Panel (a) and (b), 7 days after AMI, Western blot analysis revealed that atorvastatin treatment increased the pro-survival proteins and reduced the pro-apoptotic protein, however, this effects was diminished by either L-NAME or AMD3100. Bcl-2 (S: 1.51±0.24, B: 1.13±0.15*, A: 1.56±0.22#, AL: 1.07±0.13*$, AA: 1.16±0.16*$) and p-Akt (S: 1.33±0.19, B: 0.87±0.16*, A: 1.36±0.20#, AL: 0.91±0.15*$, AA: 0.89±0.18*$), and Bax (S: 0.10±0.02, B: 0.92±0.20*, A: 0.43±0.12*#, AL: 0.78±0.16*#$, AA: 0.76±0.13*#$). Apoptotic index of cardiomyocytes by TUNEL assay further suggested that the anti-apoptotic effects of atorvastatin was associated with increase of NO production and SDF-1α expression, and the coupling of SDF-1α with CXCR-4 (S: 6.94±2.12, B: 70.09±5.99*, A: 42.12±5.49*#, AL: 58.37±6.28*#$, AA: 55.72±7.31*#$). (*: P<0.01 vs. group S, #: P<0.01 vs. group B, $: P<0.01 vs. group A). All the measurements were repeated for 3 times to figure out the arithmetic average. S=Sham operated group; B=Blank control group; A=Atorvastatin group; AL=Atorvastatin+L-NAME group; AA=Atorvastatin+AMD3100 group.