Objective:To investigate the promotive effect of 4,5,6,7-tetrabromobenzotriazole (TBB) on the apoptosis of the human cervical cancer HeLa cells,and to clarify its effect mechanism in related signaling pathways.Methods:The human cervical cancer HeLa cells at logarithmic growth phase were divided into control group(without TBB) and experiment group(with TBB).MTT assay was used to detect the survival rate of the HeLa cells;the morphology of HeLa cells was observed under inverted microscope;Annexin Ⅴ-FITC/PI double staining and flow cytometry(FCM) were used to determine the apoptotic rates of the HeLa cells;the expression levels of apoptosis-related proteins p-Akt,Akt,Bcl-2,Bax,cleaved-caspase-3,and Pro-caspase-3 were detected by Western blotting method.Results:The MTT results showed that the survival rates of the HeLa cells in experiment group were significantly decreased(P<0.01) in a dose-dependent manner compared with control group.The apoptotic morphology of the HeLa cells in experiment group were found as cell shrinkage and karyopyknosis under inverted microscope.The Annexin Ⅴ-FITC/PI double staining and FCM results showed that the apoptotic rates of the HeLa cells in experiment group (3,6,12 and 24 h) were higher than that in control group (P<0.05 or P<0.01).The Western blotting results showed that compared with control group,the expression levels of the anti-apoptotic proteins p-Akt and Bcl-2 in HeLa cells in experiment group were decreased obviously,whereas the expression levels of the pro-apoptotic proteins Bax and cleaved-caspase-3 were increased and the expression levels of Pro-caspase-3 were decreased.Conclusion:TBB may promote the apoptosis of human cervical cancer HeLa cells by inhibiting the Akt signaling pathway.

Objective To investigate the relationship between the severity of coronary artery disease and malignant arrhythmia in the acute ST segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI), and guide clinical prevention and treatment .Methods By retrospective analysis method , 418 cases of hospitalized patients with a diagno-sis of STEMI undergoing direct PCI were continuously collected in the Department of Cardiology , the First Affiliated Hospital of China Medical University, from 2008 January to 2010 December.Electrocardiography (ECG) was given after admission.Those patients were divided into two groups according to whether the occurrence of malignant ventricular arrhythmias that was defined as sustained ventricu -lar tachycardia (sVT) or ventricular fibrillation (VF)].In sVT/VF patients, the preoperative and postoperative groups were divided according to sVT/VF time.The degree of coronary artery lesions was calculated in patients with STEMI .The incidence of sVT/VF was counted in each group with Gensini scores <60,≥60 and<120, and ≥120.The relationship between the severity of coronary le-sions and malignant arrhythmia was observed in STEMI undergoing direct PCI patients .Results ⑴In this study , a total of 47 cases ( 11.2%) occurred with sVT/VF in patients;Killip grade >I, fast heart rate , low blood pressure , and low ejection fraction were risk factors of sVT/VF( P <0.05).The occurrence of sVT/VF among the Gensini groups were significant difference (7.1%vs 10.8%vs 20.5%, P =0.012 ) .⑵The occurrence of sVT/VF was 44.8% ( 22 patients ) with direct PCI before operation; the preoperative sVT/VF rate among the Gensini groups had significant difference (2.1%vs 5.9%vs 9.6%, P =0.045).⑶The occurrence of sVT/VF is 53.3%(25 patients) with direct PCI after operation; the postoperative sVT/VF rate among Gensini groups had no significant difference(5.0%vs 4.9%vs 11.0%, P =0.142);⑷Paired with age ( x±2), gender, hypertension, and diabetes 1, Logistic re-gression analysis showed that the heart rate greater than 80 beats /min ( P =0.04 , OR:2.667 , 95%CI:1.043~6.815 ) was an independent risk factor of preoperative sVT/VF, that Gensini score was not an independent risk factor of preoperative malignant ar -rhythmia.Conclusions For STEMI PCI patients, the more serious the degree of coronary artery is , the higher may be preoperative malignant arrhythmia , while the postoperative malignant arrhythmia rate has no significant difference .

