Taurine attenuates isoproterenol-induced H9c2 cardiomyocytes hypertrophy by improving antioxidative ability and inhibiting calpain-1-mediated apoptosis

2020 ◽  
Vol 469 (1-2) ◽  
pp. 119-132
Author(s):  
Weiwei Li ◽  
Jiancheng Yang ◽  
Qiufeng Lyu ◽  
Gaofeng Wu ◽  
Shumei Lin ◽  
...  
Keyword(s):  
H9c2 Cardiomyocytes ◽  
Antioxidative Ability

scholarly journals Fisetin ameliorates Ischemia re-oxygenation injury in H9c2 cardiomyocytes via targeting the PI3K signalling pathway

2021 ◽  
pp. 100094
Author(s):  
Bhavana Sivakumar ◽  
Sri Rahavi Boovarahan ◽  
Priyanka N Prem ◽  
Gino A Kurian
Keyword(s):  
Signalling Pathway ◽  
H9c2 Cardiomyocytes ◽  
Pi3k Signalling

MicroRNA-34a regulates high glucose-induced apoptosis in H9c2 cardiomyocytes

2013 ◽  
Vol 33 (6) ◽  
pp. 834-839 ◽  
Author(s):  
Fang Zhao ◽  
Bo Li ◽  
Yin-zhi Wei ◽  
Bin Zhou ◽  
Han Wang ◽  
...  
Keyword(s):  
High Glucose ◽  
H9c2 Cardiomyocytes ◽  
Induced Apoptosis

scholarly journals Treatment effect of a flavonoid prescription on duck virus hepatitis by its hepatoprotective and antioxidative ability

2016 ◽  
Vol 55 (1) ◽  
pp. 198-205 ◽  
Author(s):  
Yun Chen ◽  
Ling Zeng ◽  
Yu Lu ◽  
Yulan Yang ◽  
Meiyun Xu ◽  
...  
Keyword(s):  
Treatment Effect ◽  
Virus Hepatitis ◽  
Antioxidative Ability

scholarly journals Ganoderic Acid A Protects Rat H9c2 Cardiomyocytes from Hypoxia-Induced Injury via Up-Regulating miR-182-5p

2018 ◽  
Vol 50 (6) ◽  
pp. 2086-2096 ◽  
Author(s):  
Xiaohong  Zhang ◽  
Can Xiao ◽  
Hong Liu
Keyword(s):  
Cell Viability ◽  
Molecular Mechanisms ◽  
Akt Pathway ◽  
H9c2 Cell ◽  
H9c2 Cells ◽  
Ganoderic Acid ◽  
Expression Levels ◽  
Protein Levels ◽  
Viability Loss ◽  
H9c2 Cardiomyocytes

Background/Aims: Ganoderic acid A (GAA) isolated from Ganoderma lucidum, shows various benefit activities, such as anti-tumor activity, anti-HIV activity and hepatoprotective activity. However, the potential effects of GAA on hypoxia-induced injury of cardiomyocytes are still unclear. In this study, we aimed to reveal the effects of GAA on hypoxic-induced H9c2 cell injury, as well as potential underlying molecular mechanisms. Methods: Rat H9c2 cardiomyocytes were cultured in hypoxia condition with different doses of GAA. Cell viability and apoptosis were detected by CCK-8 assay and flow cytometry, respectively. qRT-PCR was performed to assess the expression levels of microRNA-182-5p (miR-182-5p) and phosphatase and tensin homologue (PTEN). Cell transfection was conducted to change the expression levels of miR-182-5p and PTEN in H9c2 cells. Finally, protein levels of key factors involved in cell proliferation, cell apoptosis and PTEN/PI3K/AKT pathway were evaluated using western blotting. Results: Hypoxia treatment significantly induced H9c2 cell viability loss and apoptosis. GAA incubation remarkably protected H9c2 cells from hypoxia-induced viability loss, proliferation inhibition and apoptosis. In addition, GAA obviously enhanced the expression level of miR-182-5p in H9c2 cells. Suppression of miR-182-5p notably alleviated the protective effects of GAA on hypoxia-treated H9c2 cells. Furthermore, miR-182-5p negatively regulated the mRNA and protein levels of PTEN in H9c2 cells. GAA attenuated hypoxia-induced inactivation of PI3K/AKT pathway in H9c2 cells by up-regulating miR-182-5p and then down-regulating PTEN. Conclusion: GAA protected rat H9c2 cardiomyocytes from hypoxia-induced injury might via up-regulating miR-182-5p, down-regulating PTEN and then activating PI3K/AKT signaling pathway.

scholarly journals Shengmai San Alleviates Diabetic Cardiomyopathy Through Improvement of Mitochondrial Lipid Metabolic Disorder

2018 ◽  
Vol 50 (5) ◽  
pp. 1726-1739 ◽  
Author(s):  
Jing Tian ◽  
Wenzhu Tang ◽  
Ming Xu ◽  
Chen Zhang ◽  
Pei Zhao ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Diastolic Dysfunction ◽  
Diabetic Cardiomyopathy ◽  
Leptin Receptor ◽  
Myocardial Hypertrophy ◽  
Oxphos Complex ◽  
H9c2 Cardiomyocytes ◽  
Mitochondrial Lipid ◽  
And Function ◽  
Shengmai San

Background/Aims: Shengmai San (SMS), prepared from Panax ginseng, Ophiopogon japonicus, and Schisandra chinensisin, has been widely used to treat ischemic disease. In this study, we investigated whether SMS may exert a beneficial effect in diabetic cardiomyopathy through improvement of mitochondrial lipid metabolism. Methods: A leptin receptor-deficient db/db mouse model was utilized, and lean age-matched C57BLKS mice served as non-diabetic controls. Glucose and lipid profiles, myocardial structure, dimension, and function, and heart weight to tibial length ratio were determined. Myocardial ultrastructural morphology was observed with transmission electron microscopy. Protein expression and activity of oxidative phosphorylation (OXPHOS) complex were assessed using western blotting and microplate assay kits. We also observed cellular viability, mitochondrial membrane potential, OXPHOS complex activity, and cellular ATP level in palmitic acid-stimulated H9C2 cardiomyocytes. Changes in the sirtuin (SIRT1)/AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) pathway and mitochondrial uncoupling signaling were assessed using western blotting and quantitative real-time PCR. Results: Leptin receptor-deficient db/db mice exhibit obesity, hyperglycemia, and hyperlipidemia, accompanied by distinct myocardial hypertrophy and diastolic dysfunction. SMS at a dose of 3 g/kg body weight contributed to a recovery of diabetes-induced myocardial hypertrophy and diastolic dysfunction. SMS administration led to an effective restoration of mitochondrial structure and function both in vivo and in vitro. Furthermore, SMS markedly enhanced SIRT1 and p-AMPKα protein levels and decreased the expression of acetylated-PGC-1α and uncoupling protein 2 protein. SMS also restored the depletion of NRF1 and TFAM levels in diabetic hearts and H9C2 cardiomyocytes. Conclusion: The results indicate that SMS may alleviate diabetes-induced myocardial hypertrophy and diastolic dysfunction by improving mitochondrial lipid metabolism.

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