Adiponectin improves coronary no-reflow injury by protecting the endothelium in rats with type 2 diabetes mellitus

Figures

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  Figure 1. Establishment of type 2 diabetic rat modelwas induced by continuous high-sugar–high-fat feeding. (A) Body weight, (B) fasting plasma glucose (FPG), (C) fasting plasma insulin, (D) HOMA-IR and (E) intraperitoneal injections of glucose tolerance test (IPGTT) in high-fat–high-glucose diet-induced T2DM model in rats. **P<0.01 vs. normal diet group, n=23 rats/group.

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  Figure 2. Serum APN level in T2DM rats. (A) Dynamic change of APN in high-fat–high-glucose diet-induced T2DM model in rats (n=23 rats/group). (B) APN level in different groups at the end of 32 weeks (n=11–12 rats/group). *P<0.05, **P<0.01 vs. normal diet group; ##P<0.01 vs. T2DM group.

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  Figure 3. Endothelium-dependent vasorelaxation function in thoracic aorta. (A) ACh-induced endothelium-dependent vasorelaxation of thoracic aorta in three experimental groups (n=5 rats/group). (B) SNP-induced endothelium-independent vasorelaxation remained constant in three experimental groups (n=5 rats/group). *P<0.05, **P<0.01 vs. normal diet control group; #P <0.05, ##P<0.01 vs. T2DM group.

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  Figure 4. Serum ET-1, ICAM-1 and VCAM-1 were increased in type-2 diabetic rats, and gAd treatment reversed high-sugar–high-fat diet-related upregulation of serum ET-1 and ICAM-1. (A) Serum ET-1, (B) ICAM-1 and (C) VCAM-1 in T2DM rats at the end of 32 weeks. *P< 0.05, **P< 0.01 vs. normal diet group; ##P<0.01 vs. T2DM group. n=11–12 rats/group.

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  Figure 5. Correlation analysis of serum APN level with endothelium-dependent vasorelaxation function of thoracic aorta and serum ET-1 level. (A) Positive correlation between serum APN level and endothelium-dependent vasorelaxation function of thoracic aorta in T2DM rats at the end of 32 weeks (n=10). (B) Negative correlation between serum APN level and serum ET-1 level in T2DM rats at the end of 32 weeks (n=20).

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  Figure 6. NR injury in T2DM rats was increased after MI/R, and gAd treatment ameliorated the NR injury. (A) LVSP, (B) +dp/dtmax, (C) AAR/LV and (D) NRA/AAR in different treatment groups subjected to MI/R. (C-a) and (D-a), representative photographs of heart sections obtained from rats in sham, normal diet, DM with vehicle and gAd groups subjected to MI/R. (C-a) Dark portion by Evan's blue staining: non-ischemic, normal region; red portion: ischemic area (area at risk, AAR), negatively stained by blue dye. (C-b) Myocardial ischemic area (AAR) in different groups. (D-a) Bright blue-green fluorescence portion by Thioflavin-S staining: reflow area; bright pink fluorescence portion by fluorescent microsphere staining: reflow area; negatively stained by fluorescence: no reflow area. (D-b) No reflow area expressed as percent of AAR. *P<0.05, **P<0.01 vs. sham groups; #P<0.05, ##P<0.01 vs. normal diet group; &P <0.05 vs. T2DM group. n=6–7 rats/group.

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  Figure 7. Serum ET-1, ICAM-1 and VCAM-1 were significantly increased in the DM group after MI/R, and gAd treatment improved endothelium injury and microcirculation disturbance. (A) Serum ET-1, (B) ICAM-1 and (C) VCAM-1 in different treatments groups subjected to MI/R. **P<0.01 vs. sham groups; #P<0.05, ##P<0.01 vs. normal diet group; &P<0.05, &&P<0.01 vs. T2DM group. n=6–7 rats/group.

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  Figure 8. APN protein expression in the ischemia area of type 2 diabetic rats. #P<0.05 vs. area of no reflow. n=6–7 rats/group. RV: right ventricular; NR: no reflow; R: reflow.