1.Endosomatic transference of transplanted bone marrow mesenchymal stem cells in rat of ulcerative colitis
Journal of Chongqing Medical University 2007;0(08):-
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
2.Comparison of two experimental ulcerative colitis models in rat
Journal of Chongqing Medical University 1987;0(01):-
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..
3.Effect of survivin on the apoptosis of non-small lung cancer induced by celecoxib
Basic & Clinical Medicine 2006;0(08):-
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.
5.In vitro growth inhibition of gastric cancer cells (MFC) by siRNA targeting PKB
Ceyao YANG ; Bin ZHENG ; Wenjing DUAN ; Tide DUAN ; Wei JIA
Chinese Journal of General Surgery 1997;0(04):-
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
7.Progress of research on mTOR inhibitor in endocrine and HER-2 targeted therapy resistance in breast cancer
Haiming DUAN ; Yanni ZHENG ; Minquan WANG
Journal of International Oncology 2015;(5):377-380
Mammalian target of rapamycin(mTOR)locates at the downstream of phosphatidylinositol 3 kinase(PI3K)-protein kinase B(Akt)cell signal transduction pathway. Studies find that the abnormal activa-tion of this pathway is correlated with the endocrine and drug resistance of anti human epidermal growth factor receptor-2(HER-2)target therapy in breast cancer. The combination with mTOR inhibitors based on the past traditional drugs can block the pathway and reflect a favourable application prospect in preventing the develop-ment of resistance and restoring the initial sensitivity on tumor cells. mTOR inhibitors are expected to be the new hope for the treatment of breast cancer.
8.The inhibitory effect of celebrex on non-small cell lung cancer
Zheng DUAN ; Ling PAN ; Shuying CAO
Medical Journal of Chinese People's Liberation Army 2001;0(12):-
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.
9.THE EFFECT OF BENAZEPRIL ON PRODUCTION OF NITRIC OXIDE AND ANGIOTENSIN IN SPONTANEOUS HYPERTENSION IN RAT
Liufa DUAN ; Qiufu ZHENG ; Liping ZHANG
Medical Journal of Chinese People's Liberation Army 2001;0(07):-
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
10.Influence of VEGF antisense oligonucleotide on expression of VEGF and survivin in gastric cancer cells
Bin ZHENG ; Ceyao YANG ; Tide DUAN
Chinese Journal of General Surgery 2001;0(10):-
Objective To observe the effects of VEGF antisense oligonucleotide transfected to SGC-7091 cell line on expression of VEGF and survivin of the cell.Methods The VEGF-ASODN was synthesised artificially.There were five groups in this experiment: control group,missense group and three various concentration groups.After transfection,RNA copies were detected by real-time PT-PCR,VEGF protein in cell and culture supernate was detected by ELESA,survivin protein was measured by Western-blot,and apoptosis was detected by FCM.Growth of cells was evaluated by growth curve.ResultsVEGF-ASODN tranfection reduced the VEGFmRNA and VEGF protein expression in gastric cancer cells and supernate remarkably.It also reduced survivin protein expression and increased apoptosis in gastric cancer cells.Conclusions Transfection with VEGF-ASODN to gastric cancer cells SGC-7901 can reduce the expression of VEGF,and can increase apoptosis and suppress the proliferation of gastric cancer cells.