Figure 1
Mean myocardial TAS (Total antioxidant status) and TOS (Total oxidant status) levels in all groups. (*p < 0.05 vs. MCAo group, #p < 0.05 vs. STZ+ MCAo group, δp < 0.05 vs. STZ group. One-way ANOVA, post-hoc Tukey’s HSD test. (STZ, Streptozotocin-induced diabetic; IPreC, ischemic preconditioning; MCAo, middle cerebral artery occlusion)
Figure 2
Mean OSI (Oxidative stress index) values in all groups. (*p < 0.05 vs. MCAo group, #p < 0.05 vs. STZ+ MCAo group, δp < 0.05 vs. STZ group. One-way ANOVA, post-hoc Tukey’s HSD test. (STZ, Streptozotocin-induced diabetic; IPreC, ischemic preconditioning; MCAo, middle cerebral artery occlusion)
Figure 3
(1) Normal histological view of cardiac myofibrils in IPreC group. (Longitudinal section, Masson Trichrome stain, Magnification: 40X). (2) Congestion in IPreC+ MCAo (A) and STZ+ IPreC+ MCAo (B) groups. Overview of myofibril is nearly normal appearance. (Longitudinal section, A. H-E stain, B. Masson Trichrome stain, Magnification: 20X). (3) Eosinophilic stained areas show necrotic myofibrils that are lack of nuclei (arrow-heads) in STZ group. Arrows indicate that spaces between cardiac myofibrils. These spaces indicate necrotic area, and probably interstitial edema. (STZ, Streptozotocin-induced diabetic; IPreC, ischemic preconditioning; MCAo, middle cerebral artery occlusion, Transverse section, H-E stain, Magnification: 20X).
Figure 4
(a) Congestion (arrows) destroyed myofibrils in STZ+ MCAo group. Cardiac myofibrils are separated from each other along with congestive area. These areas probably seem to be necrotic areas accompanied by interstitial edema. (Transverse section, H-E stain, Magnification: 20X). (b) Mononuclear cell infiltration, congestion and interstitial edema in necrotic areas (arrows) destroyed cardiac myofibrils in STZ+ MCAo group (STZ, Streptozotocin-induced diabetic; IPreC, ischemic preconditioning; MCAo, middle cerebral artery occlusion, Longitudinal section, H-E stain, Magnification: 20X).
Figure 5
A) Degenerated myocardium caused by mononuclear cell infiltration (arrows) in MCAo group. B) Severely myodegeneration with interstitial edema, necrosis (arrows) and congestion (arrow-heads), in STZ+ MCAo group. (STZ, Streptozotocin-induced diabetic; IPreC, ischemic preconditioning; MCAo, middle cerebral artery occlusion, Longitudinal section, H-E stain, Magnification: 10X)
Figure 6
A) Mean congestion scores in all groups. (*p < 0.05 vs. MCAo group, #p < 0.05 vs. STZ+ MCAo group, δp < 0.05 vs. STZ group. B) Mean necrosis scores in all groups. (*p < 0.05 vs. MCAo group, #p < 0.05 vs. STZ+ MCAo group. C) Mean mononuclear cell infiltration scores in all groups. (*p < 0.05 vs. MCAo group, #p < 0.05 vs. STZ+ MCAo group (One-way ANOVA, post-hoc Tukey’s HSD test. STZ, Streptozotocin-induced diabetic; IPreC, ischemic preconditioning; MCAo, middle cerebral artery occlusion)
Figure 7
A) Western blot analysis of Bax and Bcl 2 proteins in cardiac tissues of all groups. B) Mean ratio of Bax/Bcl 2 levels in all groups. (*p < 0.05 vs. MCAo group, #p < 0.05 vs. STZ+ MCAo group, δp < 0.05 vs. STZ group. One way ANOVA, post-hoc Tukey’s HSD test. (STZ, Streptozotocin-induced diabetic; IPreC, ischemic preconditioning; MCAo, middle cerebral artery occlusion).
Figure 8
A. Western blot analysis of Caspase 3 protein in cardiac tissues of all groups. B. Mean Caspase 3 levels in all groups. (*p < 0.05 vs. MCAo group, #p < 0.05 vs. STZ+ MCAo group, δp < 0.05 vs. STZ group. One-way ANOVA, post-hoc Tukey’s HSD test. (STZ, Streptozotocin-induced diabetic; IPreC, ischemic preconditioning; MCAo, middle cerebral artery occlusion)