[Objective]To investigate the anti-proliferative effects of CEP on HCT116 cells and in mouse xenograft model. [Methods]The in vivo anti-cancer activity of CEP was determined with Xenogen bioluminescence imaging in a xenograft tumor model. The cel-based multiple signaling pathway reporter assays were carried out to determine the effects of CEP on these pathways. [Results] CEP inhibited growth of human cancer cells, the IC 50 was 0.8~11.5 μM. CEP induced cellcycle arrest in S and G2/M phase. CEP also inhibited xenograft tumor growth in athymic nude mice bearing HCT116 cells. The xenograft tumor size was significantly reduced upon the treatment with CEP(10 or 20 mg·kg-1 body weight) for up to 3 weeks. Pathway-spe-cific reporter assays indicated that CEP effectively suppressed the NF-κB and MAPK/ERK signaling pathways. [Conclusions] Our results suggest that the anticancer activity of CEP in colon cancer cells may be mediated through targeting NF-κB and MAPK/ERK signaling pathways.

[Objective]This study was aimed to research the synergistic antitumor proliferation effects and their best proportion of ursolic acid(UA) and tetrandrine(Tet), a pair of compounds isolated from Chinese herbs which showed complement inhibition on the multiple signal pathways. [Methods] The reporter assays on tumor-related signal pathways for MAPK/ERK, MAPK/JNK, NF-κB, Wnt, Notch, Cell Cycle, Myc/Max and Hypoxia were used to study the effect of five different Chinese herbal compounds on tumor proliferation,it was concluded cepharanthine(Cep), Tet, 18α-glycyrrhetinic acid(18α-Gly), UA and luteolin(Lut). MTT assay and crystal violet staining were used to study the antiproliferative effect of 15 different compounds for the tumor cells of MDA-MB-231,SW480,MG63,PC3,DU145,HCT116,143B and MDA-MB-468, which is consisted with Cep, Tet, 18α-Gly, UA and Lut for the 15 different compounds. Coefficient of drug interaction(CDI) method was used to detect the synergistic effect of the two compounds. Combination of index(CI) and isobologram method was used to screen the best ratio of compounds in their antiproliferative effects. [Results] The signal pathway reporter assay showed that UA and Tet could complementarily inhibit tumor-related signaling pathways. And the results also showed that UA and Tet could induce synergetic anti-tumor cell proliferation in vitro. Furthermore, the optimal ratio of UA and Tet was 9:1 by using isobologram and CI method. [Conclusion] UA and Tet can be inhibited and complemented by 8 tumor-related signaling pathways, and we used MTT assay and crystal violet staining or other methods to confirm the synergistic antitumor proliferation effects, furthermore, the optimal proportion for UA and Tet were screened, and it provided a new insight to develop new anticancer formula in research.

Objective To explore and analyze effect of heparin combined with urokinase therapy on lower limb venous thrombosis.Methods 90 cases with lower extremity venous thrombosis were chosed and divided into control group of 45 cases and experimental group of 45 cases according with random number table method.Control group was given pure low molecular heparin treatment, experimental group was treated with small dose of urokinase static drop on the basis of control group, 7 days for a course, a total of 2 course of treatment.Compared two groups before and after treatment of lower limb venous patency rate changes, blood coagulation function index, adverse reactions and the recurrence rate.Results Compared with control group post-treatment.patency rate of posterior divisions, popliteal vein and posterior tibial vein of experimental group were significantly better (P<0.05).Experimental group post-treatment compared with control group post-treatment, PT, APTT, TT time had significant difference ( P <0.05 ).Patients incidence of adverse reactions were significantly lower than control group ( P <0.05 ).Patients were followed up for 1 year recurrence rate was significantly lower than control group ( P <0.05 ).Conclusion Effect of low molecular heparin combined with urokinase in the treatment of venous thrombosis of lower limbs significant and its prognosis is well.

