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OBJECTIVE： To conduct structural modification of tectorigenin to search for new compounds with anti-tumor activity. METHODS： Tectorigenin was used as a lead compound， and then added into amine reagents as ethanolamine， methylamine， ethylamine， dimethylamine， diethylamine， n-propylamine and formaldehyde solution. Tectorigenin Mannich base derivatives were synthesized by mannich reaction with as the lead compound. The structures of the derivatives were identified according to IR， UV， MS and NMR data. Solubility of tectorigenin and its derivatives were investigated by solubility test method. MTT assay was used to investigate the inhibitory effects of tectorigenin and its derivatives on the proliferation of human colon cancer cell line HCT116， human lung cancer cell line A549 and human hepatoma cell line HepG2， and half inhibitory concentration （IC50） was calculated. The inhibition rate of tectorigenin and its derivatives （100 mg/kg） on H22 hepatoma-bearing mice in vivo was studied. RESULTS： Totally of 6 kinds of tectorigenin mannich base derivatives were synthesized， such as 8-（N-hydroxyethyl）-methyleneamino-5，7，4′-trihydroxy-6-methoxyisoflavone， 8-（N-methyl）-methyleneamino-5，7，4′-trihydroxy-6- methoxyisoflavone， 8-（N， N-diethyl）-methyleneamino-5，7，4′-trihydroxy-6-methoxyisoflavone， 8-（N， N-dimethyl）-methyleneamino- 5，7，4′-trihydroxy-6-methoxyisoflavone， 8-（N-ethyl）-methyleneamino-5，7，4′-trihydroxy-6-methoxyisoflavone， 8-（N-propyl）- methyleneamino-5，7，4′-trihydroxy-6-methoxyisoflavone （compounds 1-6 in turn）. Compared with tectorigenin， the water solubility of six derivatives was significantly improved， and the solubility was 5-20 times higher than that of tectorigenin. IC50 of compounds 1， 3 and 5 to HCT116 cells were （34.82±3.27）， （16.21±4.13）， （33.12±3.25） μmol/L， which were stronger than that of tectorigenin [（45.23±5.74） μmol/L]； IC50 of compounds 1， 3 and 5 to A549 cells were （37.05±5.74）， （26.88±4.52）， （30.13±6.23） μmol/L， which were stronger than that of tectorigenin [（53.24±6.34） μmol/L]； IC50 of compounds 1， 3 and 5 to HepG2 cells were （23.74±1.45）， （18.96±2.34）， （30.95±2.87） μmol/L， which were stronger than that of tectorigenin [（48.98±2.58） μmol/L]. Compounds 1， 3 and 5 showed higher inhibition rates （55.51％， 57.20％ and 49.15％） than tectorigenin （33.05％） on H22 hepatoma-bearing mice， respectively. The other three compounds had no obvious advantage over tectorigenin in anti-tumor activity. CONCLUSIONS： In this study， compounds 1， 3 and 5 of six tectorigenin mannich base derivatives synthesized in this study have stronger antitumor activity than tectorigenin.
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Objective:To explore the effects ofbufalin (BUF) combined with doxorubicin (DOX) on the proliferation and apoptosis in human lung cancer cell line A549 in vitro.Methods:Methyl thiazolyl tetrazolium (MTT) assay was used to measure the inhibitory effects of BUF,DOX and their combination on the growth ofA549 cells.Hoechst 33342 staining was used to observe the changes of nucleus.Flow cytometry was used to investigate the apoptosis and cell cycle distribution of A549 cells.Western blot was used to examine the expression of apoptotic protein.Results:BUF and DOX showed inhibitory effect on the A549 cells in a dose and time-dependent manner.Compared with BUF or DOX alone,combination of BUF (1,20,100 nmol/L) with DOX (1.0 μg/mL) could significantly increase the growth inhibition rate ofA549 cells at 24,36,72 h,respectively (all P＜0.05).BUF and DOX alone could induce apoptosis,and their combination could significantly increase the apoptosis ratio.In addition,BUF combined with DOX could block the cell stage of A549 cells,keep the cell stage stay in S stage and up-regulate the expression of caspase-3.Conclusion:BUF combined with DOX can significantly inhibit the proliferation ofA549 cells,which might be related to the induction of apoptosis,cell cycle S phase arrest and caspase-3 up-regulation.
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OBJECTIVE@#To optimize the process parameters involved in the green synthesis of silver nanoparticles (G-SNPs) by aqueous extract of Rosa damascena petals and to evaluate the biocompatibility and anti cancer activity of the synthesized silver nanoparticles against human lung adenocarcinoma (A549).@*METHODS@#The process variables that include concentration of extract, mixing ratio of reactants, silver salt concentration and interaction time were analyzed. The compatibility of the G-SNPs was verified by incubating with erythrocytes and the anticancer property of the G-SNPs against A549 cells was performed by MTT assay.@*RESULTS@#Formation of G-SNPs was confirmed by the visual change in the colour of the reaction mixture from pale yellow to brown yellow. Surface plasmon resonance of synthesized G-SNPs was observed at 420 nm; the size of G-SNPs were analyzed by DLS and found to be in the range of (84.00±10.08) nm. Field emission scanning electron microscope and high resolution transmission electron microscopy analysis confirmed that the G-SNPs were fairly spherical. Fourier transform infrared spectroscopy spectroscopy and X-ray diffraction revealed the characteristic peaks of G-SNPs. Energy dispersive X-ray analysis showed a signal of silver around 3 keV. The synthesized G-SNPs exhibited anticancer activity as evidenced by the MTT assay. IC50 value of G-SNPs was found to be 80 μg/mL.@*CONCLUSION@#The results of the present study suggest that G-SNPs can be synthesized rapidly within first minute of the reaction; they are biocompatible and possess anticancer activity against human lung adenocarcinoma.
