Figure 7: p38 MAPK activation augments isoproterenol-induced cardiac contraction decline and myocardial fibrosis in prenatal inflammation exposure offspring.

Offspring were treated as describe in Fig. 1 by adding p38 inhibitor SB202190 treatment simultaneously with ISO treatment for 2 weeks in both Con + ISO and LPS + ISO group, defined as Con + ISO + p38i and LPS + ISO + p38i group, respectively. (a) p-ATF2, the downstream targets of p38 activation, was determined by immunoblotting. Representative plots in each group and statistical data of relative densitometry, normalized by GAPDH, are shown. n = 5 offspring in each group. (b) Representative echocardiography of LVEF%, LVFS%. n = 6 offspring in each group. (c) Representative images of Masson trichrome staining of LV sections (left panel). Myocardial fibrosis was quantified as CVF (right panel). Fibrous collagen: blue; myocyte: red; scale bar = 100 um, 200 × . n = 4 rats per group. (d,e) The mRNA levels of α-MHC, β-MHC, ANP, BNP (d) and Col1a1, Col3a1, Mmp2, Mmp9 (e) in left ventricle were determined by real-time RT-PCR. β-actin was taken as internal control. n = 5 offspring in each group. Error bar represents S.D. *p < 0.05, **p < 0.01, ^#p < 0.05, and ^##p < 0.01 denote the statistical comparison between the two marked treatment groups, respectively. Two-way ANOVA.