Objective To investigate the inhibitory effect of celecoxib on non-small cell lung cancer in vitro and the role of survivin.Methods The inhibitory effect of celecoxib was detected by MTT.Flow cytometry and electron microscope were used for evaluation of apoptosis.The expression of survivin was detected by RT-PCR and Western blot.Results ①Celecoxib inhibited cell survives in a time-dependent and concentration-depended manner,and the effect of celecoxib was more significant in NCI-H520 than in A549.②Celecoxib caused apoptosis in concentration-depended manner.3.Celecoxib decreased the expression of survivin.Conclusion The decrease of the expression of survivin may play a critical role in the apoptosis of NSLLC in vitro induced by celecoxib.

Objective:To investigate the transference of transplanted bone marrow mesenchymal stem cells (BMSCs)in rat of ulcerative colitis. Methods:SD rats were randomly distributed into group A colitis induced by immune-combined TNBS/ethanol and group B as control. All rats received caudal vein injection with 1 ml of fluorescence marked BMSCs,then 5 rats were sacrificed at day 3,7 and 14 respectively in each group. Cryostat sections of bone marrow,lung,liver,spleen and gut were made to observe the distribution of BMSCs in these organs,and the fluorimetric integral optical density(IOD)were analyzed. Results:BMSCs were mainly distributed in organs which richs vessels. The highest IOD level of BMSCs in lung was on the 7th day,and was on the 14th day in bone marrow. On the 14th day,the IOD level of BMSCs in colon of group A were higher than those of other segments of digestive tube and also higher than those in group B (P

Objective:To compare the rat models of ulcerative colitis induced by 2,4,6-trinitro-benzene-sulfonic acid(TNBS) and immune-comb method.Methods:SD rats were randomly distributed into groupⅠ(immune-comb method),groupⅡ(TNBS/ethanol),groupⅢ(50% ethanol) and groupⅣ(control).The rats in groupⅠwere sensitized 2 times by antigen made of rabbit colon mucosa in 2-week intervals.After abrosia for 24 hours,each rat in four groups received enema of 0.65 ml different fluids,which were:TNBS 100mg/kg +50%ethanol for groupⅠand Ⅱ,50%ethanol for group Ⅲ,and normal sodium for control group.Rats were sacrificed on day 1,21 and week 8,12 after enema to observe the macroscopical focus of infection in bowels and the microscopical changes.Results:The typical erosion and ulcer changes appeared in groupⅠandⅡ,and there was accompanying pathological changes in the end piece of ileum in groupⅠ.The pathological changes for groupⅠcould keep for 8 weeks,while those for group Ⅱtrended to heal 3 weeks later.The pathological changes in groupⅢonly were hyperemia,oedema and a few anabrosis or superficial ulcer,keeped for 21days.There was no tissue damage in group Ⅳ.Conclusion:Immune-comb method is comparatively the ideal method to establish the model,,because it has a good reproducibility,a long persistence time,and the pathological changes resemble more to those of man..

Animals ; Dogs ; Drug Evaluation, Preclinical ; methods ; Statistics as Topic

Objective To observe the effect of PKB gene silencing on the growth of gastric cancer cell line SGC-7901 in vitro.Methods Gene transfection technique was used to transfect AKt2 siRNA into gastric cancer cells.Akt2 expression was detected by RNAi technique,Akt2 protein level was detected by Western blot,and the change of cell cycle distribution and apoptosis of SGC-7901 cells were detected by flow-cytometry,SGC-7901 proliferation was measured by MTT method.Results After SGC-7901 cells transfected with Akt2 siRNA,the expression of protein level decreased obviously(P

