Figure 8: p38 activation leads to augmented oxidative stress in offspring of LPS-treated mothers after isoproterenol treatment and schematic illustration of the current study.
Offspring were treated as described in Fig. 6. (a,b) The mRNA levels of Nox2, Nox4, p67phox, p47phox, p22phox (a) and Sod1, Sod2, Sod3, catalase, Gpx1 (b) 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 < 0.001, #p < 0.05 and ##p < 0.01 denote the statistical comparison between the two marked treatment groups, respectively. Two-way ANOVA. (c) Schematic illustration of the mechanisms responsible for the augmented myocardium damages in response to risk factor challenges in adult offspring of LPS-treated mothers. Prenatal inflammatory stimulation leads to augmented cardiac hypertrophy and fibrosis, even systolic dysfunction induced by ISO in adult offspring. The activated ROS-p38-ROS positive feedback loop results in imbalance of ROS generation and elimination might be the main reason that aggravates cardiac damages responding to a second risk factor.
