Propofol attenuates H2O2-induced oxidative stress and apoptosis via the mitochondria- and ER-medicated pathways in neonatal rat cardiomyocytes

Liu, Xue-Ru; Cao, Lu; Li, Tao; Chen, Linlin; Yu, Yiyan; Huang, Wenjun; Liu, Li; Tan, Xiaoqiu

doi:10.1007/s10495-017-1349-3

Cited by 36 publications

(27 citation statements)

References 38 publications

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“…All protocols in this study were approved by the Ethics Committee of Southwest Medical University. Neonatal rats (2–3 days) was used for the isolation and culture of neonatal rat cardiomyocytes (NRCMs) as we reported previously ( 14 ). Cultured NRCMs in DMEM with 10% FBS were further divided into four groups by different treatments: i) Control group: normal DMEM adding with 10% FBS, ii) H 2 O 2 group [with H 2 O 2 for 6 h at 500 µM ( 15 )], iii) DEX group [with DEX at 5 µM ( 16 )], and iv) H 2 O 2 + DEX group (with 5 µM DEX for 2 h before exposing to 500 µM H 2 O 2 for 6 h).…”

Section: Methodsmentioning

confidence: 99%

“…ELISA was used in this study to detect the levels of lactic dehydrogenase (LDH), glutathione (GSH) and the activities of caspase 3, 8, 9 and 12 with ELISA kits according to the instructions and our previous research ( 14 ).…”

Section: Methodsmentioning

confidence: 99%

“…The level of apoptosis, intracellular ROS level and mitochondrial membrane potential (ΔΨm) in NRCMs were detected with FCM (BD Biosciences, Franklin Lakes, NJ, USA) according to the instructions and our previous research ( 14 ). The level of apoptosis in NRCMs was analyzed with FITC-Annexin V Apoptosis Detection kit I (BD Biosciences).…”

Section: Methodsmentioning

confidence: 99%

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Dexmedetomidine attenuates H2O2-induced neonatal rat cardiomyocytes apoptosis through mitochondria- and ER-medicated oxidative stress pathways

Liu

Cao

et al. 2018

Mol Med Report

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Dexmedetomidine (DEX), an α2 adrenoceptor agonist, has sedative and analgesic properties and myocardial protective effects. However, the mechanism underlying the protective effects of DEX on the myocardium remain unclear. The present study aimed to determine whether DEX serves an important role on cardioprotection through the endoplasmic reticulum (ER)- and mitochondria-mediated apoptosis signaling pathways. Neonatal rat cardiomyocytes (NRCMs) were cultured and divided four groups: i) Normal culture medium with 10% fetal bovine serum (control group); ii) H2O2 at 500 µM (H2O2 group); iii) DEX at 5 µM (DEX group); and iv) H2O2 plus DEX (H2O2 + DEX group). The levels of apoptosis and oxidative stress of NRCMs were investigated by ELISA, western blotting, flow cytometry and cell immunofluorescence. DEX significantly suppressed H2O2-induced apoptosis, and increased activity of caspases 3, 8 and 9 of NRCMs. DEX inhibited mitochondria-mediated oxidative stress and apoptosis, as evidenced by decreased levels of reactive oxygen species and lactic dehydrogenase, alleviated mitochondrial membrane potential depolarization, and increased Bcl-2-associated X protein/B-cell lymphoma 2 ratio. In addition, DEX decreased the activity of caspase 12, and the expression levels of glucose-regulated protein 78 kDa and serine/threonine-protein kinase/endoribonuclease IRE1, three major signaling molecules involved in the ER stress-mediated apoptosis pathway. Preventive treatment with DEX alleviates cardiomyocyte against H2O2-induced oxidative stress injury through attenuating the mitochondria- and ER-mediated apoptosis pathways.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Dexmedetomidine attenuates H2O2-induced neonatal rat cardiomyocytes apoptosis through mitochondria- and ER-medicated oxidative stress pathways

