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机构地区:[1]山东大学附属省立医院神经内科,山东济南250021
出 处:《中国老年学杂志》2009年第8期935-937,共3页Chinese Journal of Gerontology
基 金:山东省科技攻关计划项目(2006GG2202036)
摘 要:目的观察亚低温对缺氧/复氧内皮细胞胞间黏附分子-1(ICAM-1)表达和黏附率的影响。方法以ECV304内皮细胞为研究对象,利用简易缺氧室,以缺氧模拟体内缺血性损伤,建立缺氧/复氧内皮细胞模型。将细胞分为33℃及37℃缺氧/复氧组。各组又分为缺氧6,12,18h后再复氧6h3个亚组。应用Western印迹检测两组各亚组ICAM-1的表达并应用细胞计数法检测各亚组细胞和中性粒细胞(PMN)的黏附率。结果①在缺氧6,12,18h亚组,37℃组内皮细胞表达ICAM-1的积分光密度值明显高于33℃组〔(0.185±0.026)vs(0.120±0.064)、(0.329±0.057)vs(0.218±0.027)、(0.443±0.068)vs(0.326±0.019)〕(P均<0.05)。②在缺氧6,12,18h亚组,33℃组内皮细胞和中性粒细胞的黏附率明显高于37℃组〔(29.41±1.77)%vs(22.30±3.25)%、(43.66±2.57)%vs(34.51±5.06)%、(62.92±4.82)%vs(49.68±4.34)%〕(P<0.05)。结论亚低温能有效抑制缺氧/复氧内皮细胞与中性粒细胞的黏附,其机制可能与降低缺氧/复氧内皮细胞ICAM-1的表达有关。Objective To observe the influence of mild hypothermia on expression of intercellular adhesion molecule (ICAM) -1 and adhesive properties of hypoxia/reoxygenation (H/R)-stimulated endothelial cells. Methods ECV304 endothelial cells were selected as object, simple and anoxie box was used to imitate the model of isehemia induced injure and to build the model of H/R-stimulated endothelial cells. The cells were divided into 33℃ and 37℃ groups. Then each group was divided into three subgroups: hypoxia for 6,12 and 18 h and then reoxygenation for 6 h. Western blot is used to detect the expression of ICAM-1 of each subgroup of two groups ; and cell count was used to investigate adhesive properties of each subgroup between H/R-stimulated endothelial ceils and PMN. Results (1)Hypoxia for 6, 12 and 18 h, the integral absorbance values of ICAM-1 protein in 37℃ group were obviously higher than those in 33℃ group [ (0. 185±0. 026) vs (0. 120±0.064) ,(0. 329±0.057) vs (0.218±0.027), (0.443±0.068) vs (0. 326±0.019)] (P 〈0.05). (2)Hypoxia for 6, 12 and 18 h, the cell adhesive properties between H/R-stimulated endothelial cells and PNM in 33℃ group were significantly higher than those in 37℃ group [(29.41±1.77)%vs (22.30±3.25)%, (43.66 ±2.57)% vs (34.51 ±5.06)%, (62.92 ±4.82)% vs (49.68 ± 4. 34) % ] ( P 〈 0. 05 ). Conclusions Mild hypothermia can effectively restrain the adhesion between H/R-stimulated endothelial cells and PMN, and mechanism of which may be related to decreasing the expression of ICAM-1 of H/R-stimulated endothelial cells.
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