中华小儿外科杂志
中華小兒外科雜誌
중화소인외과잡지
Chinese Journal of Pediatric Surgery
2015年
9期
671-674
,共4页
彭岗%俞松%陆建国%闫陶然%卓金伟%柳望舒%徐艳朋
彭崗%俞鬆%陸建國%閆陶然%卓金偉%柳望舒%徐豔朋
팽강%유송%륙건국%염도연%탁금위%류망서%서염붕
血管瘤%模型,动物%信号传递%基因表达调控
血管瘤%模型,動物%信號傳遞%基因錶達調控
혈관류%모형,동물%신호전체%기인표체조공
Hemangioma%Models,animal%Signal transduction%Gene expression regulation
目的 观察人血管瘤裸鼠移植模型中PI3Kp85、p-Akt表达,并进行正负调控,探讨PI3K/Akt信号通路在小儿血管瘤演变过程中的作用.方法 建立血管瘤裸鼠移植模型,生长45 d后,将移植成功标本48例,按区组随机平均分成3组.其中,对照组每个瘤体内注射生理盐水0.05 ml;正性调控组每个瘤体内注射0.5μmol/L的胰岛素样生长因子0.05 ml;负性调控组每个瘤体内注射25μmol/L的LY294002 0.05 ml.于药物注射当日(用药前)、注射后3d、1周、2周肉眼大体观察移植瘤形态变化,光镜观察移植瘤组织结构变化,同期免疫组化检测PI3Kp85、p-Akt蛋白的分布及表达情况,RT-PCR检测PI3Kp85 mRNA、p-Akt mRNA的表达情况.结果 负性调控组PI3Kp85、p-Akt阳性表达率分别为80.00％和86.67％,而对照组及正性调控组PBKp85及p-Akt阳性表达率均为100％.负性调控组PI3Kp85、p-Akt表达均较对照组降低,差异有统计学意义(P＜0.05或0.01),瘤体呈消退表现;正性调控组PI3Kp85、p-Akt表达均较对照组增高,差异有统计学意义(P＜0.05或0.01),血管瘤瘤体呈增生表现;PI3Kp85与p-Akt的表达呈正相关.结论 PI3K/Akt信号通路可能参与了裸鼠移植血管瘤增生与消退的调控;LY294002、胰岛素样生长因子可以通过干预PI3K/Akt信号通路中相应的靶点,抑制或激活PI3K/Akt信号通路来促使瘤体消退及增生.
目的 觀察人血管瘤裸鼠移植模型中PI3Kp85、p-Akt錶達,併進行正負調控,探討PI3K/Akt信號通路在小兒血管瘤縯變過程中的作用.方法 建立血管瘤裸鼠移植模型,生長45 d後,將移植成功標本48例,按區組隨機平均分成3組.其中,對照組每箇瘤體內註射生理鹽水0.05 ml;正性調控組每箇瘤體內註射0.5μmol/L的胰島素樣生長因子0.05 ml;負性調控組每箇瘤體內註射25μmol/L的LY294002 0.05 ml.于藥物註射噹日(用藥前)、註射後3d、1週、2週肉眼大體觀察移植瘤形態變化,光鏡觀察移植瘤組織結構變化,同期免疫組化檢測PI3Kp85、p-Akt蛋白的分佈及錶達情況,RT-PCR檢測PI3Kp85 mRNA、p-Akt mRNA的錶達情況.結果 負性調控組PI3Kp85、p-Akt暘性錶達率分彆為80.00％和86.67％,而對照組及正性調控組PBKp85及p-Akt暘性錶達率均為100％.負性調控組PI3Kp85、p-Akt錶達均較對照組降低,差異有統計學意義(P＜0.05或0.01),瘤體呈消退錶現;正性調控組PI3Kp85、p-Akt錶達均較對照組增高,差異有統計學意義(P＜0.05或0.01),血管瘤瘤體呈增生錶現;PI3Kp85與p-Akt的錶達呈正相關.結論 PI3K/Akt信號通路可能參與瞭裸鼠移植血管瘤增生與消退的調控;LY294002、胰島素樣生長因子可以通過榦預PI3K/Akt信號通路中相應的靶點,抑製或激活PI3K/Akt信號通路來促使瘤體消退及增生.
