Aim To research into the effect of diltiazem on cytokines expression in mononuclearcells induced by concanavalin A.Methods Ficoll density gradient centrifugation was used to separate the mononuclearcells from rat's spleen.There were 3 groups including control, Con A, diltiazem-Con A group in the study.The cytokines expressions in supernatant were detected by ELISA.Results Compared with control, IL-10, TNF-α, IL-6 were increased significantly in Con A group with low level IL-1β and non level TGF-β_1.But in diltiazem-Con A group, IL-10, TNF-α, IL-6 were decreased significantly compared with Con A group.Conclusion Diltiazem inhibits IL-10, TNF-α, IL-6 expressions in mononuclearcells induced by Con A.

Aim To explore the cardiac cytokine expression in rat model of myocardial calcium overload, and the intervention from diltiazem.Methods The intracellular Ca~(2+) overload was induced by the isolated rat heart subjected to 5 min Ca~(2+) depletion and 30 min Ca~(2+) repletion (Ca~(2+) paradox) by the Langendorff technique.There were five groups in this study, including Ca~(2+) overload group, normal control group, Ca~(2+) depletion control group, Ca~(2+) overload-diltiazem group, and Ca~(2+) depletion-diltiazem group.The views of myocardial pathology and ultrastruction were observed by electron microscope and light microscope respectively. The cardiac intracellular [Ca~(2+)]_i was detected by atom spectrophotometer. The expression of TNF-α, IL-1β, L-6, TGF-β1, and IL-10 was detected by RT-PCR method.Results In Ca~(2+) overload group, few inflammatory cells were found in myocardium under the light microscope. And the views of electron microscope presented that cardiocyte membranes, nucleolus, and mitochondria were disorganized obviously.Compared with normal control group, the inflammatory cytokines as TNF-α, IL-1β, and IL-6 were increased significantly whereas there was nearly no difference of the expression of TGF-β1 and IL-10 in Ca~(2+) overload group.Ca~(2+) overload-diltiazem group showed that TNF-α, IL-1β, and IL-6 were decreased significantly. There were no statistical differences in the structure of myocardium, intracellular [Ca~(2+)]_i, and cardiac cytokines expressions in the three control groups, including normal control group, Ca~(2+) depletion control group and Ca~(2+) depletion-diltiazem group.Conclusions Instead of TGF-β1 and IL-10, the expression of TNF-α, IL-1β, and IL-6 is increased obviously in myocardium of calcium paradox model. Diltiazem can inhibit the cardiac expression of TNF-α, IL-1β, and IL-6 induced by myocardial calcium overload.

Objective:To explore the effects of diltiazem on ventricular remodeling and inflammation in rat heart following acute myocardial infarction(AMI).Methods:The model of AMI rats was randomly divided into diltiazem group(D group)and control group(AMI group),besides another group of sham operation(S group).The data of ejection fraction(EF) and the left ventricular mass(LVM)were examined with echocardiography,and leukocyte infiltration in situ was analyzed on the HE staining slices,with the expression of proinflammatory cytokines(IL-I?,IL-6,TNF-?)detected by RT-PCR at 1d,3d,1w,2w and 4w intervals after AMI.Results:The results from echocardiography showed that EF increased(73.7?3.1% vs 61.0?2.6%)and LVM decreased(0.81?0.12g vs 0.92?0.12g),both significantly in D group at 4w,compared with those of the AMI group(P

Ca2+ activity has been found to associate with the immunity and inflammation within cardiovascular diseases in recent years. Researchers have begun to focus on the effect of calcium channel blockers, which could modify the immunity and inflammation. This review presented the mechanism underlying the concentration and activation of Ca2+ influenced the response of immunity and inflammation and how calcium channel blockers interfered with it, which may have potential in treatment of cardiovascular diseases.

Aim To research the effect of diltiazem on cytokine expression and inflammatory cell activity in rat heart with ischemia/reperfusion.Methods The rats, underwent ischemia reperfusion, were divided into three groups:diltiazem group(D group),ischemia/reperfusion group (I/R group),and sham group (Sgroup).Echocardiogram was detected at 1,2,4 weeks after operation. RT-PCR was used to detect the inflammatory cytokines as IL-1β,TNF-α, IL-6 and anti-inflammatory cytokines as IL-10,TGF-β.Results Compared with I/R group,EF were increased and LVM, IL-β,TNF-α,IL-6 reduced significantly in D group.There was no significant/difference for IL-10 and TGF-β in three groups .Conclusion Diltiazem inhibits IL-1β,TNF-α, IL-6 expressions and inflammatory cell infiltration in rat heart with ischemia reperfusion.