BACKGROUND:Smoking is one of the major risk factors for the formation of atherosclerosis. OBJECTIVE:To investigate the effect of cigarette smoke extract on the concentration of GATA-2 in the vascular smooth muscle cells and in which the role of the early growth response factor-1. METHODS:Vascular smooth muscle cells were cultured in vitro. The vascular smooth muscle cells were treated with various concentrations of cigarette smoke extract (0, 5%, 10%, 20%), then the reverse transcription PCR was applied to detect the mRNA expression of GATA-2. The vascular smooth muscle cells were treated with cigarette smoke extracts in the optimal concentration for 0, 4, 8, 12 and 24 hours, and then the expression of GATA-2 mRNA was observed, as wel as the changes of expression of GATA-2 mRNA after added with growth response factor-1. RESULTS AND CONCLUSION:Compared to the 0 concentration group, the expression of GATA-2 mRNA after treated with low concentration (5%) of cigarette smoke extract was increased more significantly than moderate concentration (10%) and high concentration (20%). The vascular smooth muscle cells in 0 hour group expressed GATA-2 mRNA at low level. The GATA-2 mRNA began to increase within 4 hours and reached peak at the 8 hours after stimulated with cigarette smoke extract of 5%concentration. After added with growth response factor-1 inhibitors, the expression of GATA-2 mRNA in 5%cigarette smoke extract induced vascular smooth muscle cells was decreased. Cigarette smoke extract can promote the increasing of GATA-2 by growth response factor-1, while the GATA-2 expression is reduced after the inhibition of growth response factor-1.

Cerebral vasospasm (CVS) is one of the serious complications of subarachnoid hemorrhage (SAH).Pathogenesis of CVS has not been fully clarified,and it may be associated with a variety of factors.With the development of molecular biology techniques,people have more understanding on SAH caused pathogenesis of CVS,and the research has also made considerable progress in the prevention of CVS.

Thiazolidinodiones are a synthetic ligand of peroxisome proliferator-activated receptor γ(PPARγ).PPARγhas certain protective effects for several types of tissues.The research covers the areas of glucose,lipid metabolism,cancer and atherosclerosis,etc.At present,the roles of thiazolidinediones in central nervous system diseases have received much attention,such as cerebral infarction,multiple sclerosis,and Alzheimer's disease.This article reviews the effects of PPARγ ligand thiazolidinediones on inhibiting the proliferation of glial cells,promoting angiogenesis,and antagonizing neuronal apoptosis after cerebral ischemia.

Objective To investigate the effects of peroxisome proliferators-activated receptorγ(PPARγ)agonist pioglitazone on the expressions of glial fibrillary acidic protein (GFAP) and cyclin D1 in the hippocampal CA1 region after cerebral ischemia in rats.Methods Fifty-four Sprague-Dawley rats were randomly divided into 3 groups:sham operation group,ischemia/reperfusion group,and pioglitazone intervention group (18 in each group).A rat middle cerebral artery occlusion and reperfusion model was induced by the modified suture method.Continuous pioglitazone rosiglitazone gavage (0.65 mg/kg once a day) was conducted for 5 days before modeling in the pioglitazone intervention group.At day 1,3,and 7 after modeling the rats (6 at each time point) were sacrificed and their brains were removed.HE staining was used to detecte the pathological changes of neurons in the hippocampal CA1 region.Immunohistochemical staining was use to detect the expressions of GFAP and cyclin D1 in the hippocampal CA1 region.Results Compared to the sham operation group,at day 3 and 7 after ischemia/reperfusion,the number of neuronal survival in the hippocarmpal CA1 region in the ischemia/reperfusion group was significantly reduced (all P ＜ 0.01).The expressions of GFAP and Cyclin D1 at all time points were significantly upregulated (all P ＜ 0.01).At day 3 and 7 after ischemia/reperfusion,the numbers of neuronal survival in the hippocampal CA1 region in the pioglitazone intervention group were significantly increased (all P ＜0.01).Compared to the ischemia/reperfusion group,the expressions of GFAP and Cyclin D1 at all time points were significantly down-regulated (all P ＜ 0.01).Conclusions PPARγagonist pioglitazone has a significant protective effect on neuron in the hippocampal CA1 region after cerebral ischemia/reperfusion in rats.Its mechanism may be associated with inhibiting GFAP and cyclin D1 expressions.

