Fig 1.
Dexmedetomidine preconditioning reduced I/R induced-myocardial infarct size.
A. Representative images of myocardial infarction size in each group are shown. B. Quantitative analysis of myocardial infarct sizes (INF/AAR %) in each group. Values are shown as mean ± SEM. n = 4 per group. **P < 0.01, I/R vs. sham; ## P < 0.01, DEX vs. I/R; $ P<0.05, DEX/YOH vs. DEX.
Fig 2.
Dexmedetomidine preconditioning attenuated I/R-induced myocardial structural injury.
H&E stained representative images of myocardial sections from sham (A), I/R(B), DEX (C), YOH/DEX (D), YOH (E) groups demonstrated histological changes. Magnification, ×400. Black arrows indicate the infiltrated inflammatory cells. F. Histologic scores from the hearts in each group. Bar = 200μm. Values are shown as mean ± SEM. n = 4 per group. **P < 0.01, I/R vs. sham group; ##P < 0.01, DEX vs. I/R; $ $ P<0.01, DEX/YOH vs. DEX.
Fig 3.
Dexmedetomidine preconditioning attenuated the increase in the levels of circulating and myocardial IL-6 (A) and TNF-α (B) induced by I/R. Values are shown as mean ± SEM, n = 5 per group for IL-6 and n = 4 per group for TNF-α. **P < 0.01, I/R vs. sham; ##P < 0.01, DEX vs. I/R; $P<0.05, $ $ P<0.01, DEX/YOH vs. DEX.
Fig 4.
Dexmedetomidine preconditioning attenuated the increase in the expression of HMGB1 in the I/R-injured myocardium.
A. Western blots showed the levels of HMGB1 in the hearts from the mice of each group. β-actin served as a loading control. B. Quantification of A. Values are shown as mean ± SEM. n = 4 per group. **P<0.01, I/R vs. sham; ##P<0.01, DEX vs. I/R; $ $P<0.01, YOH/DEX vs. DEX.
Fig 5.
Dexmedetomidine preconditioning attenuated the increase in the expressions of TLR-4, MyD88 and NF-κB in the I/R-injured myocardium as revealed by Western blot.
A. Western blots showed the levels of TLR-4, MyD88 and NF-κB in the hearts of mice from each group. β-actin served as a loading control. B, C and D. Quantifications of the TLR-4, MyD88 and NF-κB expressions, respectively, in each group. Values are shown as mean ± SEM. n = 4 per group. **P<0.01, I/R vs. sham group; ##P<0.01, DEX vs. I/R; $P<0.05, YOH/DEX vs. DEX.
Fig 6.
Dexmedetomidine preconditioning attenuated the increase in the expressions of TLR-4, MyD88 and NF-κB in the I/R-injured myocardium as revealed by immunohistochemistry.
Representative images of immunostaining for TLR-4 (A, D, G, J, M), MyD88 (B, E, H, K, N) and NF-κB (C, F, I, L, O) in the sections of mouse hearts from different groups are shown. Black arrows indicate the positive staining of TLR-4, MyD88 or NF-κB, respectively. Bar scale: 200 μm. n = 4 per group.
Fig 7.
Dexmedetomidine preconditioning increased the expressions of IκB-α in the I/R-injured myocardium.
A. Western blots showed the levels of IκB-α in the hearts of mice from each group. β-actin served as a loading control. B. Quantification of the IκB-α expression, respectively, in each group. Values are shown as mean ± SEM. n = 4 per group. **P<0.01, I/R vs. sham group; ##P<0.01, DEX vs. I/R; $P<0.05, YOH/DEX vs. DEX.