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表达大肠杆菌K88ac-ST1-LTB融合蛋白工程菌株的免疫原性研究 总被引:2,自引:0,他引:2
已构建的能表达大肠杆菌K88ac-ST1-LTB融合蛋白的工程菌株BL21(DE3)(pXKST3LT5)及其表达产物经动物试验证实没有毒性反应。用从IPTG诱导的工程菌中提取的包涵体或经甲醛灭活的工程菌制成抗原,免疫小鼠,结果免疫小鼠至少能抵抗2MLD的大肠杆菌强毒株C83902(K88ac,ST^ ,L^ )的攻击,用提取的包涵体免疫家兔后,采集的血清能够中和天然ST1的毒性,这表明构建的工程菌株BL21(DE3)(pXKST3LT5)可以作为预防幼畜大肠杆菌性腹泻基因工程菌苗的候选株。 相似文献
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Although the molluscicide Frescon is a strong neurotoxin to the Lymnaea stagnalis central nervous system in vitro, it is probable that the exposure of the whole animal to this molluscicide fails to result in central nervous system abnormalities: Frescon does not appear to reach the brain in sufficient quantity to disrupt its normal activity. However, only those Frescon analogs found to be neurotoxic were molluscicidal, suggesting some related mode, if not site, of action. Frescon and its analogs may act by affecting excitable tissues other than the nervous system (e.g., the snail musculature) by altering certain functional and/or structural membrane properties. 相似文献
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AIM:The effective antisense sequences targeted VEGF mRNA with computer software would be screened and designed, and effect of them on growth K562 cells and protein expression of VEGF were studied with experiments.METHODS:Seven antisense sequences were selected and synthesized, which consisted of 18-20 deoxynucleotide acid and were modified with phosphorothioate, according to principle of low free energy of overall △G37 Overall. Cell growth was assayed by trypan blue dye exclusion assay and level of VEGF protien in the media was determined by ELISA.RESULTS:Six of seven sequences were capable of inhibing growth of K562 cells and downregulating the VEGF protein expression significantly, compared with Scrambed control group. It was found that there was a close correlation between low level of overall △G37 and antisense effectiveness (r=0.887,P<0.01).CONCLUSION:VEGF mRNA antisense oliogdeoxynucleotides, which were designed by computer software of RNAstructure, were able to inhibit growth of K562 and its protein expression. The VEGF mRNA may be new target attached by drugs. At same time, the computer aided design is useful methods to obtain the effective antisense. 相似文献
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AIM: To investigate the protective effect of onychin on the endothelial cells injured by oxidative stress. METHODS: The injured model was established by endothelial cells treated with menadione. The growth inhibitory rate of endothelial cell was determined by MTT assay; NO2-/NO3- concentration in the medium was determined by nitrate reductase assay; eNOS and caveolin-1 protein levels were determined by Western blot. RESULTS: Onychin significantly decreased the growth inhibitory rate of endothelial cells injured by menadione, increased NO2-/NO3- concentration in the medium and eNOS activity and up-regulated caveolin-1 expression. CONCLUSION: Onychin possesses a protective effect against endothelial cell injury induced by menadione via caveolin-1/eNOS pathway. 相似文献
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AIM:To investigate whether the bcl-2 antisense oligonucleotide increases the sensitivity of HL60 and K562 cell lines to daunorubicin.METHODS:IC50 for HL60 and K562 was determined with MTT method, the expression levels of Bcl-2 protein were assayed by immunofluorescence using fluoresce isothiocyanate labeling. In addition, apoptosis was detected by morphological observation and flow cytometric analysis of DNA fragmentation.RESULTS:It was found that the two oligonucleotides directed against the coding region and the translation initiation of bcl-2 mRNA, combined respectively with daunorubicin, inhibited expression of bcl-2 protein, increased apoptosis in HL60 and K562 cells, and decreased IC50 of daunorubicin significantly (P<0.05). Compared to the antisense oligonucleotide directed against the translation initiation of bcl-2 mRNA, the antisense oligonucleotide directed against the coding region showed stronger effects in the aspects of increasing the sensitivity of HL60 cells to daunorubicin (P<0.05).CONCLUSIONS:These two antisense sequences in the translation initiation and the coding region of bcl-2 mRNA increased the sensitivity of HL60 and K562 cell lines to daunorubicin in a sequence-specific manner. 相似文献
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AIM:To investigate the effects of Liucha extract on the growth of tumor cells in vitro and its possible mechanism.METHODS:The capability of colony forming of human leukemia K562 cell in vitro and the cells metabolism were studied by semi-solid agar culture and MTT staining. Then , the changes in morphology in the tumor cells were examined using electronic microscope.RESULTS:Semi-solid agar culture and MTT colorimetric analysis showed that Liucha extrats could significantly inhibit the growth of the tumor cells and their capability of colony forming. Also,under the electronic microscope,it was found that the tumor K562 cell had a narrower perinuclear space,condensation of chromatin and an enlarged mitochondria , in which the cristase disappeared.CONCLUSION:The extract from Liucha possesses an inhibitory effect on K562 cell growth in vitro through affecting the metabolism of the tumor cells. 相似文献
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在陕西省关中土娄土区布置线辣椒、甘蓝、白菜、芹菜钾肥大田试验,研究不同蔬菜对钾肥的肥效反应。结果表明,增施钾肥可使蔬菜硝态氮含量降低11.8%~116.0%,维生素C含量增加0.4~147.4mg/kg;产量增加9.3%~33.8%;明显促进营养生长和生殖生长;400cm深土壤剖面硝态氮累积量减少22.7~48.0kg/hm2,尤其在80~220cm剖面减少最为明显。 相似文献
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AIM: To investigate inhibition of K562 cell growth by antisense drug targeted VEGF mRNA. METHODS: X7, 20-mer antisense sequences were selected, synthesized and modified with phosphorothioate. The drug was transfected into K562 cells in the present of lipofection. Cell growth was assayed by trypan blue dye exclusion assay and MTT. The level of VEGF protein in the media was determined by ELISA. The morphology of apoptotic cells were observed by Giemsa staining, and the propotion of apoptotic cells was detected by flow cytometry. RESULTS: The antisense drug inhibited growth of K562 and downregulated expression of VEGF protein significantly, compared with Scrambed control group and showed dose-dependent relation. Signs of apoptosis of K562 cells were not observed. CONCLUSION: Inhibition of K562 cell proliferation, but not cells apoptosis induction is the mechanism of inhibing growth of K562 cells by antisense drug targeted VEGF mRNA. At same time, VEGF has function of promoting K562 cell proliferation, and VEGF mRNA may be a new target attached by drugs. 相似文献