Aim To investigate the effects of bradykinin on the expression of IL-1? in C6 glioma cells and provide an experimental basis for the mechanism of bradykinin opening the blood tumor barrier.Methods Semi-quantitive RT-PCR and radioimmunoassay were used to detect the expression of IL-1?mRNA in C6 glioma cells and the content of IL-1? in the culture media treated with bradykinin respectively.Results RT-PCR revealed that the expression of IL-1?mRNA was significantly elevated with bradykinin treated for 15min(P

Aim To investigate the effects of PB-19 on action potential (AP) of ventricular cells in vitro and ischemia and reperfusion induced arrhythmias in vivo in rats. Methods ① We established the model of isolated rat right ventricular wall and perfused the models with normal Tyrode’s solution and PB-19.Microelectrode was inserted into the cells to record the AP. ② We ligated the left anterior descending coronary artery of rats to study the effects of PB-19 on ischemia and reperfusion induced arrhythmias. 50 rats were divided into 5 groups randomly and were given iv. injection with normal saline and PB-19 of different concentrations respectively. We recorded Ⅱ ECG of the rats. Results ①In vitro models, the APD_ 50、APD_ 90 of PB-19 group were significantly longer than that of control group respectively (P

Aim To investigate the effects of bradykinin preconditioning on the damage produced by focal cerebral ischemia-reperfusion in rats.Methods Rats were scheduled to undergo middle cerebral artery ischemia-reperfusion by intraluminal suture.Prior to ischemia,bradykinin was pumped into the brain via extra carotid artery and control group was given the same amount of normal saline.The infarct volume、brain water content、permeability of blood brain barrier and histological neuronal changes were evaluated after 2 h ischemia and 24 h reperfusion.Results Compared with other groups, bradykinin preconditioning 15min before ischemia reduced infarct volume、brain edema、permeability of blood brain barrier and histological neuronal damage.Conclusion Bradykinin preconditioning may provide protective effects against cerebral ischemic injury.This protection may be due to the protection of cerebral vasculature and the decrease of infarct volume.

Aim To assess the effect of heat shock factor-1(HSF1)and heat shock protein 70(HSP70)to tachyphylaxis by bradykinin in the opening blood-tumor barrier(BTB).Methods The C6 rat intracerebral glioma model was constructed by stereotactic implantation technique.Using western blotting method to continue monitoring the protein expression of HSF1 and HSP70 in tumor tissue after bradykinin acted on animals.The expression of occludin in tumor tissue were detected by immunohistochemistry method.Using Evans blue and electron microscope,respectively,detected the permeability and pathology of BTB after intracarotid infusion of bradykinin in C6 rats.Results Bradykinin increased the tight junction opening and the permeability of BTB in C6 animals,and the relative increments of EB were 5.19 ?g?g-1(0 min),5.06 ?g?g-1(5 min),11.35 ?g?g-1(10 min,P

Aim To investigate whether the annexation of bradykinin and papaverine had some synergetic effects on the opening of blood-tumor barrier,and find out the action of cytokine in this mechanism.Methods 160 female rats were divided into 8 groups:sham operated group;model group,PA group,BK group,PA+BK group,1/2PA+BK group,1/2BK+PA group and 1/2PA+1/2BK group.20 rats were needed in each group.The C6 brain tumor model was built.The drug was pumped into rat's brain via the carotid artery.The opening of the tight junction was detected by electron microscop.And the permeability of the blood-tumor barrier was tested by Evans blue.The expression of IL-1? was tested by Western blot and the expression of IL-1? on/around the capillary in the brain of the cerebral glioma rats was tested by SABC immunochemistry.Results In contrast to sham operated group/model group,the expression of IL-1? in PA group,BK group and PA+BK group increased obviously(P

