Objective To investigate the role of mitochondrial ATP-sensitive potassium(mito-KATP)channels in attenuation of ischemia-reperfusion(I/R)injury by lidocaine pretreatment in the isolated rat heart.Methods Adult female Wistar rats weighing 220-250 g were anesthetized with intraperitoneal 3% pentobarbital 35 mg/kg.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95%O2-5%CO2 at 37 ℃.Twenty-four isolated rat hearts with I/R injury were randomly divided into 3 groups(n = 8 each):group I/R,lidocaine group(group L)and lidocaine + glibenclamide group(group LG).After 10 min of equilibration,group C,L and LG received 20 min of perfusion with K-H solution,K-H solution containing lidocaine 2.5 mg/L and K-H solution containing lidocaine 2.5 mg/L + glibenclamide(a blocker of mito-KATP channels)10 μmol/L,respectively,then subjected to 30 min of ischemia followed by 60 min of reperfusion.HR,left ventricular developed pressure(LVDP),+ dp/dtmax and - dp/dtmax were recorded at the end of equilibration(T0)and at 15,30,45 and 60 min of reperfusion(T1-4).Coronary effluent was collected at T0 and T4 for determination of lactate dehydrogenase(LDH)and creatine kinase(CK)activities.Myocardial tissues were obtained from cardiac apex at T4 for determination of Na+ -K+ -ATPase and SOD activities and MDA and Ca2+ contents.Results Compared with group I/R,HR,LVDP,+ dp/dtmax and - dp/dtmax were significantly increased,CK and LHD activities were decreased,Na+ -K+-ATPase and SOD activities were increased,and MDA and Ca2+ contents were decreased in group L(P ＜0.05).Compared with group L,HR,LVDP,+ dp/dtmax and -dp/dtmax were significantly decreased,CK and LHD activities were increased,Na+ -K+ -ATPase and SOD activities were decreased,and MDA and Ca2+ contents were increased in group LG(P＜0.05).Conclusion The mechanism by which lidocaine pretreatment attenuates I/R injury to the isolated rat heart is related to mito-KATP channel opening.

Objective To explore the characteristic of ACE gene I/D polymorphism in Han broad jumpers .Methods Distribu‐tion of ACE gene I/D polymorphism for broad jumpers was analyzed by PCR ,DNA sequencing ,Hardy‐Weinberg and SPSS ,and the results were compared with that of normal people .Results There were II ,DD and ID in gene ACE 16 ,and the Hard‐Weinberg re‐sults showed that the subjects were group representative .The ACE DD genotype and D allele in broad jumpers was statistically higher than normal controls (P<0 .05) .Conclusion The results suggest that ACE DD genotype and D allele are associated with training sensitivity of broad jumpers and could be the molecular marker for athletes choosing genetically .

Objective To explore the effect of exercise preconditioning on inflammatory response in ischemic stroke brain tissue which mediated by miR-146a in extracellular vesicles in rats with middle cerebral artery oc-clusion(MCAO),and its mechanism.Methods Sixty 6-week-old male Sprague-Dawley rats were randomly divid-ed into a non-exercise group and an exercise group.The non-exercise group was further divided into a sham-operation control group(C,n=15)and an MCAO model group(M,n=15),while the exercise group was further di-vided into an exercise only group(E,n=15)and an exercise plus MCAO model group(EM,n=15).Rats in the E and EM groups underwent 8 weeks of treadmill exercise,6 days per week,30 minutes per day.Then rats in the M and EM groups received MCAO to induce ischemic stroke,while the C and E groups underwent a sham surgery.Twenty-four hours after the surgery,neurobehavioral tests were performed.Plasma was collected to ex-tract extracellular vesicles,and brain tissue was collected to measure the volume of cerebral infarction by using the triphenyl tetrazolium chloride(TTC)staining.Moreover,the Nissl staining was conducted to observe neuronal and Nissl body.Mean while,the content of miR-146a in plasma extracellular vesicles and brain tissue was mea-sured by using the quantitative polymerase chain reaction(qPCR),and the expression of TNF receptor associat-ed factor 6(TRAF6),nuclear factor kappa-B(NF-κB)and tumor necrosis factor-α(TNF-α)in brain tissues were determined using Western blotting.The targeting relationship between miR-146a and TRAF6 was detected by using the dual luciferase reporter gene assay.Results(1)The neurological behavioral scores of the EM and M groups were higher than those of the C group(P<0.01 and P<0.01),with that of the EM group lower than the M group(P<0.01).(2)TTC staining showed that the infarct volume of the EM and M groups was larger than that of the other two groups(P<0.01 and P<0.01),with that of the EM group smaller than the M group(P<0.01).(3)Nissl staining results showed that the neuronal arrangement was loose,the number of neurons re-duced,and the Nissl bodies were lightly stained and decreased in the M group compared with the C and E groups.Moreover,compared with the M group,the number of neurons and Nissl bodies increased in the EM group.(4)The qPCR analysis showed that the expression of miR-146a in the plasma-derived exosomes and brain tissues of the EM and M groups decreased compared with the C group(P<0.05 and P<0.01),with that of the EM group higher than the M group(P<0.05).(5)According to Western blotting,compared with the C group,the expression levels of TRAF6,NF-κB,and TNF-α proteins increased significantly(P<0.05 and P<0.01),with that of group EM signfiicantly lower than group M(P<0.05 and P<0.05).(6)Dual-luciferase report-er gene assay showed that miR-146a had a specific binding site with TRAF6.Conclusion Eight weeks of exer-cise preconditioning reduces the infarct area and the extent of brain damage,which may be mediated by miR-146a via exosomes,increasing the expression of miR-146a in brain tissue,targeting TRAF6,negatively regulat-ing TRAF6/NF-κB,and reducing the expression of TNF-α,thus alleviating the inflammatory response in brain tissue and exerting a protective effect on ischemic brain injury.