Fig. 6.

Enhanced expression of HO-1 inhibited senescence induced MI injury. Mice were 6–8 weeks. The model of MI was established by ligating left anterior descending coronary artery for a week. Mice in MI + Hemin group were i.p. injected with 20 mg/kg (once every other day) of hemin (a) Western blot detected the expression level of LaminB, p53 and p16. n = 3. *P < .01, **P < .05. Data are mean ± SEM; one-way ANOVA was used for the statistical analysis. (b) and (c) p16 level was analyzed by immunofluorescence and immunohistochemistry staining. The tissue section thickness is 6 μm. Scale bars represent 100 μm. (d) Relative mRNA levels of IL-1, IL-3 and TNF-α were analyzed by qRT-PCR. n = 4. *P < .01, **P < .05. Data are mean ± SEM; Two-tailed t-test was used for the statistical analysis. (e) Model of the role of HO-1 in cardiomyocytes senescence induced by MI injury and heart aging.