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Objective: To optimize the process parameters involved in the green synthesis of silver nanoparticles (G-SNPs) by aqueous extract of Rosa damascena petals and to evaluate the biocompatibility and anti cancer activity of the synthesized silver nanoparticles against human lung adenocarcinoma (A549). Methods: The process variables that include concentration of extract, mixing ratio of reactants, silver salt concentration and interaction time were analyzed. The compatibility of the G-SNPs was verified by incubating with erythrocytes and the anticancer property of the G-SNPs against A549 cells was performed by MTT assay. Results: Formation of G-SNPs was confirmed by the visual change in the colour of the reaction mixture from pale yellow to brown yellow. Surface plasmon resonance of synthesized G-SNPs was observed at 420 nm; the size of G-SNPs were analyzed by DLS and found to be in the range of (84.00±10.08) nm. Field emission scanning electron microscope and high resolution transmission electron microscopy analysis confirmed that the G-SNPs were fairly spherical. Fourier transform infrared spectroscopy spectroscopy and X-ray diffraction revealed the characteristic peaks of G-SNPs. Energy dispersive X-ray analysis showed a signal of silver around 3 keV. The synthesized G-SNPs exhibited anticancer activity as evidenced by the MTT assay. IC
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OBJECTIVE: To determine the inhibitory effect of EGCG on the Lewis Lung Cancer Model, to compare and preliminary to discuss the mechanism of the inhibitory effect of EGCG on the proliferation of A549 cell line and Calu-3 cell line. METHODS: Observed the inhibitory effect of EGCG on Lewis Lung Cancer in vivo. Compared the inhibitory effect of different dosages of EGCG on Calu-3 and A549 cell lines with WST-8 assay. Observed the opoptosis promotional effect of EGCG on Calu-3 cells. Compared the inhibitory effect of different dosage of EGCG on Calu-3 and A549 cell lines in PI cell number counting assay. RESULTS: EGCG inhibited the proliferation of Lewis Lung Cancer in vivo. Results of WST-8 assay showed that EGCG inhibited the proliferation of Calu-3 cell line in dose-dependent manner. However, A549 cell line showed sign of drug-resistance to EGCG. The inhibitory effect of EGCG on the proliferation of Calu-3 cell line through increasing apoptosis was observed with TUNEL assay. Cell number of Calu-3 was obviously decreased by treating of EGCG, but was not changed in A549 cell line. CONCLUSION: EGCG inhibited proliferation of Lewis Lung Cacer in vivo, and inhibited proliferation of Calu-3 cell line but didn't play the inhibitory role on A549 cell line in vitro. Copyright 2012 by the Chinese Pharmaceutical Association.
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Objective To observe the effect of Hydroxycamptothecin (HCPT) on proliferation of human lung cancer cell line A549 in vitro. Method Using cell calture and MTT assay to observe the effect of HCPT on proliferation of human lung cancer cell line A549. Result Lower concentration of HCPT had no evident inhibitory effect on the human lung cancer cell line A549 after 24 h. The effect was evident when the concentration of HCPT was up to 50 ?g/mL, and the inhibitory rate was 44.17%. The inhibitory rate was 50.28% when the concentration of HCPT was up to 100 ?g/mL. The inhibitory effect of HCPT became more significant with the stimulation of the time, and the inhibitory rate of 100 ?g/mL concentration of HCPT was 70.98% after 48 h. Conclusions HCPT can inhibit the proliferation of human lung cancer cell A549 in vitro. The effect is dose and time dependent.
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Background and purpose:The impact of the two factors of von Willnbrang factor(vWF) and integrin?3 on tumor metastasis has not been recognized. This study was done to investigate the expression of vWF and integrin?3 in human lung cancer cell line H460,the association between the two factors and tumor metastasis effect of vWF and integrin?3 on adhesion of human lung cancer cell line H460. Methods:The expression of vWF and integrin ?3 protein was examined by immunohistochemical staining. The impact of vWF and integrin?3 on adherent effect of tumor cells was evaluated by adhesion experiment, antibody inhibiting experiment and MTT.Results:Positive expression of vWF and integrin?3 was detected in H460 human lung cancer cells. H460 human lung cancer cells were able to adhere to vWF. Using anti-integrin?3, we observed that the ability of cell adhesion to vWF was inhibited,and A Value decreased from 1.59?0.06 to 0.55?0.03(P=0.01619). Using anti-vWF, we observed cell adhesion to vWF was inhibited too and A Value decreased from 1.60?0.06 to 0.54?0.03(P=0.01598),which had the same effect when using anti-integrin?3.Conclusions:H460 human lung cancer cells are capable of producing vWF, and vWF expression contributes to metastasis by adhering to cancer cells, integrin?3 is the vWF receptor on H460 human lung cancer cells.