Objective To investigate the significance and mechanism of intracerebroventricular injection viper venom nerve growth factor (Vngf) in rat neural plasticity after cerebral ischemia reperfusion injury.Methods Ninety Wistar male rats were randomly assigned into Vngf-25 U group (n = 18), Vngf-50 U group (n = 18), Vngf-100 U group (n = 18), ischemia reperfusion group (n = 18) and sham operated group.The expression of candidate plasticity-related gene 15(cpg-15) Mrna and nuclear factor of kappa B ( NF-Κb ) Mrna in rat brain tissues which were collection at 2,7,14 days after surgery were evaluated by the real time PCR.Results The expression of cpg-15 Mrna and NF-Κb Mrna began to increase after surgery( the F value of cpg-15:70.43, 34.11, 31.89, the F value of NF-Κb: 27.47, 34.56, 31.89,P＜0.01).At the same time, expression of cpg-15 Mrna and NF-Κb Mrna in the Vngf groups was significantly different from the I/R group and the sham operated group (the F value of cpg-15:48.18, 55.93, 78.43, the F value of NF-Κb: 45.92, 55.72, 50.49, P ＜0.01).The more Vngf were injected, the more cpg-15 Mrna and NF-Κb Mrna were expressed in Vngf groups.Conclusions The Vngf could accelerate neural plasticity and restore neurofunctional defect through up-regulated the expression of cpg-15 and NF-Κb.

Objective To investigate the cerebral ischemia/reperfusion protection mechanism of viper venom nerve growth factor(vNGF) by the change of expression of growth associated protein-43 (GAP-43) and neurological function.Methods 45 adult male Wistar rats (weight 220～280 g) were divided randomly into 3 groups: sham group(S, n=9), balanced salt solution group (BSS, n=9) and venom nerve growth factor group (vNGF, n=27). Each group was observed for 7 days. vNGF group was divided into 25 U, 50 U and 100 U subgroups respectively. The following indexes in 3 groups were observed respectively: neurologic deficits and the expression of GAP-43 (immunohistochemistry method).Results Neurological function: The scores of neurological function was 0 in S group. The neurological deficits score was lower at the same time in vNGF group than that in BSS group (P<0.05). Immunohistochemistry: GAP-43 expressed in both BSS group and vNGF group. The expression of GAP-43 in vNGF group increased in 25 U, and to maximum in 100 U. The expression of GAP-43 in BSS group was significantly lower than in vNGF group (P<0.05). Conclusion vNGF can effectively enhance and prolong the expression of GAP-43, increase the survival rats of nerve cells, and has the protection effect on nerve cells after cerebral ischemia injured.

Objective:To assess effect of fluvastatin on vascular endothelium-dependent diastolic function of hypercholesterolemia patients. Methods:Thirty five patients with hypercholesterolemia were treated with fluvastatin (40 mg/d,po) for 8 weeks. 25 healthy adults were as control group.The baseline of brachial angiobore and the changes of it at response to nitroglycerin and reactive hyperemia were measured by Dopple ultrasound before and after treatment in hypercholesterolemia patients. Blood lipids,blood concentrations of NO and NOS were also measured before and after treatment. Results:①In patients with primary hypercholesterolemia the vascular endothelium-dependent dilation function (EDD)was much reduced as compared with the control, so as for blood concentrations of NO and NOS. ② Serum total cholesterol,low density lipoprotein cholesterol and triglycerides were significantly lowered by 8-week treatment of fluvastatin(p

Objective To determine the influence of ginsenoside Rg1 on angiogenesis and the expression of vascular endothelial growth factor (VEGF) and hypoxia inducible factor-1? (HIF-1?) in rat acute myocardium ischemia (AMI) in rat. Methods A murine model of AMI was reproduced. Wistar rats (n=104) were randomly divided into shamoperation group, AMI control group, low ginsenoside Rg1 group (1mg/kg) and high ginsenoside Rg1 group (5mg/kg). Microvascular density, VEGF protein, VEGF and HIF-1? mRNA were assessed at 3, 7, 10 and 14 days after operation. Results The values of VEGF and HIF-1? mRNA were increasing with the duration of ischemia and hypoxia, and positive relationship was found between the time of AMI and the expression of HIF-1? mRNA. Ginsenoside Rg1 enhanced the formation of angiogenesis (P