scholarly journals Protective effects of five compounds from Livistona chinensis R. Brown leaves against hypoxia/reoxygenation, H2O2, or adriamycin-induced injury in H9c2 cells

2019 ◽  
Vol Volume 13 ◽  
pp. 1555-1566 ◽  
Author(s):  
Shaoguang Li ◽  
Shaohong Luo ◽  
Hao Chen ◽  
Yanjie Zheng ◽  
Liqing Lin ◽  
...  
Keyword(s):  
Protective Effects ◽  
H9c2 Cells ◽  
Livistona Chinensis ◽  
Hypoxia Reoxygenation

scholarly journals [Corrigendum] Protective effects of exendin‑4 on hypoxia/reoxygenation‑induced injury in H9c2 cells

2020 ◽  
Vol 22 (2) ◽  
pp. 1090-1090
Author(s):  
Kai Lu ◽  
Guanglei Chang ◽  
Lin Ye ◽  
Peng Zhang ◽  
Yong Li ◽  
...  
Keyword(s):  
Protective Effects ◽  
H9c2 Cells ◽  
Hypoxia Reoxygenation

scholarly journals Protective effects of extendin-4 on hypoxia/reoxygenation-induced injury in H9c2 cells

2015 ◽  
Vol 12 (2) ◽  
pp. 3007-3016 ◽  
Author(s):  
KAI LU ◽  
GUANGLEI CHANG ◽  
LIN YE ◽  
PENG ZHANG ◽  
YONG LI ◽  
...  
Keyword(s):  
Protective Effects ◽  
H9c2 Cells ◽  
Hypoxia Reoxygenation

scholarly journals CTRP13 Protects H9c2 Cells Against Hypoxia/Reoxygenation (H/R)-Induced Injury Via Regulating the AMPK/Nrf2/ARE Signaling Pathway

2021 ◽  
Vol 30 ◽  
pp. 096368972110332
Author(s):  
Weifeng Jiang ◽  
Jungang Song ◽  
Suitao Zhang ◽  
Yanyan Ye ◽  
Jun Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Therapeutic Potential ◽  
Ischemia Reperfusion ◽  
Myocardial Necrosis ◽  
Inhibitory Effect ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Hypoxia Reoxygenation

Myocardial infarction (MI) is identified as the myocardial necrosis due to myocardial ischemia/reperfusion (I/R) injury and remains a leading cause of mortality. C1q/TNF-related protein 13 (CTRP13) is a member of CTRP family that has been found to be involved in coronary artery disease (CAD). However, the role of CTRP13 in MI remains unclear. We aimed to explore the functional role of CTRP13 in H9c2 cells exposed to hypoxia/reoxygenation (H/R). Our results demonstrated that H/R stimulation significantly decreased the expression of CTRP13 in H9c2 cells. H/R-induced an increase in ROS production and reductions in activities of SOD and CAT were prevented by CTRP13 overexpression but were aggravated by CTRP13 silencing. Moreover, CTRP13 overexpression could reverse the inductive effect of H/R on caspase-3 activity and bax expression, as well as the inhibitory effect of H/R on bcl-2 expression in H9c2 cells. However, CTRP13 silencing presented opposite effects with CTRP13 overexpression. Furthermore, CTRP13 overexpression enhanced the H/R-stimulated the expression levels of p-AMPK and nuclear Nrf2, and Nrf2 transcriptional activity. However, inhibition of AMPK reversed the CTRP13-mediated activation of Nrf2/ARE signaling and the cardiac-protective effect in H/R-exposed H9c2 cells. Additionally, silencing of Nrf2 reversed the protective effects of CTRP13 against H/R-stimulated oxidative stress and apoptosis in H9c2 cells. Finally, recombinant CTRP13 protein attenuated myocardial I/R-induced injury in rats. Taken together, these findings indicated that CTRP13 protected H9c2 cells from H/R-stimulated oxidative stress and apoptosis via regulating the AMPK/Nrf2/ARE signaling pathway. Our results provided evidence for the therapeutic potential of CTRP13 in myocardial I/R injury.

