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 Protective Effects of Shenfuyixin Granule on H2O2-Induced Apoptosis in Neonatal Rat Cardiomyocytes

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Xinlu Wang ◽  
Xuanxuan Hao ◽  
Youping Wang ◽  
Bin Li ◽  
Lin Cui ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Caspase 3 ◽  
Neonatal Rat ◽  
Caspase 8 ◽  
Caspase 9 ◽  
Rat Cardiomyocytes ◽  
Expression Levels ◽  
Apoptosis Rate ◽  
Neonatal Rat Cardiomyocytes ◽  
Mitochondrion Membrane Potential

Shenfuyixin granule (SFYXG, i.e., Xinshuaikang granule) is a prescription, commonly used in the clinical experience, which plays a significant role in the treatment of heart failure. The purpose of this present research was to investigate the protective effect of SFYXG, and the mechanism about anti-H2O2-induced oxidative stress and apoptosis in the neonatal rat cardiomyocytes. Myocardial cells, as is well known, were divided into 4 groups: normal, model, SFYXG, and coenzyme Q10 group, respectively. Cells viability was determined by MTT assay. Flow cytometry and AO/EB staining were implemented to test the apoptosis rate and intracellular reactive oxygen species (ROS) level. Mitochondrion membrane potential (MMP) was evaluated by JC-1 fluorescence probe method. The myocardial ultrastructure of mitochondrion was measured by electron microscope. The related mRNA expression levels of Bax, Bcl-2, Caspase-3, caspase-8, and caspase-9 were detected by real-time polymerase chain reaction (PCR). Also, the expression levels of Bax and Bcl-2 protein were detected by Western blot, and the expression levels of caspase-3, caspase-8, and caspase-9 protein were tested by caspase-Glo®3 Assay, caspase-Glo®8 Assay, and caspase-Glo®9 Assay, respectively. GAPDH was used as the internal reference gene/protein. The results revealed that SFYXG (0.5 mg/ml) raised the viability of myocardial cell, weakened the apoptosis rate and ROS level, corrected the mitochondrion membrane potential stability, and improved cell morphology and ultrastructure of myocardial mitochondrion. Furthermore, SFYXG upregulated the antiapoptosis gene of Bcl-2, but downregulated the proapoptosis genes of Bax, caspase-3, and caspase-9. In conclusion, SFYXG could appear to attenuate myocardial injury by its antioxidative and antiapoptosis effect.

scholarly journals Ginsenoside Rb1 Reduces Isoproterenol-Induced Cardiomyocytes ApoptosisIn VitroandIn Vivo

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Xiu-feng Wang ◽  
Xin-jun Liu ◽  
Qian-mei Zhou ◽  
Jia Du ◽  
Tian-ling Zhang ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Herbal Remedies ◽  
Ginsenoside Rb1 ◽  
Caspase 9 ◽  
Rat Cardiomyocytes ◽  
Chinese Herbal ◽  
Induced Apoptosis ◽  
Alternative Drugs

Cardiomyocytes apoptosis can lead to heart failure. Conventional and alternative drugs, such as Chinese herbal remedies, have been developed to target cardiomyoblast cells apoptosis. In this study, we investigated the effects of ginsenoside Rb1 (Rb1), an active compound, which is isolated from Notoginseng and Ginseng on isoproterenol-(ISO-) induced apoptosis in rat cardiomyocytes and its mechanismin vivoandin vitro. Rb1 reduced the ISO-induced apoptosis in rat cardiomyocytes and H9c2 cells. The effect of Rb1 was significantly suppressed by H89 (inhibitor for PKA), but not by C-1 (inhibitor for PKC). Based on in-cell blot analysis, the ISO-induced PKA and PKC expressions were decreased by Rb1, which was inhibited by H89, but not by C-1. The expressions of caspase-3 and caspase-9 were decreased after treatment with both ISO and Rb1, but with no change for caspase-8. Our results indicated that Rb1 reducing ISO-induced rat cardiomyocytes apoptosis may be involved in PKA and caspase-9 pathways.

