The protective effect of lycopene on hypoxia/reoxygenation-induced endoplasmic reticulum stress in H9C2 cardiomyocytes

Gao, Yang; Jia, Pengyu; Shu, Wenqi; Jia, Dalin

doi:10.1016/j.ejphar.2016.02.005

Cited by 27 publications

(21 citation statements)

References 28 publications

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“…To determine whether IS-induced apoptosis is associated with ERS, cells were divided into 4 groups: i) Control group (n=4): Cells were treated with serum-free DMEM for 48 h, culture medium was changed after the first 24 h; ii) PBA group (n=4): Cells were treated with PBA (1 mM) for 24 h, and then cultured with DMEM for 24 h; iii) IS group (n=4): Cells were treated with DMEM for 24 h, and then treated with IS (1 mM) for 24 h; and iv) PBA+IS group (n=4): Cells were pretreated with PBA (1 mM) for 24 h, prior to IS (1 mM) treatment for 24 h. Serum-free DMEM was used in all experimental groups. The present study determined 1 mM to be the optimal concentration of PBA, according to a previous study (11), and determined 1 mM to be the optimal concentration of IS with respect to its induction of apoptosis and ERS, which is presented in the results.…”

Section: Endoplasmic Reticulum Stress Associated Apoptosis As a Novelmentioning

confidence: 75%

Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity

et al. 2018

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Section: Endoplasmic Reticulum Stress Associated Apoptosis As a Novelmentioning

confidence: 75%

Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity

et al. 2018

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“…Some physiological or pathological conditions that perturb ER function—such as glucose deprivation (Marjon et al, 2004), hypoxia (Gao et al, 2016), aberrant Ca 2+ regulation(Zhou et al, 2015), and elevated free fatty acid levels (Cui et al, 2013)—lead to accumulation of misfolded proteins within the ER, resulting in the induction of ER stress (Fig. 1).…”

Section: Introductionmentioning

confidence: 99%

Dual role for the unfolded protein response in the ovary: adaption and apoptosis

Qiao

2016

Protein &Amp; Cell

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The endoplasmic reticulum (ER) is the principal organelle responsible for several specific cellular functions including synthesis and folding of secretory or membrane proteins, lipid metabolism, and Ca2+ storage. Different physiological as well as pathological stress conditions can, however, perturb ER homeostasis, giving rise to an accumulation of unfolded or misfolded proteins in the ER lumen, a condition termed ER stress. To deal with an increased folding demand, cells activate the unfolded protein response (UPR), which is initially protective but can become detrimental if ER stress is severe and prolonged. Accumulating evidence demonstrates a link between the UPR and ovarian development and function, including follicular growth and maturation, follicular atresia, and corpus luteum biogenesis. Additionally, ER stress and the UPR may also play an important role in the ovary under pathological conditions. Understanding the molecular mechanisms related to the dual role of unfolded protein response in the ovarian physiology and pathology may reveal the pathogenesis of some reproductive endocrine diseases and provide a new guidance to improve the assisted reproductive technology. Here we review the current literature and discuss concepts and progress in understanding the UPR, and we also analyze the role of ER stress and the UPR in the ovary.

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“…The mechanisms of myocardial ischemia and reperfusion injury include overproduction of reactive oxygen species (ROS), overload of intracellular calcium, collapse of mitochondrial membrane potential (MMP) and prolonged opening of the mitochondrial permeability transition pore (mPTP) among other processes (4). Natural compounds, such as berberine (5), tanshinone IIA (6) and lycopene (7), serve a pivotal role in the development of effective therapeutics for myocardial ischemia and reperfusion injury.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of carnosic acid against mitochondria‑mediated injury in H9c2 cardiomyocytes induced by hypoxia/reoxygenation

Liu

Dong

2017

Exp Ther Med

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Abstract. Myocardial ischemia and reperfusion occurs in myocardial infarction. Timely reperfusion will exacerbate the injury through the mitochondria-mediated apoptosis in cardiomyocytes due to the accumulation of excessive reactive oxygen species (ROS). In order to identify novel therapeutic approaches, the cardioprotective effects of carnosic acid and the underlying mechanisms were investigated in the present study in H9c2 cardiomyocytes injured by hypoxia/reoxygenation in vitro. The viability of H9c2 cardiomyocytes was detected by MTT assay and further confirmed by the detection of intracellular lactate dehydrogenase (LDH) release. The mitochondrial function in H9c2 cardiomyocytes was evaluated using fluorescence methods. The proteins related to apoptosis, including caspase-3, B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) were analyzed by western blot analysis, and the activity of caspase-3 was determined using a colorimetric method. As a result, carnosic acid was demonstrated to improve the viability of H9c2 cardiomyocytes and suppress the leakage of cytosolic lactate dehydrogenase under hypoxia/reoxygenation. In addition, the overproduction of intracellular ROS and intracellular calcium overload were ameliorated in the presence of carnosic acid. The dysfunction of mitochondria in H9c2 cardiomyocytes was also attenuated by carnosic acid through blocking the collapse of mitochondrial membrane potential (MMP) and mitochondrial permeability transition pore (mPTP) opening. Furthermore, the apoptosis of H9c2 cardiomyocytes resulted from hypoxia/reoxygenation was inhibited by carnosic acid through the upregulation of Bcl-2 and the downregulation of Bax and caspase-3 levels. These results provided evidence for further investigation that would assist in the development of novel therapeutic approaches for myocardial infarction.

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The protective effect of lycopene on hypoxia/reoxygenation-induced endoplasmic reticulum stress in H9C2 cardiomyocytes

Cited by 27 publications

References 28 publications

Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity

Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity

Dual role for the unfolded protein response in the ovary: adaption and apoptosis

Protective effects of carnosic acid against mitochondria‑mediated injury in H9c2 cardiomyocytes induced by hypoxia/reoxygenation

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