Dexmedetomidine postconditioning attenuates myocardial ischemia/reperfusion injury by activating the Nrf2/Sirt3/SOD2 signaling pathway in the rats

Figures

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  Figure 1.. Flow chart of the study. The solid lines represent the experimental sections in Figure 2–4. The dashed lines represent the experimental sections in Figures 5 and 6. The number of rats shown in the flow chart is the final number included in each group. The specific allocation scheme is detailed in methods of the manuscript.

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  Figure 2.. The effects of Dex postconditioning on myocardial enzymes, pathological changes of myocardial damages and infarct sizes in the rats with myocardial IRI. (A) and (B) Serum CK-MB and cTnI levels (n = 5); (C) Pathological changes of myocardial damages with HE staining (n = 3), magnification: ×200, bar = 50 μm; (D) and (E) Infarct sizes determined by the Evans blue and TTC staining (n = 6). Date was expressed as the mean ± SEM. *P < .05.

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  Figure 3.. The effects of Dex postconditioning on oxidative stress and cardiomyocyte apoptosis in the rats with myocardial IRI. (A) and (B) Immunofluorescence of ROS (n = 6), magnification: ×200, bar = 50 μm; (C) Myocardial MDA level (n = 6). (D) and (E) Myocardial SOD and GSH-PX activities (n = 6); (F) Myocardial expression of Bcl-2, Bax and cleaved caspase-3 measured by western blotting (n = 3); (G–J) Quantitative analyses of myocardial Bcl-2, Bax, Bcl-2/Bax and cleaved caspase-3; (K) and (L) Cardiomyocyte apoptosis rates assessed by the Tunel assay (n = 6). Magnification, ×200, bar = 50 μm. Date was expressed as the mean ± SEM. *P < .05.

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  Figure 4.. Immunohistochemical staining, western blotting and quantitative analysis of protein expression of myocardial Nrf2/Sirt3/SOD2 signaling pathway. (A) Immunohistochemical staining of myocardial Nrf2 and Sirt3 (n = 3), arrows indicate positive results; magnification: ×200, bar = 50 μm; (B) and (C) The expression of myocardial nuclear-Nrf2, Sirt3, SOD2 and Ac-SOD2 measured by western blotting (n = 3); (D–G) Quantitative analyses of myocardial nuclear-Nrf2, Sirt3, SOD2 and Ac-SOD2. Date was expressed as the mean ± SEM. *P < .05.

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  Figure 5.. The effects of Brusatol administration on the protection of Dex postconditioning against myocardial IRI. (A) and (B) Serum CK-MB and cTnI levels (n = 5); (C) Pathological changes of myocardial damages observed by HE staining (n = 3), magnification, ×200, bar = 50 μm; (D) and (E) Infarct sizes determined by the Evans blue and TTC staining (n = 6); (F) and (G) Immunofluorescence of ROS (n = 6), magnification: ×200, bar = 50 μm; (H) Myocardial MDA level (n = 6); (I) and (J) Myocardial SOD and GSH-PX activities (n = 6); (K) and (L) Cardiomyocyte apoptosis assessed by the Tunel assay (n = 6), magnification: ×200, bar = 50 μm. Date was expressed as the mean ± SEM. *P < .05.

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  Figure 6.. Western blotting and quantitative analysis of protein expression of myocardial Nrf2/Sirt3/SOD2 signaling pathway. (A) and (B) The expression of myocardial nuclear-Nrf2, Sirt3, SOD2 and Ac-SOD2 measured by western blotting (n = 3); (C)–(F) Quantitative analyses of myocardial nuclear-Nrf2, Sirt3, SOD2 and Ac-SOD2. Date was expressed as the mean ± SEM. *P < .05.