Protective Effect of Tempol Against Hypoxia-Induced Oxidative Stress and Apoptosis in H9c2 Cells

Jing, Lin-Lin; Li, Qian; He, Lei; Sun, Wei; Jia, Zhengping; Ma, Hui‐Ping

doi:10.12659/msmbr.903764

Cited by 22 publications

(18 citation statements)

References 26 publications

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“…In addition, miR‐26a overexpression enhanced cell apoptosis, which suggested that emodin decreased cell apoptosis through downregulation of miR‐26a. This result confirmed the finding that upregulation of miR‐26a promoted apoptosis of hypoxia‐treated cardiomyocytes in H9c2 cells …”

Section: Discussionsupporting

confidence: 89%

Retracted: Emodin protects H9c2 cells against hypoxia‐induced injury via regulation of miR‐26a/survivin and the JAK1/STAT3 pathway

Huang

Liu

et al. 2019

J of Cellular Biochemistry

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Background/aim: Congenital heart disease (CHD) is a catastrophic disease. Emodin possesses biological properties in protecting against some diseases.Our study investigated to explore the effects of emodin on hypoxia-stimulated cardiomyocytes, which mimicked CHD in vitro.Methods: H9c2 cells were stimulated with hypoxia and then the cells were treated with or without emodin, and/or transfected with miR-26a mimic, pcDNA-survivin and their corresponding negative control (NC). Cell viability and cell apoptosis were detected by Cell Counting kit-8 assay and flow cytometry, respectively. In addition, the expression of apoptotic proteins, Janus kinase 1 (JNK)/signal transducer and activator of transcription 3 (STAT3) pathway factors, and survivin were evaluated by using Western blot analysis. The expression of miR-26a was analyzed by quantitative real time polymerase chain reaction (qRT-PCR). Moreover, the target of miR-26a was verified by using a luciferase report assay. Results: Hypoxia significantly decreased cell viability and increased cell apoptosis, and the accumulated levels of cleaved caspase-3 and cleaved-caspase-9 were upregulated by hypoxia compared with the control. However, emodin administration led to the opposite result. A further result showed that emodin increased the phosphorylation of JNK/STAT3 pathway-related proteins and the pathway inhibitor AG490 impaired the protective effects of emodin on hypoxia-induced injury. In addition, emodin negatively regulated the miR-26a expression, and overexpression of miR-26a enhanced cell apoptosis and upregulated the expression of cleaved-caspase-3 and cleaved-caspase-9 compared with the NC. Moreover, emodin statistically upregulated the expression of survivin, and overexpression of miR-26a decreased the expression of survivin. The luciferase of miR-26a overexpression was decreased in the wild type of the survivin group. Conclusion: Emodin protects hypoxia-induced cell injury as evidenced by increasing cell viability and decreasing apoptosis through downregulation of miR-26a as well as activation of the JNK/STAT3 pathway. K E Y W O R D SCongenital heart disease (CHD), emodin, JNK/STAT3, miR-26a, survivin

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Section: Discussionsupporting

confidence: 89%

Retracted: Emodin protects H9c2 cells against hypoxia‐induced injury via regulation of miR‐26a/survivin and the JAK1/STAT3 pathway

Huang

Liu

et al. 2019

J of Cellular Biochemistry

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“…23 Oxidative stress, along with the insufficient oxygen supplement will cause irreparable injury of cardiomyocytes and lead to the formation of myocardial fibrosis. 24,25 Previous studies demonstrated that hypoxia could inhibit cardiomyocytes viability and proliferation, and promote cell autophagy and apoptosis. 26,27 Inconsistent with the previous studies, we found that hypoxia stimulation obviously reduced the viability of H9c2 cells and primary cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Skullcapflavone I protects cardiomyocytes from hypoxia-caused injury through up-regulation of lincRNA-ROR

