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机构地区:[1]天津医科大学附属肿瘤医院高级病房,天津市“肿瘤防治”重点实验室,300060
出 处:《天津医药》2011年第12期1123-1126,共4页Tianjin Medical Journal
摘 要:目的:研究守宫硫酸多糖(Gepsin)对肝癌SMMC-7721细胞分化和增殖的影响,并进一步探讨其可能的机制。方法:将不同浓度的Gepsin加入对数生长的SMMC-7721细胞进行培养,在不同的时间利用台盼兰染色观察细胞的增殖情况。同时,收集细胞培养上清液,利用联合放免法,以溴钾酚绿法分别观察Gepsin对甲胎蛋白(AFP)、白蛋白(ALB)分泌的影响;利用酶联免疫吸附试验法观察Gepsin对转化生长因子(TGF)-β1、血管内皮生长因子(VEGF)分泌的影响;利用光镜观察Gepsin对SMMC-7721细胞形态的影响。结果:随着处理组Gepsin的浓度升高,SMMC-7721细胞的增殖明显受到抑制;而对细胞活率无明显影响。Gepsin可增加培养上清中的ALB分泌量,降低AFP分泌量。光学显微镜下可见加入Gepsin后细胞的形态由圆形变为纺锤形。Gepsin对培养上清分泌的VEGF无影响,但可使TGF-β1增加。结论:Gepsin可明显抑制肝癌细胞SMMC-7721的增殖,诱导SMMC-7721细胞分化。其机制可能是通过上调TGF-β1来诱导肝癌细胞分化实现的。Objective: To investigate the effect of Gekko sulfated polysaccharide (Gepsin) on the proliferation and differentiation in hepatic cancer cell line SMMC-7721. Methods: SMMC-7721 cells were cultured in RPM-1640 medium with different concentrations of Gepsin. Trypan blue stain was used to determine the cell proliferations in different time points. The cell culture supernatant was collected to observe the effect of Gepsin on alpha-fetoprotein (AFP) and albumin (ALB) by bromocresol green-immunology. Levels of transforming growth factor (TGF)-β1 and vascular endothelial growth factor (VEGF) influenced by Gepsin were detected using enzyme-linked immunosorbent test. The effect of Gepsin on the morphology of SMMC-7721 was examined by light microscopy. Results: The proliferation of SMMC-7721 cells was significantly inhibited with the increased concentrations of Gepsin, but no effect on the viability of SMMC-7721 cells. The AFP secretion decreased while ALB secretion increased markedly in Gepsin-treated cells. SMMC-7721 cells showed a round shape under light microscope, while cells changed to spindle shape after exposure to Gepsin. Treated with Gepsin, there was no change in the level of VEGF of cell culture supernatant, but the level of TGF-β1 significantly increased. Conclusion: Gepsin strongly inhibited the proliferation and induced the differentiation of SMMC-7721 cells, which may be induced the differentiation of SMMC-7721 cells via up-regulating the level of TGF-β1.
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