scholarly journals Wenxin Granule Ameliorates Hypoxia/Reoxygenation-Induced Oxidative Stress in Mitochondria via the PKC-δ/NOX2/ROS Pathway in H9c2 Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Qihui Jin ◽  
Yanhong Jiang ◽  
Lizhong Fu ◽  
Yanqiu Zheng ◽  
Yuxia Ding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Injury ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Cytochrome C Release ◽  
Mitochondrial Ros ◽  
Hypoxia Reoxygenation

Myocardial infarction and following reperfusion therapy-induced myocardial ischemia/reperfusion (I/R) injury have been recognized as an important subject of cardiovascular disease with high mortality. As the antiarrhythmic agent, Wenxin Granule (WXG) is widely used to arrhythmia and heart failure. In our pilot study, we found the antioxidative potential of WXG in the treatment of myocardial I/R. This study is aimed at investigating whether WXG could treat cardiomyocyte hypoxia/reoxygenation (H/R) injury by inhibiting oxidative stress in mitochondria. The H9c2 cardiomyocyte cell line was subject to H/R stimuli to mimic I/R injury in vitro. WXG was added to the culture medium 24 h before H/R exposing as pretreatment. Protein kinase C-δ (PKC-δ) inhibitor rottlerin or PKC-δ lentivirus vectors were conducted on H9c2 cells to downregulate or overexpress PKC-δ protein. Then, the cell viability, oxidative stress levels, intracellular and mitochondrial ROS levels, mitochondrial function, and apoptosis index were analyzed. In addition, PKC-δ protein expression in each group was verified by western blot analysis. Compared with the control group, the PKC-δ protein level was significantly increased in the H/R group, which was remarkably improved by WXG or rottlerin. PKC-δ lentivirus vector-mediated PKC-δ overexpression was not reduced by WXG. WXG significantly improved H/R-induced cell injury, lower levels of SOD and GSH/GSSG ratio, higher levels of MDA, intracellular and mitochondrial ROS content, mitochondrial membrane potential and ATP loss, mitochondrial permeability transition pore opening, NOX2 activation, cytochrome C release, Bax/Bcl-2 ratio and cleaved caspase-3 increasing, and cell apoptosis. Similar findings were obtained from rottlerin treatment. However, the protective effects of WXG were abolished by PKC-δ overexpression, indicating that PKC-δ was a potential target of WXG treatment. Our findings demonstrated a novel mechanism by which WXG attenuated oxidative stress and mitochondrial dysfunction of H9c2 cells induced by H/R stimulation via inhibitory regulation of PKC-δ/NOX2/ROS signaling.

scholarly journals Glaucocalyxin A Protects H9c2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of Akt/Nrf2/HO-1 Pathway

2020 ◽  
Vol 29 ◽  
pp. 096368972096767
Author(s):  
Zhuo Peng ◽  
Rui Zhang ◽  
Longfei Pan ◽  
Honghong Pei ◽  
Zequn Niu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Ischemia Reperfusion ◽  
Biologically Active ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Rat Cardiomyocytes ◽  
Myocardial Ischemia Reperfusion ◽  
Hypoxia Reoxygenation

