Salvianolic Acid B Improves Postresuscitation Myocardial and Cerebral Outcomes in a Murine Model of Cardiac Arrest: Involvement of Nrf2 Signaling Pathway

Figure 4

Salvianolic acid B treatment inhibited myocytolysis and myocardial apoptosis, and preserved mitochondrial morphology when challenged with cardiac arrest and cardiopulmonary resuscitation (CA/CPR). (a) H&E staining revealed less myocytolysis and weaving in the myocardium of Sal B-treated mice (top panel, per group). Transmission electron microscopy was performed to observe the ultrastructure of post-CA myocardial tissues. CA/CPR damaged the myocardial ultrastructure with mitochondrial swelling, outer membrane rupture, and disarrangement of the inner membrane cristae, whereas these changes were reversed by administration of Sal B (bottom panel, per group). (b) The apoptotic cell death 3 hours post-ROSC was determined using TUNEL. TUNEL (green), apoptotic nuclei; DAPI (blue), and total nuclei. (c) The apoptosis index was quantified and compared between vehicle- and Sal B-treated groups ( per group). (d) Western blot analysis of Bax, Bcl-2, and cleaved caspase-3 from the indicated groups ( per group). (e) The ratio of Bcl-2/Bax was determined from the Bcl-2 and Bax protein band densities and converted to fold change relative to the sham-operated group. (f) Quantitative value of protein expression levels of cleaved caspase-3. ^## vs. sham-operated controls; vs. vehicle group. H&E: hematoxylin-eosin; TEM: transmission electron microscopy; ROSC: return of spontaneous circulation; TUNEL: terminal dUTP nick-end labeling.

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