中国糖尿病杂志
中國糖尿病雜誌
중국당뇨병잡지
CHINESE JOURNAL OF DIABETES
2011年
5期
361-365
,共5页
汤日宁%戴厚永%李青%吕林莉%张建东%马坤岭%刘必成
湯日寧%戴厚永%李青%呂林莉%張建東%馬坤嶺%劉必成
탕일저%대후영%리청%려림리%장건동%마곤령%류필성
高糖%内皮细胞转分化%血管紧张素Ⅱ%厄贝沙坦
高糖%內皮細胞轉分化%血管緊張素Ⅱ%阨貝沙坦
고당%내피세포전분화%혈관긴장소Ⅱ%액패사탄
High glucose%Endothelial-to-mesenchymal transition% Angiotensin Ⅱ% Irbesartan
目的 探讨高糖对内皮细胞转分化的影响及其与血管紧张素Ⅱ(ATⅡ)的关系.方法 将人主动脉内皮细胞分成正常浓度葡萄糖(NG)组、高糖(HG)组和厄贝沙坦干预(HG+Irb)组.放射免疫法检测细胞上清液中ATⅡ的浓度.共聚焦显微镜观察CD31和成纤维细胞特异蛋白1(FSP1)的双染色结果.Western blot检测FSP1蛋白水平的表达.结果 与NG组比,高糖刺激的内皮细胞导致ATⅡ和FSP1表达增加(P<0.05),呈浓度和时间依赖性.共聚焦显微镜可见CD31和FSP1表达重叠,且一些细胞获得纺锤样的改变并失去CD31染色.厄贝沙坦可抑制高糖引起的上述改变(P<0.05).结论 高糖可能通过ATⅡ介导的内皮细胞转分化导致内皮细胞损伤,而厄贝沙坦抑制内皮细胞转分化.
目的 探討高糖對內皮細胞轉分化的影響及其與血管緊張素Ⅱ(ATⅡ)的關繫.方法 將人主動脈內皮細胞分成正常濃度葡萄糖(NG)組、高糖(HG)組和阨貝沙坦榦預(HG+Irb)組.放射免疫法檢測細胞上清液中ATⅡ的濃度.共聚焦顯微鏡觀察CD31和成纖維細胞特異蛋白1(FSP1)的雙染色結果.Western blot檢測FSP1蛋白水平的錶達.結果 與NG組比,高糖刺激的內皮細胞導緻ATⅡ和FSP1錶達增加(P<0.05),呈濃度和時間依賴性.共聚焦顯微鏡可見CD31和FSP1錶達重疊,且一些細胞穫得紡錘樣的改變併失去CD31染色.阨貝沙坦可抑製高糖引起的上述改變(P<0.05).結論 高糖可能通過ATⅡ介導的內皮細胞轉分化導緻內皮細胞損傷,而阨貝沙坦抑製內皮細胞轉分化.
목적 탐토고당대내피세포전분화적영향급기여혈관긴장소Ⅱ(ATⅡ)적관계.방법 장인주동맥내피세포분성정상농도포도당(NG)조、고당(HG)조화액패사탄간예(HG+Irb)조.방사면역법검측세포상청액중ATⅡ적농도.공취초현미경관찰CD31화성섬유세포특이단백1(FSP1)적쌍염색결과.Western blot검측FSP1단백수평적표체.결과 여NG조비,고당자격적내피세포도치ATⅡ화FSP1표체증가(P<0.05),정농도화시간의뢰성.공취초현미경가견CD31화FSP1표체중첩,차일사세포획득방추양적개변병실거CD31염색.액패사탄가억제고당인기적상술개변(P<0.05).결론 고당가능통과ATⅡ개도적내피세포전분화도치내피세포손상,이액패사탄억제내피세포전분화.
Objective The aim was to investigate the influence of high glucose on endothelial to mesenchymal transition (EndMT) and its relevance with the activation of angiotensin Ⅱ. Methods Human aortic endothelial cells (HAEC) were divided into three groups: normal glucose group (NG), high glucose group (HG) and the Irbesartan (1μmol/L) treated group. The concentration of angiotensin Ⅱ in the HAEC supernatant was detected by radioimmunoassay. Immunofluorescence staining was performed to detect the co-expression of CD31 and fibroblast specific protein1 (FSP1). Results HG led to a significant increase of expression of angiotensin Ⅱ and FSP1 protein in HAEC in dose and time dependent manner. Double staining of HAEC showed co-localization of CD31 and FSP1. These changes were inhibited by treatment with irbesartan (P<0.05). Conclusion These findings suggest a novel mechanism on the high glucose HG induced endothelial damage through angiotensin II mediated EndMT, which is inhibited by irbesartan.