrial natriuretic peptide (ANP). Levels of oxidative stress and phosphorylation of mitogen-activated protein kinases were also decreased after H 2 S treatment. H 2 S diminished expression of the KLF5 in myocardium of SHR and in neonatal rat cardiomyocytes rendered hypertrophy by angiotensin II (Ang II). H 2 S also inhibited ANP promoter activity and ANP expression in Ang II-induced neonatal rat cardiomyocyte hypertrophy, and these effects were suppressed by KLF5 knockdown. KLF5 promoter activity was increased by Ang II stimulation, and this was reversed by H 2 S. H 2 S also decreased activity of specificity protein-1 (SP-1) binding to the KLF5 promoter and attenuated KLF5 nuclear translocation by Ang II stimulation. Conclusion: H 2 S attenuated myocardial hypertrophy, which might be related to inhibiting oxidative stress and decreasing ANP transcription activity in a KLF5-dependent manner.

scholarly journals Tauroursodeoxycholic Acid Alleviates H2O2-Induced Oxidative Stress and Apoptosis via Suppressing Endoplasmic Reticulum Stress in Neonatal Rat Cardiomyocytes

Dose-Response ◽  
2018 ◽  
Vol 16 (3) ◽  
pp. 155932581878263 ◽  
Author(s):  
Lin Zhang ◽  
Yanmin Wang
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Reactive Oxygen Species Generation ◽  
Neonatal Rat ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Tauroursodeoxycholic Acid ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Introduction: We aimed to test the mechanism of protective effects of tauroursodeoxycholic acid (TUDCA) on cardiovascular disease using cultured cardiomyocytes. Methods: Neonatal rat cardiomyocytes (NRCMs) were isolated and cultured and then the cells were divided into 4 groups based on the treatments: control group (cells treated with culture medium), H2O2/thapsigargin (TG) group (cells treated with oxidative stress and endoplasmic reticulum [ER] stress inducer), TUDCA group, and H2O2/TG + TUDCA group. The treated NRCMs were then subjected to serial analyses including flow cytometry, enzyme-linked immunosorbent assay, and Western blotting. Results: Tauroursodeoxycholic acid significantly attenuated H2O2-induced reactive oxygen species generation and lactate dehydrogenase release and restored H2O2-induced reductions of glutathione and superoxide dismutase levels in NRCMs. Tauroursodeoxycholic acid also alleviated H2O2-induced cardiomyocytes apoptosis, as well as the Bax/Bcl2 ratio compared with that of H2O2 treated alone. In addition, TUDCA suppressed TG-induced ER stress as reflected by inversing cell viability and the expression levels of glucose-regulated protein 78 kDa and C/enhancer-binding protein homologous protein. Conclusion: Our data indicated that TUDCA-mediated inhibition on H2O2-induced oxidative stress and cardiomyocytes apoptosis was through suppressing ER stress, and TUDCA possesses the potential to be developed as therapeutic tool in clinical use for cardiovascular diseases.

Oxidative Stress Induces Senescence-like Alterations in Neonatal Rat Cardiomyocytes

2005 ◽  
Vol 11 (9) ◽  
pp. S322
Author(s):  
Yasuhiro Maejima ◽  
Susumu Adachi ◽  
Hiroshi Ito ◽  
Mitsuaki Isobe
Keyword(s):  
Oxidative Stress ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

scholarly journals Non-Lethal Levels of Oxidative Stress in Response to Short-Term Intermittent Hypoxia Enhance Ca2+Handling in Neonatal Rat Cardiomyocytes

2014 ◽  
Vol 33 (2) ◽  
pp. 513-527 ◽  
Author(s):  
Tsung-I Chen ◽  
Yu-Cheng Hsu ◽  
Chih-Feng Lien ◽  
Jian-Hong Lin ◽  
Hung-Wen Chiu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intermittent Hypoxia ◽  
Neonatal Rat ◽  
Short Term ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

scholarly journals Rapid Induction of Aldosterone Synthesis in Cultured Neonatal Rat Cardiomyocytes under High Glucose Conditions

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Masami Fujisaki ◽  
Tomohisa Nagoshi ◽  
Tetsuo Nishikawa ◽  
Taro Date ◽  
Michihiro Yoshimura
Keyword(s):  
High Glucose ◽  
Culture System ◽  
Cardiac Tissue ◽  
Current System ◽  
Experimental Models ◽  
Neonatal Rat ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

In addition to classical adrenal cortical biosynthetic pathway, there is increasing evidence that aldosterone is produced in extra-adrenal tissues. Although we previously reported aldosterone production in the heart, the concept of cardiac aldosterone synthesis remains controversial. This is partly due to lack of established experimental models representing aldosterone synthase (CYP11B2) expression in robustly reproducible fashion. We herein investigated suitable conditions in neonatal rat cardiomyocytes (NRCMs) culture system producing CYP11B2 with considerable efficacy. NRCMs were cultured with various glucose doses for 2–24 hours. CYP11B2 mRNA expression and aldosterone concentrations secreted from NRCMs were determined using real-time PCR and enzyme immunoassay, respectively. We found that suitable conditions for CYP11B2 induction included four-hour incubation with high glucose conditions. Under these particular conditions, CYP11B2 expression, in accordance with aldosterone secretion, was significantly increased compared to those observed in the cells cultured under standard-glucose condition. Angiotensin II receptor blocker partially inhibited this CYP11B2 induction, suggesting that there is local renin-angiotensin-aldosterone system activation under high glucose conditions. The suitable conditions for CYP11B2 induction in NRCMs culture system are now clarified: high-glucose conditions with relatively brief period of culture promote CYP11B2 expression in cardiomyocytes. The current system will help to accelerate further progress in research on cardiac tissue aldosterone synthesis.

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