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Protective effect of GYY4137 on rat myocardial cells infected by Coxsackie virus B3 / 中华实用儿科临床杂志
Chinese Journal of Applied Clinical Pediatrics ; (24): 59-63, 2015.
Article in Chinese | WPRIM | ID: wpr-466788
ABSTRACT
Objective To study the protective effect of GYY4137 on rat myocardial cells infected by Coxsackie virus B3 (CVB3) and its signal transduction mechanism.Methods Cardiomyocytes were treated with different concentrations of GYY4137(10,50,100 μmol/L) for 24 hours before addition of 100 TCID50 CVB3 for 2 hours before serum-free conditions.After treatment,the cell viability was ascertained with Cell Counting Kit-8 (CCK-8) assay.At the same time,the levels of tumor necrosis factor-α (TNF-α),interleukin-1β (IL-1β),interleukin-6 (IL-6) in the supernatants were analyzed by enzyme-linked immunosorbent assay (ELISA).Western blot was used to study the expression of nuclear factor kappa-B (NF-κB) protein and the inhibitory subunit of (IκBα) in myocardial cells.Results After exposure of cardiomyocytes to GYY4137 with different concentration (10,50,100 μmol/L)for 24 hours cell viability had no change.The NF-κB expression and the levels of TNF-α,IL-1β,IL-6 [(175.80 ± 5.05) ng/L,(25.80 ± 1.97) ng/L,(65.33 ± 3.51) ng/L] in the GYY4137-treated CVB3 infection group were significantly reduced when compared with untreated CVB3 infection group (P < 0.01),respectively.Compared with the normal group,the GYY4137 concentration-dependently restrained the CVB3-mediated IκBα degradation(P < 0.01).Conclusions GYY4137 exerts anti-inflammatory effects in CVB3-infected cardiomyocytes.This anti-inflammatory mechanism may be associated with suppression of the activation of the NF-κB.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Applied Clinical Pediatrics Year: 2015 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Applied Clinical Pediatrics Year: 2015 Type: Article