ABSTRACT
ObjectiveTo evaluate the role of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in attenuation of myocardial ischemia-reperfusion (I/R) injury by tetramethylpyrazine in rats.MethodsSixty-four healthy male Wistar rats weighing 250-300 g were randomly divided into 4 groups( n ＝ 16 each):sham operation group (group S),myocardial I/R group(group I/R),teramethylpyrazine group (group T) and AG,490( a JAK2 inhibitor) group (group AG).Myocardial I/R was induced by 30 min occlusion of left anterior desecending coronary artery (LAD) followed by 120 min reperfusion in groups I/R,T and A.In groups T and A teramethylpyrazine 20 mg/kg was injected iv 20 min before LAD occlusion.In group A AG490 3 tμg/g was injected iv at 5 min before reperfusion.Blood samples were then taken from inferior vena cava at 120 min of reperfusion for measurement of serum creatine phosphokinase (CK) and lactose dehydrogenase (LDH) activities.Myocardial infarct size was then measured and myocardial tissue was obtained for microscopic examination.ResultsSerum CK and LDH activities were significantly higher in group I/R than in group S.Pretreatment with tetramethylpyrazine significantly decreased myocardial infarct size and I/R-induced increase in serum CK and LDH activities and histologic damage.The protective effect of tetramethylpyrazine against myocardial 1/R injury was attenuated by postconditioning with AG490.ConclusionJAK2/STAT3 signaling pathway is involved in attenuation of myocardial I/R injury by tetramethyl pyrazine in rats.
ABSTRACT
To study the dynamics of venous plasma level of prostaglandin E_2 (PGE_2),and the relationship between PGE_2 level and immunity during and after CPB, 30 patients scheduled for open heart surgery served as the subjects. The peripheral venous blood samples were taken to measure plasma PGE_2 concentration,the expression of interleukin-2 receptor (IL-2R) on the lymphocyte membrane,and productive ability of interleukin-2 (IL-2),before and during CPB,on 1st ,7th and 14th day postoperatively,respectively. During CPB the PGE_2 level significantly ascended to the highest level,following cessation of CPB,went down but still remained higher level than baseline,even on 1st and 7th day postoperatively; Simultaneously, IL-2R expression and IL-2 generation were markedly suppressed, which were correlated negatively with the PGE_2 levels. It is suggested that cellular immunodepression induced by CPB,is partly related to the increase of plasma PGE_2, level.
