scholarly journals Safflor yellow A protects neonatal rat cardiomyocytes against anoxia/reoxygenation injury in vitro

2013 ◽  
Vol 34 (4) ◽  
pp. 487-495 ◽  
Author(s):  
Jia-lin Duan ◽  
Jing-wen Wang ◽  
Yue Guan ◽  
Ying Yin ◽  
Guo Wei ◽  
...  
Keyword(s):  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Reoxygenation Injury

Keeping the beat. Focus on “Enrichment of neonatal rat cardiomyocytes in primary culture facilitates long-term maintenance of contractility in vitro”

2012 ◽  
Vol 303 (12) ◽  
pp. C1218-C1219 ◽  
Author(s):  
John P. Konhilas ◽  
Samantha M. Behunin ◽  
Ronald M. Lynch
Keyword(s):  
Primary Culture ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Term Maintenance

scholarly journals Aldosterone increases T-type calcium channel expression and in vitro beating frequency in neonatal rat cardiomyocytes

2005 ◽  
Vol 67 (2) ◽  
pp. 216-224 ◽  
Author(s):  
N LALEVEE ◽  
M REBSAMEN ◽  
S BARRERELEMAIRE ◽  
E PERRIER ◽  
J NARGEOT ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Channel Expression ◽  
Beating Frequency

scholarly journals Ginsenoside Rb1 Protects Neonatal Rat Cardiomyocytes from Hypoxia/Ischemia Induced Apoptosis and Inhibits Activation of the Mitochondrial Apoptotic Pathway

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Xu Yan ◽  
Jinwen Tian ◽  
Hongjin Wu ◽  
Yuna Liu ◽  
Jianxun Ren ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Neonatal Rat ◽  
Ginsenoside Rb1 ◽  
Caspase 9 ◽  
Apoptotic Pathway ◽  
Rat Cardiomyocytes ◽  
Mitochondrial Apoptotic Pathway ◽  
Neonatal Rat Cardiomyocytes ◽  
Hypoxia Ischemia

Aim. To investigate the effect of Ginsenoside Rb1 (GS-Rb1) on hypoxia/ischemia (H/I) injury in cardiomyocytesin vitroand the mitochondrial apoptotic pathway mediated mechanism.Methods. Neonatal rat cardiomyocytes (NRCMs) for the H/I groups were kept in DMEM without glucose and serum, and were placed into a hypoxic jar for 24 h. GS-Rb1 at concentrations from 2.5 to 40 µM was given during hypoxic period for 24 h. NRCMs injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. Cell apoptosis, ROS accumulation, and mitochondrial membrane potential (MMP) were assessed by flow cytometry. Cytosolic translocation of mitochondrial cytochrome c and Bcl-2 family proteins were determined by Western blot. Caspase-3 and caspase-9 activities were determined by the assay kit.Results. GS-Rb1 significantly reduced cell death and LDH leakage induced by H/I. It also reduced H/I induced NRCMs apoptosis induced by H/I, in accordance with a minimal reactive oxygen species (ROS) burst. Moreover, GS-Rb1 markedly decreased the translocation of cytochrome c from the mitochondria to the cytosol, increased the Bcl-2/ Bax ratio, and preserved mitochondrial transmembrane potential (ΔΨm). Its administration also inhibited activities of caspase-9 and caspase-3.Conclusion. Administration of GS-Rb1 during H/Iin vitrois involved in cardioprotection by inhibiting apoptosis, which may be due to inhibition of the mitochondrial apoptotic pathway.

A cardiac α-actin (ACTC1) p. Gly247Asp mutation inhibits SRF-signaling in vitro in neonatal rat cardiomyocytes

2019 ◽  
Vol 518 (3) ◽  
pp. 500-505 ◽  
Author(s):  
Ashraf Yusuf Rangrez ◽  
Lucia Kilian ◽  
Katharina Stiebeling ◽  
Sven Dittmann ◽  
Eric Schulze-Bahr ◽  
...  
Keyword(s):  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Comparison of cardioprotective effects of labeled and unlabeled oleanoic acids with new BOPIM dye on primary neonatal rat cardiomyocytes following hypoxia/reoxygenation injury

