Mitochondrial dysfunction in H9c2 cells during ischemia and amelioration with Tribulus terrestris L.

Reshma, P.L.; Sainu, Neethu S.; Mathew, Anil Kuruvilla; Raghu, Kozhiparambil Gopalan

doi:10.1016/j.lfs.2016.03.055

Cited by 26 publications

(21 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Moreover, SPostC-induced mitochondrial network changes were associated to mitochondrial fusion- and fission-related proteins (Mfn2, Opa1 and Drp1). The influence of hypoxia/ischemic on fusion and fission proteins were in line with vitro studies (Dong et al, 2016; Reshma et al, 2016) on H9C2 cells and vivo study on rats (Yu et al, 2015). …”

Section: Discussionsupporting

confidence: 69%

Sevoflurane postconditioning attenuates cardiomyocyte hypoxia/reoxygenation injury via restoring mitochondrial morphology

Xie

et al. 2016

PeerJ

View full text Add to dashboard Cite

BackgroundAnesthetic postconditioning is a cellular protective approach whereby exposure to a volatile anesthetic renders a tissue more resistant to subsequent ischemic/reperfusion event. Sevoflurane postconditioning (SPostC) has been shown to exert cardioprotection against ischemia/reperfusion injury, but the underlying mechanism is unclear. We hypothesized that SPostC protects cardiomyocytes against hypoxia/reoxygenation (H/R) injury by maintaining/restoring mitochondrial morphological integrity, a critical determinant of cell fate.MethodsPrimary cultures of neonatal rat cardiomyocytes (NCMs) were subjected to H/R injury (3 h of hypoxia followed by 3 h reoxygenation). Intervention with SPostC (2.4% sevoflurane) was administered for 15 min upon the onset of reoxygenation. Cell viability, Lactate dehydrogenase (LDH) level, cell death, mitochondrial morphology, mitochondrial membrane potential and mitochondrial permeability transition pore (mPTP) opening were assessed after intervention. Mitochondrial fusion and fission regulating proteins (Drp1, Fis1, Mfn1, Mfn2 and Opa1) were assessed by immunofluorescence staining and western blotting was performed to determine the level of protein expression.ResultsCardiomyocyte H/R injury resulted in significant increases in LDH release and cell death that were concomitant with reduced cell viability and reduced mitochondrial interconnectivity (mean area/perimeter ratio) and mitochondrial elongation, and with reduced mitochondrial membrane potential and increased mPTP opening. All the above changes were significantly attenuated by SPostC. Furthermore, H/R resulted in significant reductions in mitochondrial fusion proteins Mfn1, Mfn2 and Opa1 and significant enhancement of fission proteins Drp1 and Fis1. SPostC significantly enhanced Mfn2 and Opa1 and reduced Drp1, without significant impact on Mfn1 and Fis1.ConclusionsSevoflurane postconditioning attenuates cardiomyocytes hypoxia/reoxygenation injury (HRI) by restoring mitochondrial fusion/fission balance and morphology.

show abstract

Section: Discussionsupporting

confidence: 69%

Sevoflurane postconditioning attenuates cardiomyocyte hypoxia/reoxygenation injury via restoring mitochondrial morphology

Xie

et al. 2016

PeerJ

View full text Add to dashboard Cite

show abstract

“…Cardiovascular diseases have become one of the major causes of death all over world [11]. Myocardial infarction leads to myocardial ischemia and even irreversible myocardial necrosis if blood supply is not timely restored [11,12].…”

Section: Discussionmentioning

confidence: 99%

“…Myocardial infarction leads to myocardial ischemia and even irreversible myocardial necrosis if blood supply is not timely restored [11,12]. It has been reported that myocardial ischemia results from the imbalance between the supply of oxygen to the heart and oxygen demand by the heart [13,14].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of total saponins from Ilex pubescens Hook against hydrogen peroxide-induced cardiomyocyte apoptosis

Ying¹,

Wu²,

Yin³

et al. 2018

Trop. J. Pharm Res

View full text Add to dashboard Cite

“…Currently, cardiac diseases have become one of the leading causes of death worldwide, and the prevalence of cardiac diseases are growing rapidly [16]. In addition, ischemic coronary heart diseases, such as myocardial infarction, could result in myocardial apoptosis, leading to cardiac failure [16,17].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, ischemic coronary heart diseases, such as myocardial infarction, could result in myocardial apoptosis, leading to cardiac failure [16,17]. Therefore, inhibiting myocardial apoptosis is beneficial for treating ischemic coronary heart diseases.…”

Section: Discussionmentioning

confidence: 99%

Effect of acetone extract of <i>Rumex japonicas</i> Houtt on hydrogen peroxide-induced apoptosis in rat myocardial cells

Zhou¹,

Cao²,

Song³

et al. 2017

Trop. J. Pharm Res

View full text Add to dashboard Cite

Purpose: To investigate the protective effect of the acetone extract of Rumex japonicas Houtt. (AER) on rat myocardial cells. Methods: R. japonicas was extracted with 75 % aqueous ethanol by reflux to afford total extract (TER H2O2 (p < 0.05, p < 0.01, p < 0.01, respectively). AER (50, 100 and 200 μg/mL) decreased LDH and CK contents of H9c2 cells (p < 0.01). The levels of SOD (p<0.01) and CAT (p < 0.01) were increased by AER treatments (100 and 200 μg/mL); in addition, AER (50, 100 and 200 μg/mL) decreased MDA levels (p < 0.01

show abstract

Mitochondrial dysfunction in H9c2 cells during ischemia and amelioration with Tribulus terrestris L.

Cited by 26 publications

References 43 publications

Sevoflurane postconditioning attenuates cardiomyocyte hypoxia/reoxygenation injury via restoring mitochondrial morphology

Sevoflurane postconditioning attenuates cardiomyocyte hypoxia/reoxygenation injury via restoring mitochondrial morphology

Inhibitory effects of total saponins from Ilex pubescens Hook against hydrogen peroxide-induced cardiomyocyte apoptosis

Effect of acetone extract of <i>Rumex japonicas</i> Houtt on hydrogen peroxide-induced apoptosis in rat myocardial cells

Contact Info

Product

Resources

About