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This study is to establish a paclitaxel [PTX]-resistant human cervical carcinoma HeLa cell line [HeLa/PTX] and to investigate its redox characteristics and the expression of taxol resistance gene 1 [Txr1]. HeLa cells were treated with PTX and effects of PTX on cell proliferation were detected through cell counting and the MTT assay. Levels of cellular reactive oxygen species [ROS], reduced glutathione [GSH], and oxidized glutathione [GSSG] as well as the ratio of GSH to GSSG were measured by the 2,7-difluorescein diacetate [DCFH-DA] method and the 5,5?-dithiobis[2- nitrobenzoic acid] [DTNB] method. Activities of superoxide dismutase [SOD], catalase [CAT], and glutathione peroxidase [GPx] were determined by the nitrite formation method, the molybdate colorimetric method, and the DTNB colorimetric method, respectively. The level of Txr1 mRNA was determined by real-time PCR. Compared with the regular HeLa cells, HeLa/PTX cells were larger in size and had more cytoplasmic granules. The population doubling time for HeLa/PTX cells was 1.32 times of that of HeLa cells [P < 0.01]. HeLa/PTX cells showed stronger resistance to PTX than HeLa cells with a resistance index of 122.69. HeLa/PTX cells had higher levels of ROS [P < 0.01] and Txr1 mRNA [P < 0.01], lower level of GSH [P < 0.05], and lower activities of SOD [P < 0.01] and GPx [P < 0.05] than HeLa cells. HeLa/PTX cells, with higher levels of ROS and Txr1 mRNA expression, are more resistant to PTX than HeLa cells
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Insulinoma-glucagonoma clone 20 can express at least 6 isoforms in human cells.These isoforms can affect cell apoptosis and proliferation through apoptosis related signaling pathway,such as TRAIL or TNF signaling pathways.Furthermore,insulinoma-glucagonoma clone 20,as a GTP-GDP exchange factor,participates in the transportation of nerve synaptophysins.
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Objective To study the expression of thymic stromal lymphopoietin(TSLP) and the activation of DCs in OVA-induced murine asthma model, and investigate the effects and underlying mecha-nisms of TSLP on lung inflammation. Methods Thirty BALB/c mice were randomly divided into control group, OVA group and TSLP neutralizing antibody treated group. The asthma model was evaluated by airway responsiveness and histological analysis of lung tissues ; The levels of TSLP mRNA in lungs were determined by quantitative real-time PCR; The expression of TSLP in lungs were determined by immunohistochemistry and Western blot; The expression of CD40, CD80, CD86 in BALF was detected by FACS. Results Both the histological analysis of lung tissues and the airway responsiveness were all consistent with the characteris-tic of murine asthma model. The expression of TSLP and TSLP mRNA in the OVA group was significantly in-creased compared with blank group. The expression of CD40, CD80, CD86 in BALF from OVA group was increased significantly compared with the control group. Furthermore, treating mice with TSLP neutralizing antibody reduced the expression of CD40, CD80, CD86 on dendritic cells, and IL-4, IL-5, IL-13 in the OVA group. Conclusion Our study indicate that TSLP was highly expressed in the bronchial epithelia of murine asthma model, via upregulation of CD40, CD80, CD86, induce DCs to active CD4~+ T cells and pro-duce type 2 responses, so that aggravating the lung inflammation of asthma. Blocking TSLP is capable of in-hibiting the production of Th2 cytokines, thus presents a promising strategy for the treatment of asthma.
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0.05).However,GTPase activities of Wt PgFtsZ,Z?C01 and Z?N01 were 5.84?0.20,5.25?0.18,5.73?0.13,respectively,with 10 mmol?L-1 Ca2+,and reduced by 10 mmol?L-1 Ca2+(P
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AIM: In order to evaluate the applicable value of LDL as a targeted vehicle for chemotherapeutic agents, we investigated and compared the inhibitory effects of LDL-ACM complex and free ACM on nude mice's subcutaneous implanted tumors derived from gastric cancer cell lines, SGC-7901 and NKM-45. METHODS: LDL-ACM complex was prepared and the tumor model of nude mice was established by subcutaneous implantation of SGC-7901 and NKM-45. Then, the groups of nude mice developed subcutaneous implanted tumors were received either LDL-ACM complex or free ACM. Subsequently, the tumor size, weight and leukemia cell counts were measured and the rates of tumor-inhibition and the survival were compared among the groups. RESULTS: The inhibitory effects of LDL-ACM complex on the tumors, especially on SGC-7901 implanted tumors were much more obvious than that of free ACM. It was also indicated that the action of LDL-ACM complex was mediated by LDL receptor. CONCLUSION: These results showed that LDL-ACM complex had significant inhibitory effects on the implanted tumors and the effect might be mediated by LDL receptor.