Zhang

et al. 2019

Int J Immunopathol Pharmacol

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Myocardial infarction (MI) is a serious heart disease in which cardiomyocytes are damaged, caused by hypoxia. This study explored the possible protective activity of Skullcapflavone I (SF I), a flavonoid isolated from the root of Scutellaria baicalensis Georgi, on hypoxia-stimulated cardiomyocytes cell injury in vitro. Viability and apoptosis of H9c2 cells and primary cardiomyocytes were tested using cell counting kit-8 (CCK-8) assay and Guava Nexin Reagent, respectively. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to measure the long non-coding RNA regulator of reprogramming (lincRNA-ROR) expression. si-ROR was transfected to knockdown lincRNA-ROR. Western blotting was conducted to assess the protein levels of key molecules related to cell proliferation, apoptosis, and mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK) pathway. We discovered that hypoxia stimulation obviously reduced H9c2 cell and primary cardiomyocytes' viability and proliferation, but promoted cell apoptosis. SF I treatment mitigated the cell viability and proliferation inhibition, as well as cell apoptosis caused by hypoxia. Moreover, SF I promoted the hypoxia-caused up-regulation of lincRNA-ROR in H9c2 cells and primary cardiomyocytes. Knockdown of lincRNA-ROR reversed the influence of SF I on hypoxia-stimulated H9c2 cells and primary cardiomyocytes. Besides, SF I activated MEK/ERK pathway in H9c2 cells and primary cardiomyocytes via upregulating lincRNA-ROR. To sum up, our research verified the beneficial activity of SF I on hypoxia-caused cardiomyocytes injury. SF I protected cardiomyocytes from hypoxia-caused injury through up-regulation of lincRNA-ROR and activation of MEK/ERK pathway.

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“…In addition, hypoxia exposure significantly upregulated the protein expression of Bax/Bcl‐2 ratio and the expression of caspase‐3 (Jing et al . ) (Fig. ).…”

Section: Cellular Changes During the Progress Of Oocyte Ageingmentioning

confidence: 93%

“…The general superoxide dismutase (SOD)‐mimetic drug, Tempol (4‐Hydroxy‐TEMPO), which efficiently neutralizes ROS, reduces the hypoxia‐induced oxidant stress and apoptosis by scavenging free radicals and modulating the expression of apoptosis‐related proteins (Jing et al . ). Hypoxia upregulated bax and caspase‐3 expression and downregulated bcl2 expression.…”

Section: Cellular Changes During the Progress Of Oocyte Ageingmentioning

confidence: 97%

Cellular and molecular changes associated with fish oocyte ageing

Samarin

Policar

2018

Reviews in Aquaculture

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Post-ovulatory oocyte ageing in fish is associated with limited fertilization rate, poor embryo development, larval malformation, ploidy anomalies and various other offspring abnormalities. Many studies have focused on morphological, physiological, biochemical and histological changes that occur during oocyte ageing. However, little is known about molecular changes associated with this process. This review covers the cellular and molecular characteristics of ageing oocytes with special focus on age-associated changes affected by oxidative damage. The contribution of oxidative stress and mitochondrial dysfunction, as well as new insights into oocyte ageing in higher vertebrates, is discussed to provide direction for future studies. Investigating the genomics and proteomics of oocyte ageing, including underlying molecular mechanisms, could contribute valuable information on determinants of egg quality. Such knowledge can be translated into practical applications in aquaculture, such as supplementation of oocyte culture media with antioxidants and other agents as a means to inhibit or delay development of the aged oocyte phenotype. Identification of cellular and molecular markers associated with the oocyte ageing process will benefit such developments.

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Protective Effect of Tempol Against Hypoxia-Induced Oxidative Stress and Apoptosis in H9c2 Cells

Cited by 22 publications

References 26 publications

Retracted: Emodin protects H9c2 cells against hypoxia‐induced injury via regulation of miR‐26a/survivin and the JAK1/STAT3 pathway

Retracted: Emodin protects H9c2 cells against hypoxia‐induced injury via regulation of miR‐26a/survivin and the JAK1/STAT3 pathway

RETRACTED: Skullcapflavone I protects cardiomyocytes from hypoxia-caused injury through up-regulation of lincRNA-ROR

Cellular and molecular changes associated with fish oocyte ageing

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