목적 관찰인혈관류라서이식모형중PI3Kp85、p-Akt표체,병진행정부조공,탐토PI3K/Akt신호통로재소인혈관류연변과정중적작용.방법 건립혈관류라서이식모형,생장45 d후,장이식성공표본48례,안구조수궤평균분성3조.기중,대조조매개류체내주사생리염수0.05 ml;정성조공조매개류체내주사0.5μmol/L적이도소양생장인자0.05 ml;부성조공조매개류체내주사25μmol/L적LY294002 0.05 ml.우약물주사당일(용약전)、주사후3d、1주、2주육안대체관찰이식류형태변화,광경관찰이식류조직결구변화,동기면역조화검측PI3Kp85、p-Akt단백적분포급표체정황,RT-PCR검측PI3Kp85 mRNA、p-Akt mRNA적표체정황.결과 부성조공조PI3Kp85、p-Akt양성표체솔분별위80.00％화86.67％,이대조조급정성조공조PBKp85급p-Akt양성표체솔균위100％.부성조공조PI3Kp85、p-Akt표체균교대조조강저,차이유통계학의의(P＜0.05혹0.01),류체정소퇴표현;정성조공조PI3Kp85、p-Akt표체균교대조조증고,차이유통계학의의(P＜0.05혹0.01),혈관류류체정증생표현;PI3Kp85여p-Akt적표체정정상관.결론 PI3K/Akt신호통로가능삼여료라서이식혈관류증생여소퇴적조공;LY294002、이도소양생장인자가이통과간예PI3K/Akt신호통로중상응적파점,억제혹격활PI3K/Akt신호통로래촉사류체소퇴급증생.
Objective To explore the expressions of phosphatidylinositol 3-kinase p85 (PI3Kp85) and protein kinase B (Akt) in nude mice model of human hemangioma xenograft and examine the role of PI3K/ Akt signaling pathway in evolution process of hemangioma in children.Methods The surgical specimem of proliferating hemangioma were harvested from a male 3-month-old infant.The tissues were sliced into small pieces 5 mm 4 mm 3 mm in size and grafted subcutaneously into nude mice.After growing for 45 days, a total of 48 cases of successful xenograft specimens were randomized into 3 groups: 0.05 ml saline was imratumorally injected for each tumor in control group, 0.05 ml insulin-like growth factor (0.5 μmol/L)intratumorally injected for each tumor in positive contml group and 0.05 ml LY294002 (25 μmol/L) was imratumorally injected for each tumor in negative contml group.At the day of injection and 3 days, 1 week and 2 weeks post-injection, the morphological changes of hemangioma xenografts were visually observed and their structural changes observed micmscopically.The expressions of PBKp85, p-Akt protein were determined by immunohistochemistry.And the expressions of PDKp85 mRNA and p-Aktm RNA were observed by reverse transcription-polymerase chain reaction (RT-PCR).Results The positive expression rates of PI3Kp85 and p-Akt were 100％ in control and positive control groups.And the positive expression rates were 80.00％ and 86.67％ in negative control group.The stains of PBKp85 and p-Akt became weakersignificantly in negative control group.And significant differences in PBKp85 and p-Akt stains existed between negative control and control groups (P ＜ 0.05 or 0.01) and then xenograft specimens showed regression.The stains of PI3Kp85 and p-Akt turned stronger significantly in positive control group.Significant differences of PBKp85 and p-Akt stains existed between positive control and control groups(P＜ 0.05 or 0.01).The xenograft specimens showed proliferation.And the expression levels of PI3Kp85 and pAkt had positive correlations.Conclusions PI3K/Akt signal pathway is probably participating in regulating the apoptosis of hemangioma endothelial cells in nude mice model with human hemangioma xenograft.And LY294002 and insulin-like growth factor may induce tumor regression and pmliferation by intervening the corresponding targets in PBK/Akt signaling pathway.
