ERK1/2 mediates edaravone-triggered protection against myocardial damage induced by isoprenaline in H9c2 cells / 南方医科大学学报
Journal of Southern Medical University
; (12): 2663-2666, 2010.
Article
在 Zh
| WPRIM
| ID: wpr-267713
Responsible library:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To explore the effect of extracellular signal regulated kinase 1/2 (ERK1/2) on edaravone (EDA)-triggered protection against myocardial toxicity induced by isoprenaline (ISO) in H9c2 myocardial cells (H9c2 cells).</p><p><b>METHODS</b>H9c2 cells were exposed to ISO at different concentrations to establish a cardiac toxicity model induced by persistent excitation of β1 receptor. EDA was added before ISO as a pretreatment. PD-98059, an ERK1/2 inhibitor, was administered 1 h prior to EDA to inhibit the phosphorylation of ERK1/2. Cell viability was measured using cell counter kit (CCK-8). The expressions of p-ERK1/2 and t-ERK1/2 were tested by Western blotting. Mitochondrial membrane potential (MMP) was detected by Rhodamine123 (Rh123) staining and photofluorography.</p><p><b>RESULTS</b>Exposure of H9c2 cells to 80 µmol/L ISO for 24 h down-regulated ERK1/2 phosphorylation and repressed MMP. Pretreatment with 10-40 µmol/L EDA for 1 h inhibited ISO-induced myocardial toxicity and pretreatment of 40 µmol/L EDA partially rescued ERK1/2 phosphorylation and MMP level. PD-98059 abolished cardiac protection of EDA, leading to myocardial toxicity and MMP loss.</p><p><b>CONCLUSION</b>EDA can protect H9c2 cells against myocardial injury induced by ISO by suppressing ISO-triggered inhibition of ERK1/2 activation.</p>
全文:
1
索引:
WPRIM
主要主题:
Pharmacology
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Phosphorylation
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Flavonoids
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Cell Line
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Antipyrine
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MAP Kinase Signaling System
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Myocytes, Cardiac
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Mitogen-Activated Protein Kinase 3
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Toxicity
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Isoproterenol
限制:
Animals
语言:
Zh
期刊:
Journal of Southern Medical University
年:
2010
类型:
Article