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Objective@#To investigate the efficacy of different bleaching methods on white-spot lesions of the enamel using optical coherence tomography and to evaluate its feasibility for monitoring the therapeutic effects on white-spot lesions. @*Methods@#Forty-eight sound premolars extracted for orthodontic reasons were selected and cut for 4 mm×4 mm×2 mm enamel blocks in buccal surfaces of the crowns. The samples were covered with acid-resistant varnish (except for the buccal surfaces) and immersed in demineralization solution for 18 days to establish the white-spot lesion models of the enamels. Samples were randomly divided into four groups (n=12). Group A was given demineralization only. Specimens in Group B, C and D were treated with 40% hydrogen peroxide, resin infiltration and 40% hydrogen peroxide combined with resin infiltration, respectively. Eight samples in each group were randomly selected. OCT was applied to observe the optical changes of the enamel surface and according to the OCT scanning results, the demineralization depth of enamel samples in each group was calculated. Then, the enamel blocks were embedded in epoxy resins, except the buccal surfaces, and measured for the microhardness values of the enamel surface by a microindentation hardness tester. Four samples in each group were cut longitudinally, and the ultrastructural changes of enamel samples in each group were observed by scanning electron microscope. @* Results@#OCT showed that the light scattering characteristics of enamel surface changed in all groups, and the bright layer was formed, but the thickness of bright layer in Group C and D was significantly lower than that in Group A and B (P<0.05). The microhardness values (kg/mm2) of the samples in Group A-D were (214.99±31.70), (250.66±33.64), (312.42±18.01) and(286.53±26.65), respectively. The microhardness of enamel surfaces in Group C and D was significantly higher than that in Group A and B (P<0.05), and the ultrastructure of enamel surfaces in Group C and D were more flat and dense in SEM observation (P<0.05). @*Conclusion@#The methods of resin infiltration therapy or 40% hydrogen peroxide combined with resin infiltration could effectively improve white-spot lesions of the enamel and the non-invasive OCT can be used as a better evaluation method for the diagnosis and treatment of white-spot lesions of the enamel.
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Objective To explore the anti-tumor effect and the influence of antitumor immunity of PD-L1/PD-1 blocked by PD-1 antibody combined with cisplatin. Methods Tumor models were established by injecting TC-1 cells into C57BL/6 mice, and the mice were divided into four groups (n = 4). The tumor growth curves and survival curves were drawn to observe the anti-tumor effect. The tumors were then removed; and the PD-L1 and CD8+ T cells were analyzed by immunohistochemical method. Results The anti-tumor effect was greater in the cisplatin group , PD-1 antibody group , and PD-1 antibody plus cisplatin group than in the control group (P < 0.05). Expression of PD-L1 in the tumor tissues was markedly increased in the cisplatin group and it was obviously decreased in the combination group (P < 0.05). CD8+ T cells decreased in the cisplatin group; and expression of CD8+ T cells was significantly increased the combination group (P < 0.05). Conclusion The anti-tumor effect and anti-tumor immunity of cisplatin are enhanced by blocking PD-L1/PD-1 pathway with PD-1 antibody.