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 NMDA receptor activation induces mitochondrial dysfunction, oxidative stress and apoptosis in cultured neonatal rat cardiomyocytes

2007 ◽  
pp. 559-569
Author(s):  
X Gao ◽  
X Xu ◽  
J Pang ◽  
C Zhang ◽  
JM Ding ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Caspase 3 ◽  
Receptor Activation ◽  
Nmda Receptor Antagonist ◽  
Neonatal Rat ◽  
Dependent Manner ◽  
Rat Cardiomyocytes ◽  
Peripheral Tissues ◽  
Excitatory Neurotransmitter ◽  
Neonatal Rat Cardiomyocytes

Glutamate is a well-characterized excitatory neurotransmitter in the central nervous system (CNS). Recently, glutamate receptors (GluRs) were also found in peripheral tissues, including the heart. However, the function of GluRs in peripheral organs remains poorly understood. In the present study, we found that N-methyl-D-aspartate (NMDA) could increase intracellular calcium ([Ca(2+)]i) level in a dose-dependent manner in cultured neonatal rat cardiomyocytes. NMDA at 10(-4) M increased the levels of reactive oxygen species (ROS), cytosolic cytochrome c (cyto c), and 17-kDa caspase-3, but depolarized mitochondrial membrane potential, leading to cardiomyocyte apoptosis. In addition, NMDA treatment induced an increase in bax mRNA but a decrease in bcl-2 mRNA expression in the cardiomyocytes. The above effects of NMDA were blocked by the NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801), and by ROS scavengers glutathione (GSH) and N-acetylcystein (NAC). These results suggest that stimulation of NMDA receptor in the cardiomyocyte may lead to apoptosis via a Ca(2+), ROS, and caspase-3 mediated pathway. These findings suggest that NMDA receptor may play an important role in myocardial pathogenesis.

scholarly journals Opposing effects of polysulfides and thioredoxin on apoptosis through caspase persulfidation

2020 ◽  
Vol 295 (11) ◽  
pp. 3590-3600 ◽  
Author(s):  
Ilana Braunstein ◽  
Rotem Engelman ◽  
Ofer Yitzhaki ◽  
Tamar Ziv ◽  
Erwan Galardon ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Caspase 3 ◽  
Therapeutic Potential ◽  
Thioredoxin Reductase ◽  
Caspase 9 ◽  
Apoptotic Pathway ◽  
Cellular Effects ◽  
Short Term Exposure ◽  
Biochemical Analyses

Hydrogen sulfide has been implicated in a large number of physiological processes including cell survival and death, encouraging research into its mechanisms of action and therapeutic potential. Results from recent studies suggest that the cellular effects of hydrogen sulfide are mediated in part by sulfane sulfur species, including persulfides and polysulfides. In the present study, we investigated the apoptosis-modulating effects of polysulfides, especially on the caspase cascade, which mediates the intrinsic apoptotic pathway. Biochemical analyses revealed that organic or synthetic polysulfides strongly and rapidly inhibit the enzymatic activity of caspase-3, a major effector protease in apoptosis. We attributed the caspase-3 inhibition to persulfidation of its catalytic cysteine. In apoptotically stimulated HeLa cells, short-term exposure to polysulfides triggered the persulfidation and deactivation of cleaved caspase-3. These effects were antagonized by the thioredoxin/thioredoxin reductase system (Trx/TrxR). Trx/TrxR restored the activity of polysulfide-inactivated caspase-3 in vitro, and TrxR inhibition potentiated polysulfide-mediated suppression of caspase-3 activity in situ. We further found that under conditions of low TrxR activity, early cell exposure to polysulfides leads to enhanced persulfidation of initiator caspase-9 and decreases apoptosis. Notably, we show that the proenzymes procaspase-3 and -9 are basally persulfidated in resting (unstimulated) cells and become depersulfidated during their processing and activation. Inhibition of TrxR attenuated the depersulfidation and activation of caspase-9. Taken together, our results reveal that polysulfides target the caspase-9/3 cascade and thereby suppress cancer cell apoptosis, and highlight the role of Trx/TrxR-mediated depersulfidation in enabling caspase activation.

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

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
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