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.

scholarly journals Ginsenoside-Rb1 Protects Hypoxic- and Ischemic-Damaged Cardiomyocytes by Regulating Expression of miRNAs

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Xu Yan ◽  
Jinrong Xue ◽  
Hongjin Wu ◽  
Shengqi Wang ◽  
Yuna Liu ◽  
...  
Keyword(s):  
Neonatal Rat ◽  
Control Group ◽  
Dependent Manner ◽  
The Novel ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Proliferation And Apoptosis ◽  
Novel Strategy ◽  
Dose Dependent

Ginsenoside (GS-Rb1) is one of the most important active compounds of ginseng, with extensive evidence of its cardioprotective properties. However, the miRNA mediated mechanism of GS-Rb1 on cardiomyocytes remains unclear. Here, the roles of miRNAs in cardioprotective activity of GS-Rb1 were investigated in hypoxic- and ischemic-damaged cardiomyocytes. Neonatal rat cardiomyocytes (NRCMs) were first isolated, cultured, and then incubated with or without GS-Rb1 (2.5–40μM)in vitrounder conditions of hypoxia and ischemia. Cell growth, proliferation, and apoptosis were detected by MTT and flow cytometry. Expressions of various microRNAs were analyzed by real-time PCR. Compared with that of the control group, GS-Rb1 significantly decreased cell death in a dose-dependent manner and expressions of mir-1, mir-29a, and mir-208 obviously increased in the experimental model groups. In contrast, expressions of mir-21 and mir-320 were significantly downregulated and GS-Rb1 could reverse the differences in a certain extent. The miRNAs might be involved in the protective effect of GS-Rb1 on the hypoxia/ischemia injuries in cardiomyocytes. The effect might be based on the upregulation of mir-1, mir-29a, and mir-208 and downregulation of mir-21 and mir-320. This might provide us a new target to explore the novel strategy for ischemic cardioprotection.

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.

scholarly journals Effects of the Delta Opioid Receptor Agonist DADLE in a Novel Hypoxia-Reoxygenation Model on Human and Rat-Engineered Heart Tissue: A Pilot Study

Biomolecules ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1309
Author(s):  
Sandra Funcke ◽  
Tessa R. Werner ◽  
Marc Hein ◽  
Bärbel M. Ulmer ◽  
Arne Hansen ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Ischemia Reperfusion ◽  
Heart Tissue ◽  
Contractile Force ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Engineered Heart Tissue ◽  
Hypoxia Reoxygenation

Intermittent hypoxia and various pharmacological compounds protect the heart from ischemia reperfusion injury in experimental approaches, but the translation into clinical trials has largely failed. One reason may lie in species differences and the lack of suitable human in vitro models to test for ischemia/reperfusion. We aimed to develop a novel hypoxia-reoxygenation model based on three-dimensional, spontaneously beating and work performing engineered heart tissue (EHT) from rat and human cardiomyocytes. Contractile force, the most important cardiac performance parameter, served as an integrated outcome measure. EHTs from neonatal rat cardiomyocytes were subjected to 90 min of hypoxia which led to cardiomyocyte apoptosis as revealed by caspase 3-staining, increased troponin I release (time control vs. 24 h after hypoxia: cTnI 2.7 vs. 6.3 ng/mL, ** p = 0.002) and decreased contractile force (64 ± 6% of baseline) in the long-term follow-up. The detrimental effects were attenuated by preceding the long-term hypoxia with three cycles of 10 min hypoxia (i.e., hypoxic preconditioning). Similarly, [d-Ala2, d-Leu5]-enkephalin (DADLE) reduced the effect of hypoxia on force (recovery to 78 ± 5% of baseline with DADLE preconditioning vs. 57 ± 5% without, p = 0.012), apoptosis and cardiomyocyte stress. Human EHTs presented a comparable hypoxia-induced reduction in force (55 ± 5% of baseline), but DADLE failed to precondition them, likely due to the absence of δ-opioid receptors. In summary, this hypoxia-reoxygenation in vitro model displays cellular damage and the decline of contractile function after hypoxia allows the investigation of preconditioning strategies and will therefore help us to understand the discrepancy between successful conditioning in vitro experiments and its failure in clinical trials.

Characteristics of death of neonatal rat cardiomyocytes following hypoxia or hypoxia-reoxygenation: the association of apoptosis and cell membrane disintegrity

2002 ◽  
Vol 16 (6) ◽  
pp. 241-248 ◽  
Author(s):  
Reiko Matsuoka ◽  
Kazuei Ogawa ◽  
Hiroyuki Yaoita ◽  
Wakako Naganuma ◽  
Kazuhira Maehara ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Hypoxia Reoxygenation

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
Sign in / Sign up

Export Citation Format

Share Document