Objective To investigate the effect of propofol on myocardial injury induced by hepatic ischemia/reperfusion (I/R) in rats and the role of PI3K/Akt signaling pathway. MethodsOne hundred and two male SD rats weighing 250-280 g were randomly divided into 5 groups:Ⅰ sham operation group (group S, n =6), ⅡI/R group ( n = 30), Ⅲ propofol group (group P, n = 30), Ⅳ propofol + LY294002 group (group P+ LY, n =18), and Ⅴ propofol + dimethylsulfoxide group (group P+ DMSO, n = 18). Hepatic I/R was produced by occlusion of hepatic pedicle for 30 min followed by reperfusion in group Ⅱ - Ⅴ. Propofol 12 mg/kg, propofol 12mg/kg + LY294002 (a specific PI3K inhibitor) 1.5 mg/kg, and propofol 12 mg/kg + DMSO 0.5 ml were injected I.v.via femoral vein at 10 min before ischemia in group Ⅲ -Ⅴ respectively, and then propofol was infused I.v. At a rate of 30 mg· kg- 1 · h - 1 and the administration was stopped before the rats were sacrificed in group Ⅲ - Ⅴ . At 0,30, 60, 120, and 240 min of reperfusion (T1-5) in group Ⅱ and Ⅲ , and at T3.5 in group Ⅳ and Ⅴ , six rata were sacrificed and myocardial tissues were taken for determination of the total Akt (t-Akt) and phosphorylated Akt (p-Akt) expression and Bcl-2 expression and apoptosis were detected at T3. The hepatic tissues were taken for microscopic examination. The rats were sacrificed at T1 and the parameters mentioned above were detected in group Ⅰ . ResultsCompared with group Ⅰ , p-Akt expression and apoptosis rate were significantly increased in the other4 groups, and Bcl-2 expression was up-regulated in group Ⅱ , Ⅲ and Ⅴ (P ＜ 0.05). Compared with group Ⅱ , p-Akt and Bcl-2 expression was up-regulated, and the apoptosis rate was significantly decreased in group Ⅲand Ⅴ ( P ＜ 0.05). Compared with group Ⅲ , p-Akt and Bcl-2 expression was down-regulated, and the apoptosis rate was significantly increased in group Ⅳ ( P ＜ 0.05). The microscopic examination showed that the injury to the hepatic tissues was less severer in group Ⅲ and Ⅴ than in group Ⅱ and Ⅳ. ConclusionPropofol can attenuate myocardial injury induced by hepatic I/R in rats by activation of PI3K/Akt signaling pathway.

Objective To explore the correlation between obstructive sleep apnea hypoventilation syndrome (OSAHS)and glucose metabolism disorders in patients without diabetes mellitus.Methods A total of 88 patients with OSAHS but without diabetes mellitus from 2009 to 2011 in our hospital were selected and the pulse oximeter were used to measure the oxygen saturation.Patients were divided into 2 groups:the mild OSAHS group (n=46) and the severe OSAHS group (n=42).The age-and body mass index (BMI) matched control patients without OSAHS (control group,n =48) were randomly selected.The medical history,age,body height and BMI were recorded.The levels of fasting blood glucose,glycated hemoglobin (HbA1c),cholesterol,triglyceride and low density lipoprotein cholesterol were determined.Results There were significant differences in the numbers of respiratory disorders,respiratory disturbance index,average length of apnea,the longest apnea time,low-oxygen frequency,oxygen index,the time of oxygen saturation (SaO2) below 90％,minimum SaO2 and mean SaO2 between the OSAHS group and the control group (F=2.71,2.89,1.94,2.30,2.93,2.27,3.66,3.06,1.82,respectively,all P＜0.05).There were differences in the levels of fasting blood glucose,postprandial blood glucose,HbA1c,cholesterol,triglycerideand low density lipoprotein cholesterol between the three groups(F=1.81,1.85,2.16,1.77,2.24,2.19,respectively,all P＜0.05).Conclusions The severe degree of OSAHS has the correlation with the levels of glycated hemoglobin and blood glucose,which can provide a basis to observe the duration of diabetes mellitus and to predict the risk of cardiovascular diseases.

Organ-specific tumor cell adhesion to extracellular matrix (ECM) components and cell migration into host organs often involve integrin-mediated cellular processes. Direct integrin-mediated cell adhesion to ECM components in the space of Disse appears to be required for the successful liver metastatic formation of colon cancer. In the present study, human colon cancer HT-29 cells were transfected by liposome with integrin-beta(1) antisense oligodeoxynucleotide (ASODN). The integrin-beta(1) gene expression in HT-29 cells was significantly down-regulated. The migration of HT-29 cells was assayed using transwell cell culture chambers in vitro. The number of migrating HT-29 cells in experimental group was far less than that in control group (P<0.05). The models of hepatic metastasis in nude mice were established by the intrasplenic injection of transfected HT-29 cells. Thirty days later, the nude mice were killed and the average number of hepatic metastases (4.00+/-0.93 per mouse), average volume (10.10+/-6.50 mm(3) per mouse), average weight (0.0440+/-0.0008 g per mouse) in experimental group were remarkably reduced as compared with those in control group (P<0.05). Integrin-beta(1) expression in the hepatic metastasis was studied by immunohistochemistry (SP). Positive cell percentage of hepatic metastases in experimental group was markedly decreased as compared with that in control group (P<0.05). It was concluded that integrin-beta(1) may take part in hepatic metastasis, and down-regulation of integrin-beta(1) expression may play a key role in decreasing migration and hepatic metastasis of human colon carcinoma cells (HT-29).

