Fig. 2

TLR3 activation was responsible for poly(I:C) preconditioning protective effect against I/R injury. a, b Representative western blot (a) and average data (b) for TLR3, TRIF, and TLR4 in hearts subjected I/R (n = 6). c The relative expression of TLR3, TRIF, IFN-α, IFN-β, TLR4, and Myd88, analyzed by qRT-PCR in hearts subjected to I/R with poly(I:C) or vehicle pretreatment (n = 6). (All experimental groups were compared via one-way ANOVA, bars indicate the SEM, *P < 0.05; **P < 0.01). d, e Representative microphotographs (d) and average data (e) for TLR3 (as assessed by TLR3, cTNT, and DAPI fluoresce intensity) of heart sections in mice subjected to 45 min of myocardial ischemia following 24 h of reperfusion (n = 3) (all experiment groups were compared via one-way ANOVA with a Bonferroni’s multiple comparisons test, bars indicate the SEM, *P < 0.05; **P < 0.01). Blue, DAPI; green, cTNT; red, TLR3, scale bars, 50 μm. f, g Infarct size was identified with TTC-Evans blue double stain in tlr3^−/− mice, scale bars, 1 mm (n = 3) (two experimental groups were compared via unpaired student’s t test, bars indicate the SEM, *P < 0.05; **P < 0.01). h The cardiac functional markers were analyzed with ELISA kit (n = 6) (all experiment groups were compared to tlr3^−/− mice +I/R group via one-way ANOVA with a Dunnett’s multiple comparisons test, bars indicate the SEM, *P < 0.05; **P < 0.01). TLR3 KO, TLR3 knockout mice; ns not statistically significant