Post-Ischemic Treatment of Recombinant Human Secretory Leukocyte Protease Inhibitor (rhSLPI) Reduced Myocardial Ischemia/Reperfusion Injury

Figures

• 

  Figure 1. Schematic diagram of experimental protocol.

• 

  Figure 2. Determination of body weight of experimental animal before performing the surgical procedure of myocardial I/R injury (a), heart weight harvested at the end of the surgery (b) and heart weight to body weight ratio in rats of the study cohort (c). 3.2. Effect of Post-Ischemic rhSLPI Treatment on Infarct Size.

• 

  Figure 3. Determination of the percentage of area at risk (AAR) to ventricle volume (V) (a), percentage of infarct size to area at risk (b), activity of Lactate Dehydrogenase (LDH) (c) and Creatine kinase-MB (CK-MB) (d) (* p < 0.05 vs. sham) (# p < 0.05 vs. I/R) (n = 8).

• 

  Figure 4. Determination of effect of post-ischaemic treatment of rhSLPI on cardiac inflammatory cytokines level including IL-1β (a), IL-6 (b) and TNF-α (c) in the sham group, I/R group, rhSLPI-DI and rhSLPI-OR (* p < 0.05 vs. sham) (# p < 0.05 vs. I/R) (n = 6).

• 

  Figure 5. Determination of cardiac (a,c) and serum (b,d) protein modifications (protein carbonylation and ischemia-modified albumin). (* p < 0.05 vs. sham) (# p < 0.05 vs. I/R) (n = 6).

• 

  Figure 6. Determination of rhSLPI on activation of MAPK kinase involved in cell injury and survival in MI rat by Western blot analysis (a). The quantitative analysis for the MAPK phosphorylation was presented for p38 (b), JNK (c), ERK (d) and Akt (e). (* p < 0.05 vs. sham) (# p < 0.05 vs. I/R) (n = 6).

• 

  Figure 7. Determination of rhSLPI on apoptosis regulatory protein levels in MI rat by Western blot analysis (a). The quantitative analysis for the expression was presented for bax (b), caspase-3 (c) and caspase-8 (d) (* p < 0.05 vs. sham) (# p < 0.05 vs. I/R) (n = 6).

• 

  Figure 8. A schematic diagram of the major findings in this study. rhSLPI that was treated in the timing of the post-ischemia duration. rhSLPI could protect the heart from the ischemic condition. The mechanisms for this could be associated with the attenuation of intracellular ROS production, activation of Akt and p38 MAPK phosphorylation, reduction in inflammatory cytokines (TNF-α, IL-1β and IL-6) and reduction in apoptosis regulatory proteins (Bax, caspase-3, caspase-8).