The effects of prostaglandin E_2 on hemodynamics and cardial function in normal rabbits and on cardioprotection in experimental acute myocardial infarction rabbits were investigated. To determine the action of prostaglandin E_2 in normal rabbits (n = 10), we measured arterial systolic pressure (ASP), arterial diastolic pressure (ADP), mean arterial pressure (MAP), heart rate (HR), left ventricular ejection time (LVET), +dp/dt max, -dp/dt max, Vc_E-50, T time after injected prostaglandin E_2 (1?g/min/kg). The results showed that ASP, ADP, MAP were decreased. HR, Vc_E-50, LVET were unchanged. To determine the effects of prostaglandin E_2 on the cardioprotection in acute myocardial infarction in rabbits (n=8), left ventricular systolic pressure (LVEP), +dp/dt max,-dp/dt max, ST of ECG, infarct size were also measured by us. The results showed that +dp/dt max, -dp/dt max were higher than control (n=9), ST lower than control, LVSP and infarct size were unchanged. Thus, prostaglandin E_2 could relax vascular smooth muscle, reduce laod of heart, decrease myocardial oxygen demands, maintain cardiac function during acute myocardial infarction.

AIM: The effects of BDM on isolated rat heart in cold cardioplegia were studied METHODS: Rat heart were subjected to cold cardioplegia at 4℃ for 8, 18 and 24 h Then each heart was perfused (90 cm H 2O) in Langendorff model at 37℃ for 40 min In the high K + group( n =24) the hearts were preserved in St Thomas cardioplegic solution, in BDM group( n =24) hearts were preserved in K-H solution with BDM 30 mmoL/L RESULTS: After 18 h, heart rate and the coronary flow in BDM group were significantly higher than in high K + group( P

AIM and METHODS: The protective effects of multi-enzyme Ⅱ was studied on cultured endothelial cells which was injuried by hyperlipidemia serum. RESULTS: Hyperlipidemia serum increased ICAM-1 expression on the surface of endothelial cells, and decreased NO- 2 release significantly (P

ObjectiveTo study the anatomical abnormalities of basal ganglia and research their influence on depression status in patients with post stroke depression (PSD)by diffusion tensor imaging (DTI) of MRI.MethodsPatients with basal ganglia infarction were recruited,and divided into groups of PSD and non depression control group by Hamilton Depression Rating Scale (HAMD) assessment. All the patients were evaluated with National Institute of Health Stroke Scale ( NIHSS). And the patients were checked by DTI sequence.Fractional anisotropy (FA),average diffusion coefficient (ADC) values and the number of nerve fiber were measured in bilateral caudatum,pallidum,putamen and thalamus.ResultsThe score of NIHSS (6.29 ± 3.45 ) was significantly higher in PSD group than that in non-depression group (3.95 ± 1.90 ;t =2.219,P =0.036). No significant difference was found between the two groups for the DTI data of the basal ganglia nuclei ( t =0.056-1.618,all P ＞ 0.05 ). Compared with contralateral construction (0.40 ± 0.02 ),the FA value decreased in the left putamen ( 0.37 ± 0.03 ) in the PSD group ( t =2.243,P =0.045 ).By Spearman correlations analysis,the HAMD score was positively correlated with NIHSS score ( r =0.464,P =0.017 ),and negatively correlated with the FA values of left pallidum (r=-0.563,P=0.005),right pallidum (r=-0.416,P=0.035) and left putamen (r =-0.428,P =0.029).Conclusions The occurrence of PSD was associated with neurological functional deficit following basal ganglia infarction.The depression level was correlated with the increasing of NIHSS score,the reductions in bilateral pallidum and left putamen FA values.This research contributes to evaluation of the PSD status in patients with basal ganglia infarction.