Aim To study the effect of sodium aescinate (10 mg?kg-1?d-1) on brain edema induced by intracerebral hemorrhage and the mechanism. Methods Male Wistar rats received an injection of 50 ?lautologous whole blood into the right basal ganglia and were killed 6, 24, 48 or 72 h later. Dry-wet-weighting technique, zymologic, immunohistochemical and Western blot methods were used to examine changes of water content, Na+ and K+ contents, glial fibrillary acidic protein(GFAP)-positive cells and expression of occludin, which is a tight junction(TJ)-associated protein. Results Compared with sham operation group, contents of water and Na+ were significantly higher(P

Aim To study the activation of transcription factor cAMP response element binding protein(CREB)in the rat C6 glioma cells induced by bradykinin,and discuss its possible significance.Methods Immunocytochemistry and western-blot method were used to determine the phosphorylation of CREB after stimulated by 1 ?mol? L-1 bradykinin at various time points(0,5,10,15,20,30min).Results Bradykinin at 1 ?mol? L-1 induced phosphorylation of CREB inthe glioma cells at the indicated time points(0～30min)(P

Objective To investigate the expression of miR-29s in the glioma stem cells,and explore how the members of miR-29s affect the bio-logical behaviors of glioma stem cells. Methods Eight patient specimens were used to culture glioma stem cells. Real-time PCR was adopted to test the expression of miR-29s. CCK-8 analysis was performed to test the proliferation ,Transwell was used to test cell migration and invasion ,and flow-cytometry analysis was carried out to test apoptosis. Results miR-29a,miR-29b and miR-29c were decreased in glioma stem cells. Over-ex-pression of miR-29s could inhibit the proliferation,cell migration and invasion,but promote apoptosis of glioma stem cells. Conclusion miR-29s acts as a cancer suppressor gene in the glioma stem cells ,and miR-29a plays the dominant functional role in the family.

Objective To investigate the changes of expression of N-methyl-D-aspartate receptor(NMDAR)and mitogen activated protein kinase(MAPK)in Alzheimer disease(AD)rat model. Methods AD rat model was established by injection of amyloid-beta protein 1-40 1?l(10 g/L)into hippocampus of rat.NMDAR-mRNA and MAPK protein were immunostained by in situ hybradization histochemistry and immunohistochemistry respectively.Learning and memory ability,LTP were determined by Morris water maze and electrophysiological methods respectively. Results The escape latent was prolongated in Alzheimer rats two weeks after injection of A? than in control rats and in rats before the injection of A?(P

Objective To study the mechanism of miR?200c in regulating RMP7?induced increases of blood?tumor barrier(BTB)permeability by targeting Ras homolog gene family member A(RhoA). Methods Endogenous expression of miR?200c was detected by real?time PCR in hu?man cerebral microvascular endothelial cell line hCMEC/D3(ECs)after RMP7 treatment. miR?200c mimic and miR?200c inhibitor were transfect?ed into GECs(ECs with U87 glioma cells co?culturing),respectively. Transfection efficiency of miR?200c mimic and miR?200c inhibitor were de?termined by real?time PCR. HRP flux and TEER assays revealed BTB permeability. The protein expression level of RhoA was assessed by West?ern blotting. The distribution of RhoA was assessed by immunofluorescence microscopy. RhoA luciferase assays were performed using the Dual?Lucif?erase reporter assay system. Results RMP7 significantly induced a decrease in miR?200c expression in GECs of BTB. miR?200c mimic and miR?200c inhibitor were successfully transfected into GECs. Overexpression of miR?200c inhibited endothelial leakage and restored normal transendo?thelial electric resistance values. Simultaneously ,overexpression of miR?200c significantly reduced the protein expression level of RhoA. In addi?tion,immunofluorescence analysis revealed that the distribution of RhoA in the cytoplasm and nuclei of GECs were decreased in miR?200c mimic group. RhoA was one of the direct targets of miR?200c with the specific binding site being located at the seed sequence. The results of miR?200c si?lencing were opposite to that of the miR?200c overexpression group. Conclusion miRNA?200c regulated RMP7?induced increases in BTB perme?ability by targeting RhoA.