Hepatitis C, Chronic ; Humans

BACKGROUND: Biliary ischemia-reperfusion injury is one of the main reasons for the injury bile duct following liver transplantation, liver resection and hepatic artery thrombosis after chemotherapy. However, nothing has been decided yet concerning liver can tolerate long intrahepatic bile ducts ischemia under normal temperature. OBJECTIVE: To use the rabbit biliary ischemia-reperfusion injury, model, analyze the rabbit intrahepatic bile ducts ischemia security time. METHODS: Rabbits were randomly divided into sham operation, hepatic artery and common bile duct joint blocking 1.5, 2, 2.5, 3 h groups. Sham operation group only free common bile duct, hepatic artery and portal vein. Hepatic artery and common bile duct joint blocking 1.5, 2, 2.5, 3 h groups, left and right hepatic duct openings superior margin was clamped using artery clamps, and hepatic artery, common bile duct and loose connective tissue were occluded. Following 1.5, 2, 2.5 and 3 hours, artery clamps were removed to recover hepatic artery or biliary tract blood flow. After a week, animal survival was calculated and liver function was tested. RESULTS AND CONCLUSION: None animals in the sham operation and hepatic artery and common bile duct joint blocking 1.5 hour groups died;survival rate was 87.5% following 2 hours of blocking. Animal survival rate was decreased gradually with prolonged blocking time of blood flow. These indicated that the maximum safety time of blocking biliary duct blood flow was 2 hours. Pathological and histological changes were mild within 2 hours of blocking, mainly presenting cell edema and inflammatory cell infiltration, and necrotic focus was punctiform or fragmentis, reversible. While ischemia above 2 hours, bile duct epithelial necrotic shape was significant. The obvious, hepatic necrosis was multifocal, flake, irreversible damage. Histological change also confirmed that 2 hours may be maximum security limitation of rabbit tolerance intrahepatic bile duct flow blocking under normal temperature.

Objective:To observe the clinical effects of oral Tedral SA on the elderly patients with sinus bradycardia. 　　Methods:Tedral SA(1/2 to one tablet/day in two divided doses)was administered orally to 14 elderly patients with sinus bradycardia.Twenty-four-hour Holter monitoring was performed before and one month after oral Tedral SA. 　　Results:After oral Tedral SA,resting heart rate of 14 patients was maitained between 50 to 70 beats/min.The minimum heart rates before and during therapy has significant difference statistically(34.93±2.79 vs.44.21±2.91,p＜0.001).The heart rate during oral Tedral SA was significantly increased.A few patients complained of palpitation,which disappeared as the dosage of Tedral SA was decreased.Subjective symptoms associated with sinus bradycardia such as dizziness,faintness disappeared completely in 14 patients. 　　Conclusion:Tedral SA was a effective and safe drug for treatment of elderly patients with severe sinus bradycardia.

To investigate the changes in nitric oxide (NO) and angiotensin (AⅡ) in rat with spontaneous hypertension (SHR) and the effect of benazepril on production of NO/AⅡ. The animals were divided into three groups: normotensive (WKY) group, SHR control group and benazepril group. Blood pressure was measured by the tail-cuff method. NO - 3 concentration in serum was assayed by activated cadmium reduction method; cGMP and AⅡ levels in vascular tissue were assayed by RIA (radioimmunoassay). The results showed that blood NO - 3 concentration and vascular cGMP level were all lower in SHR group compared with WKY rats(P

Objective To investigate the inhibitory effect of celebrex on non-small cell lung cancer and its mechanisms.Methods the inhibitory effect of celebrex on NSCLC were detected by MTT Flow cytometry, electron microscope were used for evaluation of apoptosis and cell cycle block. The expression of P27 KIP1, XIAP were detected by reverse transcription-polymerase chain reaction.Results 1. celebrex inhibited cell survival of NSCLC in a time-dependent and concentration-depended manner, and the effect of celebrex were more pronounced in NCI-H520 than in A549.2.Flow cytometry show that celebrex induced a G0/G1 cell arrest in NSCLC. 3. The result of these apoptosis test' indicate that celebrex caused apoptosis in concentration-depended manner. 4.celebrex increased the expression of P27 KIP1,and decreased the expression of XIAP.Conclusions celebrex inhibited cell survival of NSCLC.Its mechanisms involved in cell cycle arrest and apoptosis.