Objective To investigate the targeted combination and anti-inflammatory effects of anti-intercellular adhesion molecule 1 (ICAM-1) targeted perfluorooctylbromide (PFOB) particles on myocardial ischemia-reperfusion injury in rat model. Methods Seventy-six adult Sprague Dawley rats (male or female, weighing 250-300 g) were selected for experiment. The models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery for 30 minutes in 30 rats. The expression of ICAM-1 protein was detected by immunohistochemistry staining at 6 hours after reperfusion, and the normal myocardium of 10 rats were harvested as control; then the content of interleukin 8 (IL-8) in serum was tested every 6 hours from 6 hours to 48 hours after reperfusion. The other 36 rats were randomly divided into 6 groups (n=6): ischemia-reperfusion injury model/targeted PFOB particles group (group A), ischemia-reperfusion injury model/untargeted PFOB group (group B), normal control/targeted PFOB particles group (group C), normal control/untargeted PFOB particles group (group D), ischemia-reperfusion injury model/normal saline group (group E), and sham operation group (group F). The ischemia-reperfusion injury models were established in groups A, B, and E; while a thread crossed under the coronary artery, which was not ligated after open-chest in group F. After 6 hours of reperfusion, 1 mL of corresponding PFOB particles was injected through juglar vein in groups A, B, C, and D, while 1 mL of nomal saline was injected in group E. Ultrasonography was performed in groups A, B, C, and D before and after injection. The targeted combination was tested by fluorescence microscope. The content of IL-8 was tested after 6 and 24 hours of reperfusion by liquid chip technology in groups A, B, E, and F. Results After 6 hours of reperfusion, the expression of ICAM-1 protein significantly increased in the anterior septum and left ventricular anterior wall of the rat model. The content of IL-8 rised markedly from 6 hours after reperfusion, and reached the peak at 24 hours. Ultrasonography observation showed no specific acoustic enhancement after injection of PFOB particles in groups A, B, C, and D. Targeted combination was observed in the anterior septum and left ventricular anterior wall in group A, but no targeted combination in groups B, C, and D. There was no significant difference in the content of IL-8 among groups A, B, and E after 6 hours of reperfusion (P gt; 0.05), but the content in groups A, B, and E was significantly higher than that in group F (P lt; 0.05). After 24 hours of reperfusion, no sigificant difference was found in the content of IL-8 between groups A and B (P gt; 0.05), but the content of IL-8 in groups A and B were significantly lower than that in group E (P lt; 0.05). Conclusion Anti-ICAM-1 targeted PFOB particles can target to bind and pretect injured myocardium of rat by its anti-inflammation effects.
ObjectiveTo compare the myocardial protective effect of HTK solution and St.ThomasⅡ(STH) solution in immature rabbit myocardium at different cardiac arrest time. MethodsAccording to cardioplegia and cardiac arrest time, 32 immature New Zealand white rabbits (aged 2-3 weeks) were randomly divided into four groups. A group SO (8 rabbits) underwent 1 hour cardiac arrest with STH solution, a group ST (8 rabbits) underwent 2 hours cardiac arrest with STH solution, a group HO (8 rabbits) underwent 1 hour cardiac arrest with HTK solution, a group Ht (8 rabbits) underwent 2 hours cardiac arrest with HTK solution. Compare the myocardial protective effect of HTK and STH solution in immature myocardium at different cardiac arrest time. ResultsThe Langendorff models were successfully established in 30 cases (8 cases in the group SO and HO, 7 cases in the group ST and HT). There were no statistical differences in hemodynamics and myocardial enzyme (CK-MB, LDH) (P > 0.05), but HTK solution reduced the activity of nitric oxide synthase (NOS) and content of malonaldehyde (MDA) and NO, maintained high activity of superoxide dismutase (SOD) and Ca2+-ATPase (P < 0.05), performed more effective myocardial protection for immature myocardium. ConclusionHTK solution has more effective myocardial protection for immature myocardium than STH solution does, but STH solution still has good outcomes within short cardiac arrest time (1h).
Objective To study the effect and mechanism of recombinant human brain natriuretic peptide (rh-BNP) in alleviating myocardial ischemia-reperfusion (I/R) injury by regulating mitogen activated protein kinase (MAPK) pathway. Methods A total of 128 adult male Sprague-Dawley (SD) rats with specific pathogen free were selected. The SD rats were divided into groups according to random number table, including, sham operation (Sham) group, I/R group, I/R+rh-BNP group, negative control adenovirus (Ad-NC)+Sham group, Ad-NC+I/R group, Ad-NC+I/R+rh-BNP group, p38 mitogen-activated protein kinase adenovirus (Ad-p38MAPK)+I/R group and Ad-p38MAPK+I/R+rh-BNP group, with 16 SD rats in each group. Myocardial I/R injury model was established by ligation of left anterior descending coronary artery. Before modeling, rh-BNP was injected intraperitoneally or adenovirus was injected into myocardium; 180 minutes after reperfusion, the contents of lactate dehydrogenase (LDH), creatine kinase isoenzyme (CK-MB) in serum, myocardial infarction size, the contents of reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α) and the expression of phosphorylated p38MAPK (p-p38MAPK), phosphorylated JNK (p-JNK) and phosphorylated extracellular regulated protein kinases 1/2 (p-ERK1/2) were detected. Results The contents of LDH, CK-MB, myocardial infarction size, the contents of TNF-α, ROS and the expression of p-p38MAPK and p-JNK in I/R group were higher than those in Sham group, p-ERK1/2 expression level was lower than that in Sham group (P<0.05). The contents of LDH, CK-MB, myocardial infarction size, the contents of TNF-α, ROS and the expression of p-p38MAPK in I/R+rh-BNP group were lower than those in I/R group (P<0.05), the expression of p-JNK and p-ERK1/2 had no significant difference compared with I/R group (P>0.05). The contents of LDH, CK-MB, myocardial infarction size, the contents of TNF-α, ROS and the expression of p-p38MAPK in Ad-p38mapk+I/R+rh-BNP group were higher than those in Ad-NC+I/R-rh-BNP group (P<0.05). Conclusion rh-BNP can alleviate myocardial I/R injury, which is related to inhibiting p38MAPK pathway, reducing inflammation response and oxidative stress response.