Myocardial infarction (MI) is one of the most serious cardiovascular diseases associated with myocardial ischemia/reperfusion (I/R) injury. Glaucocalyxin A (GLA) is a biologically active ent-kauranoid diterpenoid that has been found to ameliorate myocardial I/R injury in mice. However, the mechanism has not been fully investigated. In the present study, we aimed to investigate the effect of GLA on rat cardiomyocytes H9c2 cells exposed to hypoxia/reoxygenation (H/R). The results showed that GLA treatment improved cell viability of H/R-stimulated H9c2 cells. Administration with GLA suppressed the H/R-stimulated reactive oxygen species (ROS) production in H9c2 cells. GLA also elevated the activities of antioxidant enzymes, including superoxide dismutase and glutathione peroxidase in H/R-stimulated H9c2 cells. Moreover, GLA prevented H/R-stimulated cell apoptosis in H9c2 cells, as evidenced by increased bcl-2 expression, decreased bax expression, as well as reduced caspase-3 activity. Furthermore, GLA enhanced the activation of protein kinase B (Akt)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in H9c2 cells exposed to H/R. Additionally, treatment with LY294002 reserved the protective effects of GLA on H/R-stimulated oxidative injury in H9c2 cells. In conclusion, these findings suggested that GLA protected H9c2 cells from H/R-stimulated oxidative damage, which was mediated by the Akt/Nrf2/HO-1 signaling pathway. Thus, GLA might be a promising therapeutic agent for the prevention and treatment of myocardial I/R.

scholarly journals Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Rong-Hui Han ◽  
He-Meng Huang ◽  
Hong Han ◽  
Hao Chen ◽  
Fei Zeng ◽  
...  
Keyword(s):  
Transcription Factors ◽  
High Glucose ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Cardiac Cells ◽  
H9c2 Cell ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Hypoxia Reoxygenation

Abstract Background Administration of propofol, an intravenous anesthetic with antioxidant property, immediately at the onset of post-ischemic reperfusion (propofol postconditioning, P-PostC) has been shown to confer cardioprotection against ischemia–reperfusion injury, while the underlying mechanism remains incompletely understood. The FoxO transcription factors are reported to play critical roles in activating cardiomyocyte survival signaling throughout the process of cellular injuries induced by oxidative stress and are also involved in hypoxic postconditioning mediated neuroprotection, however, the role of FoxO in postconditioning mediated protection in the heart and in particular in high glucose condition is unknown. Methods Rat heart-derived H9c2 cells were exposed to high glucose (HG) for 48 h (h), then subjected to hypoxia/reoxygenation (H/R, composed of 8 h of hypoxia followed by 12 h of reoxygenation) in the absence or presence of postconditioning with various concentrations of propofol (P-PostC) at the onset of reoxygenation. After having identified the optical concentration of propofol, H9c2 cells were subjected to H/R and P-PostC in the absence or presence of FoxO1 or FoxO3a gene silencing to explore their roles in P-PostC mediated protection against apoptotic and autophagic cell deaths under hyperglycemia. Results The results showed that HG with or without H/R decreased cell viability, increased lactate dehydrogenase (LDH) leakage and the production of reactive oxygen species (ROS) in H9c2 cells, all of which were significantly reversed by propofol (P-PostC), especially at the concentration of 25 µmol/L (P25) (all P < 0.05, NC vs. HG; HG vs. HG + HR; HG + HR + P12.5 or HG + HR + P25 or HG + HR + P50 vs. HG + HR). Moreover, we found that propofol (P25) decreased H9c2 cells apoptosis and autophagy that were concomitant with increased FoxO1 and FoxO3a expression (all P < 0.05, HG + HR + P25 vs. HG + HR). The protective effects of propofol (P25) against H/R injury were reversed by silencing FoxO1 or FoxO3a (all P < 0.05, HG + HR + P25 vs. HG + HR + P25 + siRNA-1 or HG + HR + P25 + siRNA-5). Conclusion It is concluded that propofol postconditioning attenuated H9c2 cardiac cells apoptosis and autophagy induced by H/R injury through upregulating FoxO1 and FoxO3a under hyperglycemia.