Liu

Cao

et al. 2018

Mol Med Report

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“…A key beginning event in the initiation of UPR is the dissociation of GRP78 from the three transmembrane sensor proteins, freeing them to activate distinct UPR pathways. In most examples of ER stress and UPR signaling, GRP78 is upregulated and UPR signaling is stimulated [ 29 , 30 ]. However, as seen in Figure 6 C, levels of GRP78 are reduced in the 3-month-old TauTKO heart, an effect associated with inhibition of UPR signaling.…”

Section: Resultsmentioning

confidence: 99%

Role of Mitochondria and Endoplasmic Reticulum in Taurine-Deficiency-Mediated Apoptosis

et al. 2017

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Taurine is a ubiquitous sulfur-containing amino acid found in high concentration in most tissues. Because of its involvement in fundamental physiological functions, such as regulating respiratory chain activity, modulating cation transport, controlling inflammation, altering protein phosphorylation and prolonging lifespan, taurine is an important nutrient whose deficiency leads to severe pathology and cell death. However, the mechanism by which taurine deficiency causes cell death is inadequately understood. Therefore, the present study examined the hypothesis that overproduction of reactive oxygen species (ROS) by complex I of the respiratory chain triggers mitochondria-dependent apoptosis in hearts of taurine transporter knockout (TauTKO) mice. In support of the hypothesis, a 60% decrease in mitochondrial taurine content of 3-month-old TauTKO hearts was observed, which was associated with diminished complex I activity and the onset of mitochondrial oxidative stress. Oxidative damage to stressed mitochondria led to activation of a caspase cascade, with stimulation of caspases 9 and 3 prevented by treatment of 3-month-old TauTKO mice with the mitochondria specific antioxidant, MitoTempo. In 12 month-old, but not 3-month-old, TauTKO hearts, caspase 12 activation contributes to cell death, revealing a pathological role for endoplasmic reticulum (ER) stress in taurine deficient, aging mice. Thus, taurine is a cytoprotective nutrient that ensures normal mitochondrial and ER function, which is important for the reduction of risk for apoptosis and premature death.

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“…Hydrogen peroxide (H 2 O 2 ), a highly reactive oxygen species (ROS), gives rise to wide spread oxidative damage, and has been widely used to mimic oxidative stress in vitro 7 . Previous studies have demonstrated that H 2 O 2 may also activate apoptosis in vivo 8 . The mitochondria-mediated intrinsic pathway and the cell death receptors-mediated extrinsic pathway are the main pathways involved in cell apoptosis 9 .…”

Section: Introductionmentioning

confidence: 97%

Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor

Xue

et al. 2017

Sci Rep

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Epigallocatechin-3-gallate (EGCG) is one of the major polyphenolic compounds present in green tea extracts and has been used as a potential drug for the treatment of numerous diseases. The present study aimed to elucidate the role and mechanism of EGCG in protecting against H2O2-induced apoptosis in mouse vascular smooth muscle cells (VSMCs). VSMCs were pretreated with various concentrations of EGCG for 2 hours prior to treatment with H2O2. Treatment with H2O2 significantly decreased the cell viability and induced apoptosis of VSMCs, which were attenuated by pretreatment with EGCG. In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2. Moreover, the antioxidation effect of EGCG on VSMCs was determined to be associated with the 67kD laminin receptor (67LR). Our results demonstrated that EGCG improved cell viability and protected VSMCs against oxidative stress through both extrinsic and intrinsic pathways, while 67LR is likely to be an active and key receptor of EGCG. These findings provide a novel molecular mechanism of EGCG in inhibiting H2O2-induced apoptosis in VSMCs, as well as its function in preventing the development of atherosclerosis.

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Propofol attenuates H2O2-induced oxidative stress and apoptosis via the mitochondria- and ER-medicated pathways in neonatal rat cardiomyocytes

Cited by 36 publications

References 38 publications

Dexmedetomidine attenuates H2O2-induced neonatal rat cardiomyocytes apoptosis through mitochondria- and ER-medicated oxidative stress pathways

Dexmedetomidine attenuates H2O2-induced neonatal rat cardiomyocytes apoptosis through mitochondria- and ER-medicated oxidative stress pathways

Role of Mitochondria and Endoplasmic Reticulum in Taurine-Deficiency-Mediated Apoptosis

Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor

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