OBJECTIVE: To investigate the effect of nicotine on inflammatory cytokines in myocardial ischemia/reperfusion (I/R) injury in rat. METHODS: Fifty male Sprague-Dawley (SD) rats were divided into five groups by random numbers table (each n=10): sham operation group (S group), I/R group, nicotine 400 μg/kg group (H group), nicotine 40 μg/kg group (L group) and α-bungarotoxin (α-BGT,1 μg/kg) group. The anterior descending branch of left coronary artery was occluded for 30 minutes followed by 90 minutes reperfusion to reproduce myocardial I/R injury rat model, while in S group the anterior descending branch of left coronary artery was only exposed without occlusion procedure. Thirty minutes before myocardial ischemia, drugs in corresponding doses were given intravenously via jugular vein. At the end of 90 minutes of reperfusion, blood samples were collected from carotid artery to determine the levels of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), IL-10, MB isoenzyme of creatine kinase (CK-MB), and cardiac troponin I (cTnI), then the animals were sacrificed and the hearts were harvested for pathological study and determination of myeloperoxidase (MPO) activity. Immunohistochemistry and reverse transcription- polymerase chain reaction (RT-PCR) were used to assess intercellular adhesion molecule-1 (ICAM-1) protein and mRNA expression in heart tissue. RESULTS: Compared with the S group, the concentrations of TNF-α, IL-8, IL-10, CK-MB, cTnI, MPO activity, ICAM-1 protein and mRNA expression were significantly increased in I/R group [TNF-α (ng/L): 158.7±32.7 vs. 31.5±5.8, IL-8 (ng/L): 0.71±0.06 vs. 0.30±0.04, IL-10 (ng/L): 69.0±7.8 vs. 41.4±4.3, CK-MB (U/L): 2 540±169 vs. 1 120±120, cTnI (μg/L): 26.2±4.6 vs. 0.9±0.2, MPO (U/g): 4.2±0.6 vs. 1.6±0.4, ICAM-1 protein: 0.210±0.025 vs. 0.100±0.018, ICAM-1 mRNA: 1.82±0.23 vs. 1.18±0.20, P<0.05 or P<0.01]. Injury to myocardial ultrastructure was worse in I/R group. Compared with the I/R group, the plasma levels of TNF-α and IL-8 were lower [TNF-α (67.3±9.8) ng/L, IL-8 (0.47±0.04) ng/L], IL-10 was higher [(147.5±12.5) ng/L], CK-MB, cTnI, MPO, ICAM-1 protein and mRNA were lower obviously in H group [CK-MB (1 282±145) U/L, cTnI (4.7±1.4) μg/L, MPO (2.5±0.4) U/g, ICAM-1 protein 0.140±0.026, ICAM-1 mRNA 1.31±0.25, P<0.05 or P<0.01]. Injury to the myocardial ultrastructure was less marked in H group. The indexes of those in L group and α-BGT group compared with I/R group were not statistically significantly different. CONCLUSION: Nicotine can block endothelial expression of adhesion molecules and neutrophil adhesion and infiltration to promote a balance of anti-inflammatory and pro-inflammatory response, thus prevents excessive inflammatory response to myocardial I/R injury in rat.
OBJECTIVE: To investigate the effect of nicotine on inflammatory cytokines in myocardial ischemia/reperfusion (I/R) injury in rat. METHODS: Fifty male Sprague-Dawley (SD) rats were divided into five groups by random numbers table (each n=10): sham operation group (S group), I/R group, nicotine 400 μg/kg group (H group), nicotine 40 μg/kg group (L group) and α-bungarotoxin (α-BGT,1 μg/kg) group. The anterior descending branch of left coronary artery was occluded for 30 minutes followed by 90 minutes reperfusion to reproduce myocardial I/R injury rat model, while in S group the anterior descending branch of left coronary artery was only exposed without occlusion procedure. Thirty minutes before myocardial ischemia, drugs in corresponding doses were given intravenously via jugular vein. At the end of 90 minutes of reperfusion, blood samples were collected from carotid artery to determine the levels of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), IL-10, MB isoenzyme of creatine kinase (CK-MB), and cardiac troponin I (cTnI), then the animals were sacrificed and the hearts were harvested for pathological study and determination of myeloperoxidase (MPO) activity. Immunohistochemistry and reverse transcription- polymerase chain reaction (RT-PCR) were used to assess intercellular adhesion molecule-1 (ICAM-1) protein and mRNA expression in heart tissue. RESULTS: Compared with the S group, the concentrations of TNF-α, IL-8, IL-10, CK-MB, cTnI, MPO activity, ICAM-1 protein and mRNA expression were significantly increased in I/R group [TNF-α (ng/L): 158.7±32.7 vs. 31.5±5.8, IL-8 (ng/L): 0.71±0.06 vs. 0.30±0.04, IL-10 (ng/L): 69.0±7.8 vs. 41.4±4.3, CK-MB (U/L): 2 540±169 vs. 1 120±120, cTnI (μg/L): 26.2±4.6 vs. 0.9±0.2, MPO (U/g): 4.2±0.6 vs. 1.6±0.4, ICAM-1 protein: 0.210±0.025 vs. 0.100±0.018, ICAM-1 mRNA: 1.82±0.23 vs. 1.18±0.20, P<0.05 or P<0.01]. Injury to myocardial ultrastructure was worse in I/R group. Compared with the I/R group, the plasma levels of TNF-α and IL-8 were lower [TNF-α (67.3±9.8) ng/L, IL-8 (0.47±0.04) ng/L], IL-10 was higher [(147.5±12.5) ng/L], CK-MB, cTnI, MPO, ICAM-1 protein and mRNA were lower obviously in H group [CK-MB (1 282±145) U/L, cTnI (4.7±1.4) μg/L, MPO (2.5±0.4) U/g, ICAM-1 protein 0.140±0.026, ICAM-1 mRNA 1.31±0.25, P<0.05 or P<0.01]. Injury to the myocardial ultrastructure was less marked in H group. The indexes of those in L group and α-BGT group compared with I/R group were not statistically significantly different. CONCLUSION:Nicotine can block endothelial expression of adhesion molecules and neutrophil adhesion and infiltration to promote a balance of anti-inflammatory and pro-inflammatory response, thus prevents excessive inflammatory response to myocardial I/R injury in rat.