基础医学与临床
基礎醫學與臨床
기출의학여림상
Basic & Clinical Medicine
2015年
10期
1346-1350
,共5页
黄海良%丁伟伟%张胜权%罗欣
黃海良%丁偉偉%張勝權%囉訢
황해량%정위위%장성권%라흔
白细胞介素-31%16HBE%血管内皮生长因子%细胞表皮生长因子%P38 MAPK%JNK
白細胞介素-31%16HBE%血管內皮生長因子%細胞錶皮生長因子%P38 MAPK%JNK
백세포개소-31%16HBE%혈관내피생장인자%세포표피생장인자%P38 MAPK%JNK
IL-31%16HBE%VEGF%EGF%P38 MAPK%JNK
目的:探讨IL-31对16HBE细胞VEGF、EGF和EGFR表达的影响及作用机制。方法 IL-31单独及分别联合P38 MAPK信号阻断剂SB203580或JNK信号阻断剂SP600125处理16HBE细胞,分别用real-time PCR和Western blot检测VEGF、EGF和EGFR mRNA及蛋白表达水平;采取Western blot分别检测P38 MAPK和JNK的磷酸化表达水平。结果与对照组相比,IL-31显著上调VEGF、EGF和EGFR mRNA和蛋白的表达( P<0.01),并且能显著上调P38 MAPK和JNK的磷酸化表达(P<0.01)。与IL-31组相比,IL-31+SB203580或SB203580组p-P38 MAPK的表达水平均明显下降(P<0.01),而IL-31+SP600125或SP600125组p-JNK的表达水平均明显下降(P<0.01)。与IL-31组相比,IL-31联合SB203580或SP600125组VEGF的表达均明显下降( P<0.01),而EGF和EGFR的表达在IL-31联合SB203580组显著下降(P<0.01)。结论 IL-31可通过激活P38 MAPK及JNK信号通路而诱导VEGF表达;而IL-31诱导的EGF和EGFR表达则主要通过P38 MAPK信号通路介导。
目的:探討IL-31對16HBE細胞VEGF、EGF和EGFR錶達的影響及作用機製。方法 IL-31單獨及分彆聯閤P38 MAPK信號阻斷劑SB203580或JNK信號阻斷劑SP600125處理16HBE細胞,分彆用real-time PCR和Western blot檢測VEGF、EGF和EGFR mRNA及蛋白錶達水平;採取Western blot分彆檢測P38 MAPK和JNK的燐痠化錶達水平。結果與對照組相比,IL-31顯著上調VEGF、EGF和EGFR mRNA和蛋白的錶達( P<0.01),併且能顯著上調P38 MAPK和JNK的燐痠化錶達(P<0.01)。與IL-31組相比,IL-31+SB203580或SB203580組p-P38 MAPK的錶達水平均明顯下降(P<0.01),而IL-31+SP600125或SP600125組p-JNK的錶達水平均明顯下降(P<0.01)。與IL-31組相比,IL-31聯閤SB203580或SP600125組VEGF的錶達均明顯下降( P<0.01),而EGF和EGFR的錶達在IL-31聯閤SB203580組顯著下降(P<0.01)。結論 IL-31可通過激活P38 MAPK及JNK信號通路而誘導VEGF錶達;而IL-31誘導的EGF和EGFR錶達則主要通過P38 MAPK信號通路介導。
목적:탐토IL-31대16HBE세포VEGF、EGF화EGFR표체적영향급작용궤제。방법 IL-31단독급분별연합P38 MAPK신호조단제SB203580혹JNK신호조단제SP600125처리16HBE세포,분별용real-time PCR화Western blot검측VEGF、EGF화EGFR mRNA급단백표체수평;채취Western blot분별검측P38 MAPK화JNK적린산화표체수평。결과여대조조상비,IL-31현저상조VEGF、EGF화EGFR mRNA화단백적표체( P<0.01),병차능현저상조P38 MAPK화JNK적린산화표체(P<0.01)。여IL-31조상비,IL-31+SB203580혹SB203580조p-P38 MAPK적표체수평균명현하강(P<0.01),이IL-31+SP600125혹SP600125조p-JNK적표체수평균명현하강(P<0.01)。여IL-31조상비,IL-31연합SB203580혹SP600125조VEGF적표체균명현하강( P<0.01),이EGF화EGFR적표체재IL-31연합SB203580조현저하강(P<0.01)。결론 IL-31가통과격활P38 MAPK급JNK신호통로이유도VEGF표체;이IL-31유도적EGF화EGFR표체칙주요통과P38 MAPK신호통로개도。
Objective_To explore the influence and mechanism of IL-31 on the expression of VEGF, EGF and EG-FR in 16HBE cells.Methods_16HBE cells were cultured and treated with IL-31 with or without SB203580 or SP600125, real-time PCR and Western blot were applied to determine the mRNA and protein expression of VEGF, EGF and EGFR respectively.Meanwhile, Western blot was used to examine the changes of P38 MAPK and JNK signaling pathways.Results_Compared with control group, the mRNA expression of VEGF, EGF and EGFR was increased markedly under the stimulation of IL-31 ( P<0.01 ) , the expression of p-P38 MAPK and p-JNK signifi-cantly increased ( P<0.01) .Compared with IL-31 group, the expression of p-P38 MAPK significantly decreased in IL-31 combined with SB203580 or SB203580 group ( P <0.01 ) , while the expression of p-JNK markedly decreased in IL-31 combined with SP600125 or SP600125 group( P<0.01) .Compared with IL-31 group, the expression of VEGF was significantly decreased in IL-31 combined with SB203580 or SP600125 group ( P <0.01 ) , while the expression of EGF and EGFR was markedly declined in IL-31 combined with SB203580 group ( P<0.01 ) .Conclusions_IL-31 may up-regulate the expression of VEGF through activating P38 MAPK and JNK signaling pathways and up-regulate the expression of EGF and EGFR through activating P38 MAPK signaling path-way in16 HBE cells.