中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2013年
41期
7235-7240
,共6页
组织构建%血管组织构建%烟草烟雾提取物%生长反应因子1%GATA-2%基质金属蛋白酶2%血管平滑肌细胞%国家自然科学基金
組織構建%血管組織構建%煙草煙霧提取物%生長反應因子1%GATA-2%基質金屬蛋白酶2%血管平滑肌細胞%國傢自然科學基金
조직구건%혈관조직구건%연초연무제취물%생장반응인자1%GATA-2%기질금속단백매2%혈관평활기세포%국가자연과학기금
plant extracts%matrix metalloproteinase 2%GATA transcription factors%muscle,smooth,vascular
背景：吸烟是动脉粥样硬化形成的主要危险因素之一。目的：观察烟草烟雾提取物对大鼠血管平滑肌细胞中GATA-2浓度的影响及早期生长反应因子1在其中的作用。方法：体外培养大鼠血管平滑肌细胞，用不同浓度(0，5%，10%，20%)烟草烟雾提取物刺激，采用RT-PCR的方法检测烟草烟雾提取物对GATA-2的影响。用筛选出的最适合的烟草烟雾提取物浓度处理大鼠血管平滑肌细胞不同时间(0，4，8，12，24 h)后，检测GATA-2 mRNA的变化，以及加入生长反应因子1抑制剂后GATA-2 mRNA的变化。结果与结论：与0浓度烟草烟雾提取物相比，5%低浓度烟草烟雾提取物刺激后，GATA-2 mRNA表达较10%中浓度和20%高浓度增加的更显著。不加烟草烟雾提取物组即0 h 组血管平滑肌细胞中有少量 GATA-2的mRNA，5%烟草烟雾提取物刺激后于4 h内开始增加，8 h达高峰。加入生长反应因子1抑制剂后5%烟草烟雾提取物诱导的血管平滑肌细胞GATA-2 mRNA表达明显降低。提示烟草烟雾提取物可通过生长反应因子1促进GATA-2增加，抑制生长反应因子1后，GATA-2的表达减少。
揹景：吸煙是動脈粥樣硬化形成的主要危險因素之一。目的：觀察煙草煙霧提取物對大鼠血管平滑肌細胞中GATA-2濃度的影響及早期生長反應因子1在其中的作用。方法：體外培養大鼠血管平滑肌細胞，用不同濃度(0，5%，10%，20%)煙草煙霧提取物刺激，採用RT-PCR的方法檢測煙草煙霧提取物對GATA-2的影響。用篩選齣的最適閤的煙草煙霧提取物濃度處理大鼠血管平滑肌細胞不同時間(0，4，8，12，24 h)後，檢測GATA-2 mRNA的變化，以及加入生長反應因子1抑製劑後GATA-2 mRNA的變化。結果與結論：與0濃度煙草煙霧提取物相比，5%低濃度煙草煙霧提取物刺激後，GATA-2 mRNA錶達較10%中濃度和20%高濃度增加的更顯著。不加煙草煙霧提取物組即0 h 組血管平滑肌細胞中有少量 GATA-2的mRNA，5%煙草煙霧提取物刺激後于4 h內開始增加，8 h達高峰。加入生長反應因子1抑製劑後5%煙草煙霧提取物誘導的血管平滑肌細胞GATA-2 mRNA錶達明顯降低。提示煙草煙霧提取物可通過生長反應因子1促進GATA-2增加，抑製生長反應因子1後，GATA-2的錶達減少。
배경：흡연시동맥죽양경화형성적주요위험인소지일。목적：관찰연초연무제취물대대서혈관평활기세포중GATA-2농도적영향급조기생장반응인자1재기중적작용。방법：체외배양대서혈관평활기세포，용불동농도(0，5%，10%，20%)연초연무제취물자격，채용RT-PCR적방법검측연초연무제취물대GATA-2적영향。용사선출적최괄합적연초연무제취물농도처리대서혈관평활기세포불동시간(0，4，8，12，24 h)후，검측GATA-2 mRNA적변화，이급가입생장반응인자1억제제후GATA-2 mRNA적변화。결과여결론：여0농도연초연무제취물상비，5%저농도연초연무제취물자격후，GATA-2 mRNA표체교10%중농도화20%고농도증가적경현저。불가연초연무제취물조즉0 h 조혈관평활기세포중유소량 GATA-2적mRNA，5%연초연무제취물자격후우4 h내개시증가，8 h체고봉。가입생장반응인자1억제제후5%연초연무제취물유도적혈관평활기세포GATA-2 mRNA표체명현강저。제시연초연무제취물가통과생장반응인자1촉진GATA-2증가，억제생장반응인자1후，GATA-2적표체감소。
BACKGROUND:Smoking is one of the major risk factors for the formation of atherosclerosis. OBJECTIVE:To investigate the effect of cigarette smoke extract on the concentration of GATA-2 in the vascular smooth muscle cells and in which the role of the early growth response factor-1. METHODS:Vascular smooth muscle cells were cultured in vitro. The vascular smooth muscle cells were treated with various concentrations of cigarette smoke extract (0, 5%, 10%, 20%), then the reverse transcription PCR was applied to detect the mRNA expression of GATA-2. The vascular smooth muscle cells were treated with cigarette smoke extracts in the optimal concentration for 0, 4, 8, 12 and 24 hours, and then the expression of GATA-2 mRNA was observed, as wel as the changes of expression of GATA-2 mRNA after added with growth response factor-1. RESULTS AND CONCLUSION:Compared to the 0 concentration group, the expression of GATA-2 mRNA after treated with low concentration (5%) of cigarette smoke extract was increased more significantly than moderate concentration (10%) and high concentration (20%). The vascular smooth muscle cells in 0 hour group expressed GATA-2 mRNA at low level. The GATA-2 mRNA began to increase within 4 hours and reached peak at the 8 hours after stimulated with cigarette smoke extract of 5%concentration. After added with growth response factor-1 inhibitors, the expression of GATA-2 mRNA in 5%cigarette smoke extract induced vascular smooth muscle cells was decreased. Cigarette smoke extract can promote the increasing of GATA-2 by growth response factor-1, while the GATA-2 expression is reduced after the inhibition of growth response factor-1.
