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.

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 establish a method for the in-vitro culture of astrocytes from cerebral cortex of neonatal rats.Methods Astrocytes were isolated from cerebral cortex of the neonatal SD rats aged 24 hours,and then were cultured in the high-glucose DMEM medium with 10% fetal bovine serum added.The morphological features of astrocytes were examined under inverted microscope.The growth of the third generation of astrocytes was observed with counting plate method and methyl thiazolyl tetrazolium (MTT) assay.Results The astrocytes from cerebral cortex of neonatal rats grew well,the astrocytes showed typical morphological features,and no other kinds of cells was found.Conclusion A simple and practical in-vitro culture method for rats astrocytes is established.

OBJECTIVE To establish a fingerprinting method by randomly amplified polymorphic DNA.Epidemiological study was carried out on Pseudomonas aeruginosa in Ruijin Hospital. METHODS To obtain optimum scheme on reaction system for randomly amplified polymorphic DNA(RAPD) of P.aeruginosa. RESULTS P.aeruginosa strains isolated from the same ward shared the same RAPD fingerprint type,except for pulmonary ward.Different ward was with different fingerprint type. CONCLUSIONS Prevalent strain was not found in the whole hospital,but within ward exists hospital-acquired infection phenomenon.

Objective To explore the influence of ozone therapy on high-sensitivity C-reactive protein (hs-CRP) and matrix metalloproteinases-3 (MMP-3) in synovial fluid of patients with knee osteoarthritis,and to investigate the possible mechanism.Methods Sixty-two patients with knee osteoarthritis were divided into observation group and control group by random digits table method with 31 cases each.The patients of observation group were treated with ozone,while the patients of control group were treated with hyaluronic acid once a week for 5 weeks.The efficacy was evaluated and the level of hs-CRP and MMP-3 in synovial fluid were detected before and after treatment.Results The total effective rate in observation group was 100.00％ (31/31),significantly higher than that in control group [87.10％ (27/31)],and there was significant difference (x2 =4.28,P ＜ 0.05).After treatment,the level of hs-CRP and MMP-3 in observation group was (6.68 ±2.15) mg/L,(69.84 ± 16.97) μ g/L,significantly lower than that in control group [(8.72 ± 2.39) mg/L,(85.43 ± 19.52) tμ g/L],and there was significant difference (t =3.53,3.36,P ＜ 0.01).Conclusion There is significant effect of ozone therapy of patients with knee osteoarthritis,its mechanism may be reducing the level of MMP-3 and inhibiting inflammatory reaction.

AIM: Recent studies have identified the importance of inflammation in the development and progression of heart failure.Chemokines are essential factors in the recruitment and activation of leukocytes.They are closely related with inflammation.So the relation between chemokines expression and lymphocytes recruitment and cardiac function after acute myocardial infarction(AMI) was studied.METHODS: Ligating left interventricular branch induced AMI.Experimental rats were divided into three groups: heart failure group(MI-HF),non-heart failure group(MI-NF) and sham group(sham).Sham group was made by the same procedure only without ligation.The blood dynamics of rats was examined after 3 days,1 week and 2 weeks following ligation.Rats,which had a left ventricular end-diastolic pressure(LVEDP) above 15 mmHg,were considered to be in heart failure.Reverse transcription polymerase chain reaction(RT-PCR) was used to analyze the mRNA expression of chemokines,including monokine induced by IFN-?(MIG),macrophage inflammatory protein-1 alpha(MIP-1?) and regulated upon activation,normal T cell expressed and secreted(RANTES),in the infarcted region(circumjacent region included).The numbers of lymphocytes infiltrated in the infarcted region were also counted.RESULTS: MIP-1?,RANTES and MIG mRNA increased at 3 days and reached the peak at 1 week after AMI,significantly higher in MI-HF group than those in MI-NF group(RANTES,0.83?0.05 vs 0.51?0.19,P

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