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Objective To investigate effect of paclitaxel on expression of programmed death ligand-1 ( PD-L1 ) in the surface of cervical cancer TC-1 cells and its mechanism. Methods ①The cells were divided into two groups: paclitaxel group, paclitaxel combined with PKD blocker (G? 6976) group. There were 4 concentration gradient and 5 holes for each group, and each hole has its corresponding concentration of drugs. Influence of paclitaxel on TC-1 cell viability and effect of PKD blocker G? 6976 on IC50 value of paclitaxel were evaluated by MTT method.②The cells were divided into 0. 9% sodium chloride solution ( NS) group and paclitaxel group, There were 5 holes of each group. Effect of paclitaxel on PD-L1 expression on the surface of TC-1 cells were measured by immunohistochemistry.③The cells were divided into 4 groups:NS+DMSO group, G? 6976 group, paclitaxel group and paclitaxel+G? 6976 group. There were 5 holes for each group. Effect of paclitaxel and G? 6976 on PD-L1 expression on the surface of TC-1 cells were measured by immunohistochemistry. The expressions of PD-L1 on the surface of cells were measured by immunofluorescence treated with different drugs. Results The IC50 value of paclitaxel was 40 μg·mL-1 in paclitaxel group, and 38. 9 μg·mL-1 in paclitaxel combined with PKD blocker G? 6976 group, without significant difference between the two groups (P>0. 05). The expression of PD-L1 in the surface of TC-1 cells were significantly higher in paclitaxel group than in negative control group [(88. 48±13. 44)% vs. (39. 59±5. 99)%, P<0. 05]. The expression of PD-L1 in the surface of TC-1 cells was (79. 7%±4. 7)% after treatment with paclitaxel combined with PKD blocker G? 6976 for 24 h, and it was significantly lower than that in paclitaxel group [(96. 8±2. 5)%, P<0. 05]. Conclusion Paclitaxel promotes the expression of PD-L1 in the surface of TC-1 cells, which could be significantly inhibited by blocking PKD pathway. Paclitaxel may exert its effect through PKD pathway.
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Objective Drug resistance is a major problem for the successful chemotherapeutic treatment and prognosis of cervi -cal cancer .The article investigated the role of Twist on cisplatin resistance of Hela cervical cancer cells in hypoxia microenvironment and its possible mechanism to provide an experimental basis to improve the therapeutic efficacy for cervical cancer . Methods Hela Cells were divided into two groups, normal oxygen group A (no CoCl2) and hypoxia group A (addition of 150μmol/L CoCl2 medium).6 hours later, different degrees(10-3, 10-4, 10-5, 10-6, 10-7 mol/L) of cisplatin (10 -3 , 10 -4 , 10 -5 , 10 -6 , 10 -7 mol/L) were added into two groups .24 hours later , MTT were added to measure IC 50 and growth inhibition ratio .CoCl2 were used to mimic hypoxia environ-ment.The working concentration and the treatment duration of Cispla-tin was optimized by MTT method.The expressions of Twist and MDR1 in normal oxygen group , cisplatin group , hypoxic group B and hypoxic cisplatin group B were determined by immunofluores-cence and western blot . Results The IC50 values were 10 -5.3 mol/L and 10 -4.5 mol/L of cisplatin respectively in normal oxygen group and hypoxia group, and there was significantly difference between them (P<0.05).The optimized working concentration and work time of cisplatin was 10 -5 mol/L and 24 h.Compare to the normal oxygen group (13.08 ±2.39, 29.57 ±12.80), the expres-sions of Twist (20.81 ±2.07, 24.25 ±4.51, 33.14 ±4.24) and MDR1 (35.26 ±8.41, 60.13 ±22.32, 76.00 ±9.96) was signifi-cantly higher than those in other three groups and which were the highest in hypoxic cisplatin group (P<0.05).There were significant positive correlations among them in hypoxic group and hypoxic cisplatin group (r =0.686,P <0.05;r =0.546,P <0.05). Conclusion The hypoxia microenvironment may be related to the cisplatin resistance of Hela cervical cancer cells .The possible mechanism is hypoxia activates Twist and upregulates MDR 1 expression , resulting in cisplatin resistance of Hela cells .
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Objective To investigate the effects and mechanism of hypoxia on the growth and invasion of human cervical cancer Hela cells. Methods Hypoxia microenvironment was mimicked by cobalt chloride (CoCl2), in which the growth of Hela cells were determined by MTT method, the migration ability was detected by scratch test, and the expressions of HIF-1αand Vimentin protein were measured by immunofluorescence. Results The growth of Hela cells treated with 150 μmol/L of CoCl2 for 6 h was promoted. The migration ability in hypoxia group at 48 h was significantly higher than that in ordinary oxygen group. The expressions of HIF-lαand Vimentin in Hela cells in hypoxia group were significantly higher than those in ordinary oxygen group. There was significantly positive correlation between the expressions of HIF-1α and Vimentin (P < 0.05). Conclusion Hypoxia could promote the expression of HIF-lα, which then could up-regulate the expression of Vimentin , and finally enhanced the ability of invasion and metastasis of Hela cells.