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Objective: To investigate the effect and mechanism of brain-derived neurotrophic factor (BDNF) pretreatment for reducing myocardial ischemia/reperfusion (I/R) injury in experiment rats. Methods: Rat’s myocardial I/R model was established by left anterior descending artery ligation for 30min followed-by reperfusion for 180 min. The rats were divided into 5 groups:Sham operation group, I/R group and IR with BDNF pretreatment (1, 10, 100) nmol/(kg·ml) groups respectively. The LVSP, LVEDP, ±dp/dtmax were recorded after I/R;serum levels of LDH, CK and the cardiac tissue levels of MDA, SOD were examined;the ratios of left ventricular myocardial infarction area in different groups were observed by by Evans blue staining;cell apoptosis rates were evaluated by Tunel staining;the total-TrkB and p-TrkB in myocardium were detected by Western-blot analysis. Result: Compared with I/R group, in 3 IR with BDNF pretreatment groups, LVSP, ±dp/dtmax were gradually increasing and LVEDP were gradually decreasing, all P Conclusion: BDNF pretreatment could maintain the cardiac function in experiment rats after I/R injury, it may reduce MI area, decrease oxidative damage and apoptosis, therefore, protect myocardial cells for reducing IR injury.
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Objective To evaluate the effect of delayed preconditioning with morphine on ischemic cerebral injury in mice and the role of classical protein kinase C (cPKC).Methods Forty male BALB/C mice,weighing 20-22 g,were randomly divided into 4 groups (n =10 each):sham operation group (group S),ischemic cerebral injury group (group ICI),morphine preconditioning group (group MP) and cPKC inhibitor Go6983 group (group G).Ischemia was induced by middle cerebral artery occlusion (MCAO).In S group,the middle cerebralartery was only exposed but not occluded.In MP group,morphine 10 mg/kg was injected intraperitoneally 24 h before MCAO.In G group,morphine 10 mg/kg was injected intraperitoneally 24 h before MCAO and 5 μl Go6983 (6nmol) was injected into the left lateral cerebral ventricle immediately before MCAO.The neurologic deficit was evaluated and scored according to neurological disability status scale in a blind nanner 6 h after MCAO.The animals were sacrificed and brains were immediately removed for measurement of the brain edema and infarct volume.Apoptotic rate was calculated.Results Compared with S group,the neurologic deficit scores,infarct volume,brain edema and apoptotic rate were significantly increased in ICI,MP and G groups (P ＜ 0.01).Compared with group ICI,the neurologic deficit scores,infarct volume,brain edema and apoptotic rate were significantly decreased in group MP (P ＜ 0.01),and no significant change was found in the parameters mentioned above in group G (P ＞ 0.05).Conclusion Delayed preconditioning with morphine can reduce ischemic cerebral injury in mice and activation of classical cPKC signaling pathway is involved in the mechanism.
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Objective To investigate the FOS expression changes in rat brain after ischemic pretreatment and the relationship between FOS and ischemic tolerance.Method The cerebral ischemia model of the wister rats was established by occluding four blood vessels.The FOS experssion in the hippocampus neurons was determined by using SABC immunocytochemical technique with against c-fos protooncogene antibody of rabbit.Results The FOS expression in the 30',12h,24h and 72h four experimental groups following cerebral ischemic pretreatment were obviously higher than that of false operafion control group (all P