2014 ◽  
Vol 66 (4) ◽  
pp. 677-685 ◽  
Author(s):  
Sa Wang ◽  
Hai-bo He ◽  
Shu-zhang Xiao ◽  
Jun-zhi Wang ◽  
Cai-hong Bai ◽  
...  
Keyword(s):  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Reoxygenation Injury ◽  
Cardioprotective Effects ◽  
Hypoxia Reoxygenation

The protective effect of Ganoderma atrum polysaccharide against anoxia/reoxygenation injury in neonatal rat cardiomyocytes

Life Sciences ◽  
2009 ◽  
Vol 85 (17-18) ◽  
pp. 634-641 ◽  
Author(s):  
Wen-juan Li ◽  
Shao-ping Nie ◽  
Yan Yan ◽  
Shang-bin Zhu ◽  
Ming-yong Xie
Keyword(s):  
Protective Effect ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Reoxygenation Injury

scholarly journals Aldosterone Rapidly Represses Protein Kinase C Activity in Neonatal Rat Cardiomyocytes in Vitro

Endocrinology ◽  
1997 ◽  
Vol 138 (8) ◽  
pp. 3410-3416 ◽  
Author(s):  
Atsuhisa Sato ◽  
Jun-Ping Liu ◽  
John W. Funder
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Kinase C ◽  
Protein Kinase C Activity

scholarly journals Delayed Protection of Tetramethylpyrazine on Neonatal Rat Cardiomyocytes Subjected to Anoxia-Reoxygenation Injury

2007 ◽  
Vol 100 (6) ◽  
pp. 366-371 ◽  
Author(s):  
He-Ping Chen ◽  
Ming He ◽  
Qi-Ren Huang ◽  
Guo-Hua Zeng ◽  
Dan Liu
Keyword(s):  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Reoxygenation Injury

scholarly journals Beta-1-Adrenergic Receptors Mediate Nrf2-HO-1-HMGB1 Axis Regulation to Attenuate Hypoxia/Reoxygenation-Induced Cardiomyocytes Injury in Vitro

2015 ◽  
Vol 35 (2) ◽  
pp. 767-777 ◽  
Author(s):  
Jichun Wang ◽  
Xiaorong Hu ◽  
Jing Xie ◽  
Weipan Xu ◽  
Hong Jiang
Keyword(s):  
Adrenergic Receptors ◽  
Pi3k Inhibitor ◽  
Neonatal Rat ◽  
Control Group ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Nf Kappab ◽  
Cultured Cardiomyocytes ◽  
Hypoxia Reoxygenation

Backgroud/Aims: The aim of the study was to evaluate the effects of beta1-adrenergic receptors (β1-ARs) -mediated nuclear factor erythroid 2-related factor 2 (Nrf2)-heme oxygenase-1 (HO-1)-high mobility group box 1 protein (HMGB1) axis regulation in hypoxia/reoxygenation (H/R)-induced neonatal rat cardiomyocytes. Methods: The neonatal cultured cardiomyocytes were concentration-dependently pretreated by dobutamine (DOB), a selective β1-adrenergic receptor agonist, in the absence and/or presence of LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor), SB203580 (a p38mitogen-activated-protein kinase (p38MAPK) inhibitor), Nrf2siRNA and HO-1siRNA, respectively, and then treated by H/R. The effects and mechanisms by which H/R-induced cardiomyocytes injury were evaluated. Results: Significant increase of HO-1 was found in neonatal cultured cardiomyocytes treated with DOB, when compared to the control group. Significant change for Nrf2 translocation was also revealed in neonatal cultured cardiomyocytes treated with DOB. Insignificant decreases of NF-kappaB p65 activation and HMGB1 release were observed in H/R-induced neonatal cultured cardiomyocytes treated with DOB, when compared to the control group. Importantly, DOB treatment significantly increased the cell viability and decreased the levels of LDH and MDA in H/R-induced cardiomyocytes injury. However, DOB failed to increase HO-1, inhibit NF-kappaB p65 activation, prevent HMGB1 release and attenuate H/R-induced cardiomyocytes injury when the cultured cardiomyocytes were pretreated by Nrf2siRNA, HO-1siRNA, PI3K inhibitor (LY294002) and p38MAPK inhibitor (SB203580), respectively. Conclusions: β1-ARs-mediated Nrf2-HO-1-HMGB1 axis regulation plays a critical protective role in H/R-induced neonatal rat cardiomyocytes injury in vitro via PI3K/p38MAPK signaling pathway.

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