糖皮质激素对人胃癌细胞肿瘤坏死因子受体的调节  被引量:1

MODULATION OF TUMOR NECROSIS FACTOR RECEPTOR OF HUMAN GASTRIC CANCER CELLS BY GLUCOCORTICOIDS

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作  者:冉瑞琼[1,2,3] 付华 王国平[1,2,3] 曹世龙[1,2,3] 

机构地区:[1]上海医科大学肿瘤医院 [2]上海瑞金医院消化科 [3]中科院上海原子核研究所

出  处:《中国免疫学杂志》1997年第2期81-83,共3页Chinese Journal of Immunology

摘  要:用放射配体结合分析法和MTT比色法研究了地塞米松对胃癌细胞肿瘤坏死因子受体数目和亲和力以及肿瘤坏死因子突变体(TNF-m)细胞毒效应的影响。结果表明:地塞米松可显著降低TNF受体的亲和力而不改变受体的数目,地塞米松明显抑制TNF-m的内化、降解,并增加与其受体的解离。地塞米松作用后的胃癌细胞对TNF-m的抗性增加,提示地塞米松上述调节作用可能是其抗炎、抗内毒素休克的机制之一。The effect of dexamethasone on the number and affinity of TNFR on gastric cancer cells,and the cytotoxicity of tumor necrosis factor mutant(TNF m)was studied with radioligand binding assay and MTT coloremetric.Results showed:dexamethasone could significantly decrease the affinity of TNFR to 125 I TNF m,without changing the number of TNFR on the surface of gastric cancer cells.Dexamethasone could obviously inhibit the internalization,degradation and promote the dissociation of TNF m from its receptors.The gastric cancer cells treated with dexamethasone had a greater resistance against TNF m than the control.The results mentioned above suggest that downregulation of TNF receptor by dexamethasone may be involved in the mechanisms of glucocorticoids therapy in inflammation and septic shock.

关 键 词:胃肿瘤 癌细胞 肿瘤坏死因子 地塞米松 

分 类 号:R735.205[医药卫生—肿瘤]

 

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