Aim To investigate the effects of 17β-es-tradiol on the apoptosis induced by ketamine in primary cultured cortical neurons. Methods Primary cultured cortical neurons were treated with different concentra-tions of ketamine or 17β-estradiol respectively. 24 hours after various treatments, neuron viability was measured by MTT assay. The structure of neurons was analyzed using microscope. Apoptotic neurons were de-termined by the TUNEL assay. The level of pAkt ex-pression was analyzed by Western blot. ResultsCompared with the control group, ketamine decreased neuron viability in a dose-dependent manner. Com-pared with ketamine group, 17β-estradiol increased neuron viability in a dose-dependent manner. Lack of three-dimensional sense,faded color,uncleared outline
were observed, and fractured neuron axons or neurons death were also observed in neurons treated by 100μmol · L-1 ketamine. 100 μmol · L-1 ketamine in-creased the number of apoptotic neurons and decreased the expression of pAkt. 0.1 μmol · L-1 17β-estradiol decreased the number of apoptotic neurons and in-creased the expression of pAkt. LY294002 inhibited the protective effects of 17β-estradiol, the number of apoptotic neurons increased, and the level of pAkt de-creased significantly. Conclusion 17β-estradiol ex-erts the neuroprotective effects against ketamine-in-duced neuroapoptosis by activating the PI3 K/Akt sig-naling pathway.

ObjectiveTo evaluate radio-frequency hemostasis in hepatectomy.MethodsFrom January 2009 to February 2011,the clinical data of 60 patients undergoing curative liver resection were divided into two groups using radio-frequency hemostasis (RFH) and clamp crushing method (CCM) respectively,RFH group (30 cases) and CCM group (30 cases).There was no difference between the 2 groups regarding the age,sex.hepatic function and tumor size.Data regarding the intra-operative and postoperative courses of the patients were analyzed.ResultsNo damage of hepatic vein occured in RFH group.Hepatic veins rupture occurred in 5 cases and massive bleeding occurred in 3 cases in CCM group.lntra-operative blood loss was significantly less in FRH group [ (219 ±62) ml] than in CCM group [ (416 ±96) ml ] (P ＜ 0.05 ).The postoperative drainage volume in RFH group was significantly less than that in CCM group on the third postoperative day.The serum ALT and T-BIL in RFH group was significantly lower than that in CCM group on postoperative day 1 and day 7 ( separately t =5.987,16.803,22.264,8.386,8.255,all P ＜0.05 ).Postoperative hepatic function in RFH group was significantly better than that in CCM group.ConclusionsThe use of radio-frequency hemostasis in hepatectomy is less traumatic,of less bleeding,faster recovery than clamp crashing method.

Objective To determine the effect of signal transducers and activators of transcription 3 (STAT3) gene silencing by shRNA mediated by lentiviral vector for the treatment of colorectal cancer. Methods The recombinant lentiviral vector pRNAT-shSTAT3, empty lentiviral vector pRNAT-GFP, and lentiviral packaging plasmids in supernatant were collected to transfect HT-29 cells for harvesting the HT-29-shSTAT3 cells and HT29-GFP cells. Fifteen male rats were divided into three groups (n = 5 ), and then they were inoculated with HT-29cells, HT-29-GFP cells and HT-29-shSTAT3 cells, respectively. Cell growth was assessed by MTT assay and the changes in cell cycle were detected by flow cytometry. The changes in microvessel density (MVD) of tumors were detected by immunohistochemistry. All data were analysed by one-way analysis of variance. Results The growth of HT-29-shSTAT3 cells was significantly suppressed compared with HT-29 and HT-29-GFP cells (F = 632.50,P ＜ 0. 05 ). The proportions of cells at the G0/G1 phase were 68.7% ± 2.9% in HT-29-shSTAT3 cells, 38.5% ±1.6% in HT-29-GFP cells and 38.7% ± 2.3% in HT-29 cells, with a significant difference among the three groups (F = 166.53, P ＜ 0.05 ). The MVDs of HT-29 cells, HT-29-GFP cells and HT-29-shSTAT3 cells were 29 ±5, 28 ±4 and 10 ±3, respectively, with a significant difference among the three groups (F=31.60, P ＜0.05). Conclusion STAT3 gene silencing by shRNA mediated by lentiviral vector can significantly inhibit the growth of colorectal cancer cells.