摘要
目的观察4-氨基水杨酸半乳糖苷(4-ASA半乳糖苷)对脂多糖诱导RAW264.7细胞产生肿瘤坏死因子-α(TNF-α)、细胞核转录因子核因子κB(NF-κB p65)的作用。方法实验设正常对照组、模型组(脂多糖组)、4-ASA半乳糖苷低、中、高剂量组,给药24 h后,酶联免疫吸附法(ELISA法)检测细胞上清中TNF-α的表达,细胞免疫法检测NF-κB p65的表达。结果模型组TNF-α的表达显著高于正常对照组(P<0.05),而4-ASA半乳糖苷10、40、160 mg/L组与模型组相比,细胞上清中TNF-α的表达显著降低(P<0.01);模型组NF-κB p65的表达显著高于正常对照组(P<0.01),细胞核与细胞质中NF-κB p65的表达在10 mg/L组显著低于模型组(P<0.05),40、160 mg/L组的表达降低更显著(P<0.01)。结论 4-ASA半乳糖苷在10、40、160 mg/L时可抑制细胞上清中TNF-α的表达,亦能抑制细胞质和细胞核中NF-κB p65的表达。
Objective To investigate the effects of 4-aminosalicylic acid galactoside （4-ASA galactoside） on TNF-α and NF-κB p65 in RAW264.7 cell induced by lipopolysaccharide （LPS）.Methods After the intervention was conducted on normal control group,model group,4-aminosalicylic acid galactoside with low,medium and high dose group for 24 hours,expression of TNF-α was identified with enzyme-linked immunosorbent assay （ELISA） and NF-κB p65 was detected by immune cytochemistry.Results Expression of TNF-α in model group was significantly higher than that of normal control group （P ＜ 0.05）,under doses of 10,40,160 mg/L,concentration of TNF-α in supermatants decreased significantly than that of model group （P ＜ 0.01）.NF-κB p65 in model group was significantly higher than that of normal control group （P ＜ 0.01）.But expression of NF-κB p65in cytoplasm and nucleus was remarkably lower than model group at 10 mg/L （P ＜ 0.05）,and group of 40,160 mg/L was more lower （P ＜ 0.01）.Conclusion 4-ASA galactoside can inhabit expression of TNF-α in supermatants and NF-κB p65 in cytoplasm and nucleus.
出处
《中国医药导报》
CAS
2013年第32期10-12,16,共4页
China Medical Herald
基金
山西省留学人员科研资助项目(编号2011-047)
