郑州大学学报(医学版)
鄭州大學學報(醫學版)
정주대학학보(의학판)
JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES)
2015年
1期
91-94
,共4页
侯长春%梁悦%邬丽红%罗劲%刘丽华%陈一强
侯長春%樑悅%鄔麗紅%囉勁%劉麗華%陳一彊
후장춘%량열%오려홍%라경%류려화%진일강
支气管哮喘%高迁移率族蛋白B1%16 HBE%血管内皮生长因子
支氣管哮喘%高遷移率族蛋白B1%16 HBE%血管內皮生長因子
지기관효천%고천이솔족단백B1%16 HBE%혈관내피생장인자
bronchial asthma%high-mobility group protein B1%16HBE%vascular endothelial growth factor
目的:探讨高迁移率族蛋白B1(HMGB1)对人支气管上皮细胞(16HBE)血管内皮生长因子(VEGF)表达和分泌的影响及可能调控机制。方法:16HBE按以下方法分组。①HMGB1不同质量浓度组:0、100、500、2000μg/L HMGB1刺激16HBE 24 h。②HMGB1不同作用时间组:对照组,2000μg/L HMGB1分别刺激16HBE 6、12、24 h组。 MTT检测上述各组干预后16 HBE的细胞活力,实时荧光定量PCR检测16 HBE VEGF mRNA表达水平的变化,ELISA检测细胞培养上清中VEGF水平。应用P38 MAPK通路特异性抑制剂SB-202190观察其对HMGB1诱导VEGF表达和分泌的影响。结果:随HMGB1作用浓度的增加和作用时间的延长,VEGF的表达和分泌呈上升趋势(P均<0.05),但细胞活力无明显改变(P均>0.05)。 HMGB1刺激增加了16HBE细胞VEGF的表达和分泌,SB-202190几乎完全抑制了HMGB1诱导的VEGF的表达和分泌( P均<0.05)。结论:HMGB1可能通过P38 MAPK通路介导支气管上皮细胞VEGF的表达和分泌。
目的:探討高遷移率族蛋白B1(HMGB1)對人支氣管上皮細胞(16HBE)血管內皮生長因子(VEGF)錶達和分泌的影響及可能調控機製。方法:16HBE按以下方法分組。①HMGB1不同質量濃度組:0、100、500、2000μg/L HMGB1刺激16HBE 24 h。②HMGB1不同作用時間組:對照組,2000μg/L HMGB1分彆刺激16HBE 6、12、24 h組。 MTT檢測上述各組榦預後16 HBE的細胞活力,實時熒光定量PCR檢測16 HBE VEGF mRNA錶達水平的變化,ELISA檢測細胞培養上清中VEGF水平。應用P38 MAPK通路特異性抑製劑SB-202190觀察其對HMGB1誘導VEGF錶達和分泌的影響。結果:隨HMGB1作用濃度的增加和作用時間的延長,VEGF的錶達和分泌呈上升趨勢(P均<0.05),但細胞活力無明顯改變(P均>0.05)。 HMGB1刺激增加瞭16HBE細胞VEGF的錶達和分泌,SB-202190幾乎完全抑製瞭HMGB1誘導的VEGF的錶達和分泌( P均<0.05)。結論:HMGB1可能通過P38 MAPK通路介導支氣管上皮細胞VEGF的錶達和分泌。
목적:탐토고천이솔족단백B1(HMGB1)대인지기관상피세포(16HBE)혈관내피생장인자(VEGF)표체화분비적영향급가능조공궤제。방법:16HBE안이하방법분조。①HMGB1불동질량농도조:0、100、500、2000μg/L HMGB1자격16HBE 24 h。②HMGB1불동작용시간조:대조조,2000μg/L HMGB1분별자격16HBE 6、12、24 h조。 MTT검측상술각조간예후16 HBE적세포활력,실시형광정량PCR검측16 HBE VEGF mRNA표체수평적변화,ELISA검측세포배양상청중VEGF수평。응용P38 MAPK통로특이성억제제SB-202190관찰기대HMGB1유도VEGF표체화분비적영향。결과:수HMGB1작용농도적증가화작용시간적연장,VEGF적표체화분비정상승추세(P균<0.05),단세포활력무명현개변(P균>0.05)。 HMGB1자격증가료16HBE세포VEGF적표체화분비,SB-202190궤호완전억제료HMGB1유도적VEGF적표체화분비( P균<0.05)。결론:HMGB1가능통과P38 MAPK통로개도지기관상피세포VEGF적표체화분비。
Aim:To investigate the effect of high-mobility group protein B1( HMGB1) on the expression and secretion of vascular endothelial growth factor (VEGF) in human bronchial epithelial cell line 16HBE and mechanism underlying this process.Methods:16HBE cells were allocated into different groups according to the following methods .1)different con-centrations:16HBE cells were coincubated with different concentrations of HMGB 1(0, 100, 500, 2 000 μg/L).2)differ-ent intervention time:16HBE cells were incubated with HMGB1 at 2 000 μg/L for 6, 12, 24h, respectively.MTT assay was used to assess the viability of 16HBE cells.The expression of VEGF mRNA was determined by real-time PCR and the level of VEGF in the supernatant was determined by ELISA .The effect of P38 MAPK pathway on HMGB-induced expres-sion and secretion of VEGF was analyzed by use of a special inhibitor ,SB-202190 .Results:The expression and secretion of VEGF had an increasing tendency with the increase of concentration and treatment time of HMGB 1(P<0.05), but there was no obvious changes in 16HBE viability.P38 inhibitor SB-202190 abolished the HMGB1-induced VEGF expression and secretion(P<0.05).Conclusion:HMGB1 increases VEGF expression and secretion via a P 38 MAPK-dependent pathway in bronchial epithelial cells .