Figure 5
From: PRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium
The overexpression of PRDX2 inhibits ROS levels and myocardial injury after AMI but promotes inflammatory responses. After 2 weeks of coronary artery ligation, serum from mice was harvested for ELISA analysis and after 1 month, myocardial tissue was used for immunohistochemical analysis. (A–C) ELISA for inflammatory cytokines. The data are presented as means ± SD from three separate experiments from five to six mice in each group. *p < 0.05, **p < 0.01, ***p < 0.001 vs control. (D) Representative images of infarct size as stained by TTC. (E) PRDX2 decreased infarct size compared with other groups. The data are presented as means ± SD from five to six separate mice in each group. **p < 0.01, ***p < 0.001 vs control. (F) Immunofluorescence for ROS generation by DCF-DA. (G) The results show that the expression of PRDX2 inhibits generation of oxidative stress and the inhibition of PRDX2 on ROS was enhanced with TLR4 knock out. The data are presented as means ± SD from ten separate fields. ***p < 0.001 vs control. (H and I) TUNEL analysis of apoptosis in myocardial infarction. Statistical analysis of apoptosis. AB, aortic banding. The data are presented as means ± SD from three separate experiments. ***p < 0.001 vs control.