To investigate the effect of selective N-methy-D-aspartate receptor antagonist MK-801 on dentate granule cell neurogenesis after diffuse brain injury in the adult rat, so as to explore the role of glutamic acid on dentate granule cell neurogenesis after diffuse brain injury. 45 adult male SD rats were subjected to diffuse brain injury and randomized into MK-801-treatment group, vehicle-treatment group and control group (n=15 each). By using bromodeoxyuridine ( BrdU ) labelling method and immunohistochemistry to observe dividing cells, the proliferation rates of neural precursor cells in the dentate gyrus(DG) were compared between MK-801-treatment group and corresponding control groups on 2, 4, 6, 8, and 12 days after diffuse brain injury. The results showed that MK-801 (1mg/kg i.p.) significantly reduced the number of BrdU labeled cells in the dentate gyrus on 4, 6, 8 and 12 days after diffuse brain injury (P

Based on a review of research and application of the clinical decision support system (CDSS) at home and abroad,a KB-CDSS building model is proposed.The authors rounded up the architecture,principle,process,construction of the knowledge base,system design and application value of the system.In the end,the paper introduced the application of WanFang Data Clinical Diagnosis and Treatment Knowledge Base.

Objective To assessed the ability of FK506 and antilymphocyte serum(ALS) to induce mixed chimerism and tolerance for knee composite tissue allograft in rabbits without chronic immunosuppression. Methods Male Flap-eared rabbits were used as donors,and female New Zealand white rabbits were used as recipients. Vascularized heterotopic knee allotransplantation was performed. Treatment consisted of ALS(1 ml/kg) only,FK506(0.5 mg/kg) only and a combination of FK506 and ALS which were administered 24h before transplantation. ALS was administered intraperitoneally every day in the first three days. FK506 was administered gastric intubation every day for fifteen days. Survival times of knee allografts were observed. Donor specific hematopoietic chimerism and histology sections were tested. Results Survial time of knee allografts with ALS single was(17.4?1.8)d,and(23.8?1.5)d with FK506 single,(40.4?2.9)d with FK506 and ALS,contrasting with(13.6?0.8)d of control. Chimerism rate show a stabilization of 3 weeks above 10% after protocol discontinue in groups with FK506 and ALS. Conclusions Short-term administration of FK506 and ALS in this ways prolong survival time of vascularized knee allograft in rabbits and could maintain mixed chimerism and tolerance for 3 weeks.

Objective To explore the effect of pharmacological preconditioning wtith low-dose FK506 reducing subsequent ischemia-reperfusion injury in rabbit knee joint and to explore the possible mechanism of that. Methods Twenty four animal model of allograft heterootopic knee joint were established and divided randonly into three groups: IR group ( Ischemia-reperfusion group), KK506 group ( FK506 preconditioning group) and ST group(Sham control group). Vessels were clamped for 1 hour, and then grafts received reper-fusion. Tissues(for example muscles tissues) of pro-ischemia and reperfusion after 12 hours were obtained, and they were observed by microscope and electron microscope and were at aiysised with reverse transcription-polymerase chain reaction( RT-PCR) , Western Blot, DNA ladder, flow cvtometer. Moreover, the contents of MDA , NO and SOD in these tissues were examined by spectrophotometer Results As a result, we observed disoranized tissues and swollen cells in IR groups but trenchant tissues and intact cells in FK506 groups by microscope, vaeuolated and tumid mitochondrion in IR groups but non-vacuolated and intact that in FK506 groups. With FK506 preconidtioning, the contents MDA and NO were distiactly reduced but significant raised in FK506 group. Compared with IR group, DNA ladder of FK506 group were weakly, and apoptotic raetes reduce from 20% to 10% and the expression of TNF, IL-1 , Fas and FasL mRNA obviously down-regulated. At the same time, expression of HSP70 significantly up-regulated on protein and mRNA levels with RT-PCR and Western blotting analysis in FK506 group. Conclusion Pharmacological preconditioning with low-dose FK506(0. 3mg/kg) can induce tolerance of ischemia-reperfusion injury in rabbit allograft knee joint. Over-expression of HSP70 may he key factor of that.

Objective To study the effect of simvastatin on improve ventricular remodeling in rats after myocardial infarction(MI). Methods The MI models of rat were constructed,and divided into three groups:(1)MI group(MI-C),only ligation of left anterior descending coronary artery(LAD);(2)Simvastatin group(MI-S),ligation of LAD and gavage with simvastatin 40 mg?kg~(-1)?d~(-1);(3)Sham group(sham),no ligation of LAD.Cardiac architecture and function were determined by the echocardiography.The TNF-? mRNA expression in infarction and non-infarction regions was measured by RT-PCR. TNF-? protein was determined by Western blot and immunohistochemical staining.Results The echocardiography showed that the left ventricular end-diastolic diameter(LVEDd,(7.5?0.4)mm versus(4.5?0.3)mm) significantly increased in MI-C group,compared with sham group.The fractional shortening(FS,(20.5?2.5)% versus(51.6?3.1)%) and ejection fraction(EF,(41.4?4.3)%versus(85.2?3.7)%)markedly decreased in MI-C group,while compared with sham group. Simvastatin obviously reduced left ventricle(LV) expansion and improved LV function(P