CAJ | 학술논문

目的评价NF-κB在七氟醚诱发小鼠小胶质细胞释放炎性因子中的作用.方法新生C57BL/6小鼠,分离培养小胶质细胞,以1×105个/ml密度接种于24孔板,1 ml/孔,80个培养孔,采用随机数字表法,将其分为4组(n=20):正常对照组(C组)、七氟醚组(S组)、NF-κB抑制剂吡咯烷二硫代氨基甲酸组(P组)和吡咯烷二硫代氨基甲酸+七氟醚组(P+S组).S组和P+S组通入4.1％七氟醚6h,P+S组通入七氟醚前1h加入10μmol/L吡咯烷二硫代氨基甲酸.七氟醚孵育6h时,收集细胞悬液,测定NF-κB的活性及其表达和IL-6、TNF-α的表达;收集上清液,测定IL-6和TNF-α的浓度.结果与C组比较,S组NF-κB活性、IL-6和TNF-α的水平升高(P＜0.01),其它2组上述指标差异无统计学意义(P＞0.05);与S组比较,P+S组NF-κB活性、IL-6和TNF-α的水平降低(P＜0.01);各组间NF-κB表达差异无统计学意义(P＞0.05).结论 NF-κB完全介导了七氟醚诱发小鼠小胶质细胞释放炎性因子.
목적 평개NF-κB재칠불미유발소서소효질세포석방염성인자중적작용.방법 신생C57BL/6소서,분리배양소효질세포,이1×105개/ml밀도접충우24공판,1 ml/공,80개배양공,채용수궤수자표법,장기분위4조(n=20):정상대조조(C조)、칠불미조(S조)、NF-κB억제제필각완이류대안기갑산조(P조)화필각완이류대안기갑산+칠불미조(P+S조).S조화P+S조통입4.1％칠불미6h,P+S조통입칠불미전1h가입10μmol/L필각완이류대안기갑산.칠불미부육6h시,수집세포현액,측정NF-κB적활성급기표체화IL-6、TNF-α적표체;수집상청액,측정IL-6화TNF-α적농도.결과 여C조비교,S조NF-κB활성、IL-6화TNF-α적수평승고(P＜0.01),기타2조상술지표차이무통계학의의(P＞0.05);여S조비교,P+S조NF-κB활성、IL-6화TNF-α적수평강저(P＜0.01);각조간NF-κB표체차이무통계학의의(P＞0.05).결론 NF-κB완전개도료칠불미유발소서소효질세포석방염성인자.
Objective To evaluate the role of nuclear factor kappa B (NF-κB) in sevofluraneinduced release of inflammatory factors in mouse microglias.Methods Microglial cells obtained from newborn C57BL/6 mice (aged 2-3 days) were seeded in 24-well plates (density 1 × 105 cells/ml, 1 ml/well) , a total of 80 wells.The cells were randomly divided into 4 groups using a random number table (n =20 each) : control group (group C);sevoflurane group (group S);NF-κB selective inhibitor pyrrolidine dithiocarbamate (PDTC) group (group P);PDTC + sevoflurane group (group P +S).In S and P+S groups, 4.1％ sevoflurane was inhaled for 6 h.In P+S group, 10 μmol/L PDTC was added at 1 h before sevoflurane inhalation.At 6 h of incubation with sevoflurane, NF-κB activity and expression and levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were determined.Results Compared with group C, the NF-κB activity and levels of IL-6 and TNF-α were significantly increased in group S, and no significant change in the above parameters was found in the other two groups.Compared with group S, the NF-κB activity and levels of IL-6 and TNF-α were significantly decreased in group P+S.There was no significant difference in NF-κB expression between the four groups.Conclusion NF-κB mediates sevoflurane-induced release of inflammatory factors in mouse microglias.