Objective:To observe the affection of angiotensin Ⅱ antagonists on the cultured subtype 2 receptor of angiotensin II transfected aortic vascular smooth muscle cells of rat.Methods:After transfected the plasmid that contained the cDNA of subtype 2 receptor of angiotensin II into cultured rat vascular smooth muscle cells, the cells were divided into three groups：cells of group 1 were treated with angiotensinⅡ,cells of group 2 were treated with angiotensinⅡand losartan,cells of group 3 were treated with angiotensinⅡ and PD123319 .After experiments，the expression of PCNA, NOS and the cell number was tested, respectively.Results：After treated with Losartan，the cell number of group 2 was(4.17±0.15)×105，the OD value of PCNA was 0.202 6±0.007 6，both of which were less than that of cells of group 3；the OD value of NOS of cells was more in group 2(0.027 5±0.002 1 ) than that in group 3 (0.016 9±0.002 0) (P＜0.01).Conclusions:It suggests that when being activated,subtype 2 receptor of angiotensin Ⅱ could inhibit the proliferation of vascular smooth muscle cells and antagonist the effect of subtype 1 receptor of angiotensin Ⅱ,such an effect may be related to the activation of NOS.

AIM To compare the protective effects of norepinephrine preconditioning(NEPC)and ischemic preconditioning(IPC)on myocardial ischemic/reperfused injury in rats in vivo . METHODS Rats were divided into control, ischemia/ reperfusion, classic IPC and NEPC groups. After 20 min reperfusion, several indexes including cardiac function indexes, MDA were tested, the myocardial ultrastr ucture and the injury reaction of catalase observed. RESULTS Both IPC and NEPC could protect myocardial ultra structure, ameliorate left heart function, decrease cardiac MDA content and protect the activity of catalase. CONCLUSION Extra micro norepinephrine preconditioning as a non injury method can mimic the protective effects of classic IPC and shows its clinical values.

Objective:To explore the role of long non-coding RNA rhabdomyosarcoma 2 associated transcript(lncRNA RMST)and microRNA-24-3p(miR-24-3p)in proliferation,migration and invasion of oral squamous cell carcinoma cells(OSCCs).Methods:The RMST expression in head and neck squamous cell carcinoma(HNSC)was analyzed by UALCAN data base.qRT-PCR was used to detect the expression of RMST and miR-24-3p in 5 human OSCC cell lines.CAL27 cells were in vitro cultured and allocated into con-trol group,pcDNA3.1 group(vector),pcDNA3.1-RMST+mimics-NC group(overexpression of RMST+negative control of miR-24-3p)and pcDNA3.1-RMST+miR-24-3p mimics group(overexpression of RMST+miR-24-3p).Dual luciferase reporter assay was per-formed to analyze the interaction between RMST and miR-24-3p.MTT assay,wound-healing and transwell assay were applied to de-tect the proliferation,migration and invasion of the cells.Western blot and qRT-PCR were conducted to measure the expression of E-cadherin,N-cadherin and c-myc in the cells.Results:RMST level were down-regulated in HNSC tissues and OSCC cell lines(P＜0.01).While miR-24-3p level was elevated in OSCC cell lines(P＜0.01).miR-24-3p was identified and confirmed as a potential binding partner to RMST.miR-24-3p level was lower in pcDNA3.1-RMST group than in pcDNA3.1 group(P＜0.01).The prolifera-tion,migration and invasion abilities of CAL27 cell in pcDNA3.1-RMST+mimics-NC group were lower than in pcDNA3.1 group(P＜0.01).While those of CAL27 cells in pcDNA3.1-RMST+miR-24-3p mimics group were higher than in pcDNA3.1-RMST+mimics-NC group(P＜0.01).Compared with pcDNA3.1 group,pcDNA3.1-RMST+miR-24-3p mimics showed higher expression of E-cad-herin,lower expression of N-cadherin and c-myc(P＜0.01).Compared with pcDNA3.1-RMST+miR-24-3p mimics group,pcD-NA3.1-RMST+miR-24-3p mimics group showed lower expression of E-cadherin,higher expression of N-cadherin and c-myc(P＜0.01).Conclusion:Down-expressed RMST may suppress the proliferation,migration and invasion progression of OSCC cells through targeting miR-24-3p.