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

2018 ◽  
Vol 104 ◽  
pp. 712-717 ◽  
Author(s):  
Shuang Wang ◽  
Yanfang Zhu ◽  
Ruixia Qiu
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
H9c2 Cardiomyocytes ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

scholarly journals Puerarin attenuates myocardial hypoxia/reoxygenation injury by inhibiting autophagy via the Akt signaling pathway

2017 ◽  
Vol 15 (6) ◽  
pp. 3747-3754 ◽  
Author(s):  
Huixiong Tang ◽  
Xudong Song ◽  
Yuanna Ling ◽  
Xianbao Wang ◽  
Pingzhen Yang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Myocardial Hypoxia ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

scholarly journals Knockdown of Tripartite Motif 8 Protects H9C2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of PI3K/Akt Signaling Pathway

2020 ◽  
Vol 29 ◽  
pp. 096368972094924
Author(s):  
Xiaoyan Dang ◽  
Yong Qin ◽  
Changwei Gu ◽  
Jiangli Sun ◽  
Rui Zhang ◽  
...  
Keyword(s):  
Cell Viability ◽  
Signaling Pathway ◽  
Ischemia Reperfusion ◽  
Akt Signaling ◽  
H9c2 Cells ◽  
Loss Of Function ◽  
Akt Signaling Pathway ◽  
Tripartite Motif ◽  
Myocardial Ischemia Reperfusion ◽  
Hypoxia Reoxygenation

Tripartite motif 8 (TRIM8) is a member of the TRIM protein family that has been found to be implicated in cardiovascular disease. However, the role of TRIM8 in myocardial ischemia/reperfusion (I/R) has not been investigated. We aimed to explore the effect of TRIM8 on cardiomyocyte H9c2 cells exposed to hypoxia/reoxygenation (H/R). We found that TRIM8 expression was markedly upregulated in H9c2 cells after stimulation with H/R. Gain- and loss-of-function assays proved that TRIM8 knockdown improved cell viability of H/R-stimulated H9c2 cells. In addition, TRIM8 knockdown suppressed reactive oxygen species production and elevated the levels of superoxide dismutase and glutathione peroxidase. Knockdown of TRIM8 suppressed the caspase-3 activity, as well as caused significant increase in bcl-2 expression and decrease in bax expression. Furthermore, TRIM8 overexpression exhibited apposite effects with knockdown of TRIM8. Finally, knockdown of TRIM8 enhanced the activation of PI3K/Akt signaling pathway in H/R-stimulated H9c2 cells. Inhibition of PI3K/Akt by LY294002 reversed the effects of TRIM8 knockdown on cell viability, oxidative stress, and apoptosis of H9c2 cells. These present findings defined TRIM8 as a therapeutic target for attenuating and preventing myocardial I/R injury.

scholarly journals 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

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Ruibin Jiang ◽  
Yan Guo ◽  
Nipi Chen ◽  
Chengxian Gao ◽  
Zhishan Ding ◽  
...  
Keyword(s):  
Akt Signaling ◽  
Total Flavonoids ◽  
Protective Effects ◽  
H9c2 Cells ◽  
H9c2 Cardiomyocytes ◽  
Reoxygenation Injury ◽  
Carya Cathayensis ◽  
Carya Cathayensis Sarg ◽  
Signaling Activity ◽  
Hypoxia Reoxygenation

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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