Skip to main content
. 2016 Mar 24;37(5):1281–1289. doi: 10.3892/ijmm.2016.2538

Figure 3.

Figure 3

Effect of sodium hydrosulfide on rat myocardial tissue necrosis and cell apoptosis. (A) Hematoxylin and eosin (H&E) staining to determine histopathological changes under a light microscope (×20 magnification; scale bar, 100 µm). Circles indicate the disorganization of cell structures and inflammatory cell infiltration. (B) Serum lactate dehydrogenase (LDH) concentration, (C) cardiomyocyte apoptosis evaluated by TUNEL staining (×20 magnification; scale bar, 100 µm). (D) Quantification of TUNEL-positive nuclei. Data are expressed as the means ± SEM. **p<0.01 vs. sham-operated group; #p<0.05 and ##p<0.01 vs. acute myocardial infarction (AMI) group. Sham, sham-operated group; AMI, rats subjected to AMI (ischemia) and not treated with any agents; AMI + NaHS-L, rats subjected to AMI and treated with low-dose (0.78 mg/kg) NaHS; AMI + NaHS-M, rats subjected to AMI and treated with medium-dose (1.56 mg/kg) NaHS; AMI + NaHS-H, rats subjected to AMI and treated with high-dose (03.12 mg/kg) NaHS; AMI + SB, rats subjected to AMI and treated with the glycogen synthase kinase-3β (GSK-3β) inhibitor, SB216763 (0.6 mg/kg); AMI + vehicle, rats subjected to AMI and treated with the vehicle (DMSO, 2 ml/kg).