1.Effects of Quercetin on Human Lung Cancer NCI-H1395 Cell Apoptosis
Lin LI ; Dijin WANG ; Ke WAN ; Guohui XU
China Pharmacy 2015;(34):4786-4788
OBJECTIVE:To investigate the effects of quercetin on human lung cancer NCI-H1395 cell apoptosis. METHODS:CCK-8 was used to detect the effects of 0-200 μmol/L quercetin on human lung cancer NCI-H1395 cell proliferation after treated for 12,24 and 48 h. Hochest33258 staining and flow cytometry were used to detect the effects of 0,20,50,100 μmol/L quercetin on NCI-H1395 cell apoptosis after treated for 24 h. The effects of 100 μmol/L quercetin on NCI-H1395 cell apoptosis was investi-gated after treated with Caspase-8,Caspase-9,Caspase-3 inhibitor. RESULTS:Quercetin could inhibit NCI-H1395 cell prolifera-tion in dose and time-dependent manner. 20,50,100 μmol/L quercetin could induce the apoptosis of NCI-H1395 cell,and apoptot-ic rates were (18.6 ± 4.1)%,(39.1 ± 4.5)% and (58.2 ± 3.5)%. Caspase-8 and Caspase-3 activation inhibition could obviously weaken the inhibitory effects of quercetin on cell(P<0.05). CONCLUSIONS:Quercetin can inhibit NCI-H1395 cell proliferation and induce cell apoptosis,which is related to the external way of cell apoptosis through activating Caspase-8 and Caspase-3.
2.A randomized clinical study on efficacy of Aidi injection combined with chemotherapy in the treatment of advanced non-small cell lung cancer.
Dijin WANG ; Yinglan CHEN ; Jian REN ; Yun CAI ; Minzhi LIU ; Qinyuan ZHAN
Chinese Journal of Lung Cancer 2004;7(3):247-249
BACKGROUNDTo compare the therapeutic effect, adverse reaction and effect on immunity of chemotherapy combined Aidi injection (AI) with those of chemotherapy alone in the treatment of advanced non small cell lung cancer (NSCLC).
METHODSNinety eight cases of advanced NSCLC were randomly divided into two groups, trial group and control group. In the trial group, NP plus AI (60 80 ml) were given intravenously by dissolving in 400 ml of normal saline per day for 8-10 days, while in the control group, only NP chemotherapy was given. Navelbine (25 mg/m², d1, 8) and cisplastin (40 mg/m², d1-3) were chosen in the chemotherapy. Each patient received at least two cycles of treatment.
RESULTSThe effective rate in the trial group and the control group was 53.1% and 44.9% respectively, without significant difference between the two groups ( P > 0.05). But the rate of progression, adverse reactions in bone marrow and digestive tract, and change of immunity in the trial group were all lower than those in the control group ( P < 0.05), and the improvement in Karnofsky score in the trial group was higher than that in the control group ( P < 0.05).
CONCLUSIONSChemotherapy of NP combined with AI shows benefit in the treatment of advanced NSCLC. AI could decrease the influence on immunity and adverse reaction of chemotherapy, and improve the quality of life in patients with NSCLC.
3.NRSF Plays a Regulatory Role in Human Insulin Gene Transcription
Qingbin LIU ; Yanhua LI ; Yinxiang YANG ; Hongfeng YUAN ; Rui ZHANG ; Lipeng QIN ; Yang L ; Sainan ZHANG ; Dijin SUN ; Lin CHEN ; Cixian BAI ; Xue NAN ; Yunfang WANG ; Xuetao PEI
Progress in Biochemistry and Biophysics 2006;0(09):-
The transcriptional repressor RE1 silencer transcription factor(NRSF/REST) is an important factor that restricts some neuronal traits in neurons.Since these traits are also present in pancreatic islet cells,NRSF-regulated genes involved in islet function are searched.A NRSE-like motif was analysed in human insulin promoter.The role of NRSE was evaluated by generating a model of insulin-secreting cells that firmly express NRSF.The presence of NRSF led to a decrease in activity of human insulin promoter by stable or transient transfection with human insulin-promoter luciferase.The predicted NRSE-like motif also confers NRSF-dependent transcriptional repression in the context of a surrogate gene promoter.Specific binding activity of NRSF/REST to the NRSE-like motif was confirmed by EMSA.Moreover,the binding activity is competed by consensus NRSE sequence.These data showed that human insulin promoter is regulated by the transcriptional repressor NRSF/REST via the NRSE-like motif.