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.

Objective To explore the relationship between the polymorphism of angiotensin converting enzyme (ACE) gene and essential hypertension complicated with left ventricular hypertrophy (LVH). Methods ACE gene I/D polymorphism in 150 healthy subjects, 80 essential hypertensive(ET)patients with LVH and 152 ET patients without LVH was detected by PCR. Left ventricular mass (LVM) was measured by echocardiography, and then left ventricular mass index (LVMI) was calculated. Results The frequencies of the ACE D allele in the ET patients with or without LVH were 0.493 and 0.514, respectively, and significantly higher than those in the healthy subjects (P

Objective To explore the role of the autoantibodies against angiotensin Ⅱtype 1 receptor(AT1-receptor) and ?1-adrenergic receptor(?1-receptor)in the development of chronic glomerulonephritis(CGN) with renal failure.Methods The epitopes of the second extracellular loop of AT1 receptor(165-191),?1 receptor(192-21),M2 receptor(169-191) were synthesized and used respectively to screen sera autoantibodies from patients with chronic renal failure(n=66),hypertension without renal failure(n=58) and healthy blood donors(n=40,control) by ELISA.Results In patients of chronic glomerulonephritis with renal failure,the positive rates of the autoantibodies against AT1-receptor and ?1-receptor were 56.1% and 53.0% respectively.The positive rates were all higher than those in patients of the hypertension without renal failure(the positive rates were 15.5% and 12.1%,respectively) and in the healthy donors(10% and 12.5%,respectively)(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.

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

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 study the autoimmune response against self myocardial tissue in an experimental rats model of acute myocardial infarction (AMI) and reveal a potential role of autoimmune mediated myocardial injury involved in ventricular remodeling after AMI.Methods:An experimental animal model of AMI was adopted by in vivo ligation of left anterior descending branch (LAD) in Wistar rats After six weeks, spleens were removed and splenocytes were collected About 100?10 6～150?10 6 splenocytes were freshly transferred to syngeneic inbred rats Four weeks later, these recipient rats were anesthetized for hemodynamics analysis by catheter technique Antibody against cardiac myosin heavy chain (MHC) was screened by enzyme linked immunosorbent assay Histopathological studies were performed on all hearts Results:The antibody against cardiac MHC was positive in 8 of 22 AMI rats and recipient rats, and in 0 of 20 sham operation and recipient rats,P

AIM: We sought to evaluate the expression of apoptosis related genes, p53 and bcl-2, in cultured vascular smooth muscle cells (VSMCs) in which apoptosis was induced by the ligands of PPAR?-ox-LDL,ciglitazone and 15-deoxy-△ 12,14-PGJ 2,and then influenced by PGF 2?,an antagonist of PPAR?. To clarify whether PPAR? is involved in the regulations of p53 and bcl-2.METHODS: Rat aorta smooth muscle cells were isolated and cultured in DMEM containing 10%FBS. ox-LDL,ciglitazone and 15 d-PGJ 2 were added into the medium for 24 h, respectively. Using PGF 2? to inhibit PPAR? activation via activation of MAP kinase. We employed the flow cytometry analysis to quantitatively analyze the apoptosis of VSMCs. Also, we measured and analyzed the discrepancies of the expression of p53 and bcl-2 between every groups. RESULTS: During the process of apoptosis induced by PPAR?,the expression of P53 protein increased (P

AIM: To investigate the effect of human iNOS gene transfection on blood pressure in SD rats. METHODS: Human iNOS cDNA was transfected using gene transfection technique via enterocolia. The iNOS gene expression in rat celiac macrophages was also observed. RESULTS: The significant lowering of blood pressure in rats transfected with iNOS gene was observed from second day to sixth day after transfection, compaered to the control group ( P