Total Flavonoids from Carya cathayensis Sarg. Leaves Alleviate H9c2 Cells Hypoxia/Reoxygenation Injury via Effects on miR-21 Expression, PTEN/Akt, and the Bcl-2/Bax Pathway

This study aimed to investigate whether the total flavonoids (TFs) from Carya cathayensis Sarg. leaves alleviate hypoxia/reoxygenation (H/R) injury in H9c2 cardiomyocytes and to explore potential mechanisms. H9c2 cells pretreated with TFs for 24h were exposed to H/R treatment. The results indicated that TFs significantly alleviate H/R injury, which include inhibiting apoptosis and enhancing antioxidant capacity. The protective effects of TFs resulted in higher expression of miR-21 in H/R-induced H9c2 cells than that of controls, which in turn upregulated Akt signaling activity via suppressing the expression of PTEN together with decreasing the ratio of Bax/Bcl-2, caspase3, and cleaved-caspase3 expression in H/R-induced H9c2 cells. Conversely, blocking miR-21 expression with miR-21 inhibitor effectively suppressed the protective effects of TFs against H/R-induced injury. Our study suggests that TFs can decrease cell apoptosis, which may be mediated by altering the expression of miR-21, PTEN/Akt, and Bcl/Bax.

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Naringin Effectively Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury

VNU Journal of Science Natural Sciences and Technology ◽

10.25073/2588-1140/vnunst.5294 ◽

2021 ◽

Vol 37 (3) ◽

Author(s):

Vu Thi Thu ◽

Ngo Thi Hai Yen

Keyword(s):

Membrane Potential ◽

Mitochondrial Membrane Potential ◽

Mitochondrial Membrane ◽

Cell Group ◽

H9c2 Cell ◽

H9c2 Cells ◽

H9c2 Cardiomyocytes ◽

Reoxygenation Injury ◽

Hypoxia Reoxygenation

This study was conducted to evaluate the protective effect of Naringin (NAR) on H9C2 cardiomyocytes in hypoxia/reoxygenation (HR) injury in vitro induced by the hypoxia chamber. Methods: H9C2 cells were grown under normal (control) and HR conditions. The viability, cardiolipin content and mitochondrial membrane potential of H9C2 cells in experimental groups were analyzed by using suitable kits. Results: The obtained results showed that the addition of Naringin (16÷160 µM) significantly increased the survival rate of H9C2 cells under HR conditions. In particular, NAR had the highest efficiency in preserving mitochondrial function at concentrations of 80 µM and 160 µM. In HR-exposed H9C2 cell group, the cardiolipin content and mitochondrial membrane potential values of H9C2 cells were decreased sharply with that of control (71,64±1,37% and 68,12±2,78%, p<0,05). Interestingly, mitochondrial cardiolipin contents were signigicantly increased in H9C2 cells post-hypoxic treated wtih NAR at dose of 80 µM 160 µM to 87,76±1,89% and 81,09±1,21%. Additionally, post-hypoxic supplementation of NAR at concentration of 80 µM and 160 µM effectively increased mitochondrial membrane potential values. Conclusion: The obtained results are preliminary data on the effects of NAR in protecting mitochondrial-targeted cardiomyocytes against HR injury.

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Shikonin protects H9C2 cardiomyocytes against hypoxia/reoxygenation injury through activation of PI3K/Akt signaling pathway

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2018.04.144 ◽

2018 ◽

Vol 104 ◽

pp. 712-717 ◽

Cited By ~ 14

Author(s):

Shuang Wang ◽

Yanfang Zhu ◽

Ruixia Qiu

Keyword(s):

Signaling Pathway ◽

Akt Signaling ◽

Akt Signaling Pathway ◽

H9c2 Cardiomyocytes ◽

Reoxygenation Injury ◽

Hypoxia Reoxygenation

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Intermedin attenuates high-glucose exacerbated simulated hypoxia/reoxygenation injury in H9c2 cardiomyocytes via ERK1/2 signaling

European Journal of Inflammation ◽

10.1177/1721727x17744096 ◽

2017 ◽

Vol 15 (3) ◽

pp. 229-238 ◽

Cited By ~ 1

Author(s):

Hong Li ◽

Chuan-Shi Xiao ◽

Yun-Fei Bian ◽

Rui Bai ◽

Fen Gao

Keyword(s):

Oxidative Stress ◽

High Glucose ◽

Culture Medium ◽

Annexin V ◽

H9c2 Cells ◽

Propidium Iodide Staining ◽

H9c2 Cardiomyocytes ◽

Reoxygenation Injury ◽

Simulated Hypoxia ◽

Hypoxia Reoxygenation

Objective: This study investigated whether and how intermedin (IMD) exerted a protective effect against simulated hypoxia/reoxygenation (H/R) injury in high-glucose-treated H9c2 cells. Methods: Cellular viability was assessed via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Oxidative stress was determined by malondialdehyde and superoxide dismutase content in the culture medium supernatant. Flow cytometry with Annexin V/propidium iodide staining was used to detect the cardiomyocyte apoptosis rate. The protein expression of Bax, Bcl-2, caspase-3, and ERK1/2 was determined by western blot. Results: IMD administration to H9c2 cells during H/R injury decreased oxidative stress product generation and inhibited apoptosis ( P < 0.05 or P < 0.01) while these effects were blocked by the ERK1/2 inhibitor ( P < 0.05 or P < 0.01). Through the application of a specific ERK1/2 inhibitor, it was demonstrated that IMD mitigates high-glucose-induced oxidative stress and apoptosis via ERK1/2 signaling. Conclusion: Intermedin may be a novel therapeutic agent for mitigating diabetic cardiovascular injury in the clinical setting.

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