Fig. 5.

Inhibition of PI3K or transfection of Akt siRNA abolished poly(I:C)-induced cardioprotection following myocardial I/R injury. a Representative photographs of TTC-stained, perfused heart sections obtained from poly(I:C) with or without LY294002 pretreated mice subjected to I/R injury, scale bars, 1 mm. b Quantitative data of left ventricular infarct size (MI) and area at risk (AAR) in poly(I:C) with or without LY294002 pretreated mice (n = 6). c Representative transthoracic echocardiography of 24 h before and after I/R injury with or without LY294002 pretreated. d Average of data LVIDd, LVIDs, EF, and FS measured by echocardiography in poly(I:C) or vehicle pretreated mice subjected to I/R (n = 6) (all experiment groups were compared via one-way ANOVA with a Bonferroni’s multiple comparisons test, bars indicate the SEM, *P < 0.05). e Expression of TLR3 and TLR4 as assessed by qRT-PCR in hearts subjected I/R after poly(I:C) preconditioning with or without LY294002 pretreatment (n = 6). f, g Representative western blot (f) and average data (g) for PI3K, phospho-PI3K, Akt, phospho-Akt, and p70 S6 kinase in hearts subjected to I/R with poly(I:C) and/or LY294002 pretreatment (n = 6) (all experiment groups were compared with poly(I:C) I/R group via one-way ANOVA with a Dunnett’s multiple comparisons test, *P < 0.05; **P < 0.01). h, i Representative western blot (h) and average data (i) for protein level of phospho-PI3K, PI3K, phospho-Akt, and Akt in neonatal cardiomyocytes transfected with Akt siRNA and poly(I:C) before OGD (n = 6). j Cell viability was detected in neonatal cardiomyocytes transfected with Akt siRNA for 24 h and received OGD performance (n = 6) (all experimental groups were compared via one-way ANOVA with a Turkey’s multiple comparisons test, bars indicate the SEM, *P < 0.05; **P < 0.01). LY, LY294002