scholarly journals Total Flavonoids from Carya cathayensis Sarg. Leaves Alleviate H9c2 Cells Hypoxia/Reoxygenation Injury via Effects on miR-21 Expression, PTEN/Akt, and the Bcl-2/Bax Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Ruibin Jiang ◽  
Yan Guo ◽  
Nipi Chen ◽  
Chengxian Gao ◽  
Zhishan Ding ◽  
...  
Keyword(s):  
Akt Signaling ◽  
Total Flavonoids ◽  
Protective Effects ◽  
H9c2 Cells ◽  
H9c2 Cardiomyocytes ◽  
Reoxygenation Injury ◽  
Carya Cathayensis ◽  
Carya Cathayensis Sarg ◽  
Signaling Activity ◽  
Hypoxia Reoxygenation

This study aimed to investigate whether the total flavonoids (TFs) from Carya cathayensis Sarg. leaves alleviate hypoxia/reoxygenation (H/R) injury in H9c2 cardiomyocytes and to explore potential mechanisms. H9c2 cells pretreated with TFs for 24h were exposed to H/R treatment. The results indicated that TFs significantly alleviate H/R injury, which include inhibiting apoptosis and enhancing antioxidant capacity. The protective effects of TFs resulted in higher expression of miR-21 in H/R-induced H9c2 cells than that of controls, which in turn upregulated Akt signaling activity via suppressing the expression of PTEN together with decreasing the ratio of Bax/Bcl-2, caspase3, and cleaved-caspase3 expression in H/R-induced H9c2 cells. Conversely, blocking miR-21 expression with miR-21 inhibitor effectively suppressed the protective effects of TFs against H/R-induced injury. Our study suggests that TFs can decrease cell apoptosis, which may be mediated by altering the expression of miR-21, PTEN/Akt, and Bcl/Bax.

scholarly journals Myostatin Deficiency Protects C2C12 Cells from Oxidative Stress by Inhibiting Intrinsic Activation of Apoptosis

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1680
Author(s):  
Marius Drysch ◽  
Sonja Verena Schmidt ◽  
Mustafa Becerikli ◽  
Felix Reinkemeier ◽  
Stephanie Dittfeld ◽  
...  
Keyword(s):  
Intracellular Signaling ◽  
Ischemia Reperfusion ◽  
C2c12 Cell ◽  
C2c12 Cells ◽  
Ros Generation ◽  
Protective Effects ◽  
Activity Increase ◽  
Mitogen Activated Protein ◽  
Myostatin Inhibition ◽  
Hypoxia Reoxygenation

Ischemia reperfusion (IR) injury remains an important topic in clinical medicine. While a multitude of prophylactic and therapeutic strategies have been proposed, recent studies have illuminated protective effects of myostatin inhibition. This study aims to elaborate on the intracellular pathways involved in myostatin signaling and to explore key proteins that convey protective effects in IR injury. We used CRISPR/Cas9 gene editing to introduce a Myostatin (Mstn) deletion into a C2C12 cell line. In subsequent experiments, we evaluated overall cell death, activation of apoptotic pathways, ROS generation, lipid peroxidation, intracellular signaling via mitogen-activated protein kinases (MAPKs), cell migration, and cell proliferation under hypoxic conditions followed by reoxygenation to simulate an IR situation in vitro (hypoxia reoxygenation). It was found that mitogen-activated protein kinase kinase 3/6, also known as MAPK/ERK Kinase 3/6 (MEK3/6), and subsequent p38 MAPK activation were blunted in C2C12-Mstn−/− cells in response to hypoxia reoxygenation (HR). Similarly, c-Jun N-terminal kinase (JNK) activation was negated. We also found the intrinsic activation of apoptosis to be more important in comparison with the extrinsic activation. Additionally, intercepting myostatin signaling mitigated apoptosis activation. Ultimately, this research validated protective effects of myostatin inhibition in HR and identified potential mediators worth further investigation. Intercepting myostatin signaling did not inhibit ROS generation overall but mitigated cellular injury. In particular, intrinsic activation of apoptosis origination from mitochondria was alleviated. This was presumably mediated by decreased activation of p38 caused by the diminished kinase activity increase of MEK3/6. Overall, this work provides important insights into HR signaling in C2C12-Mstn−/− cells and could serve as basis for further research.

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