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作 者:景香香[1] 王志刚[1] 李晓东[1] 彭晓琼[1] 杨春江[1] 张群霞[1] 郑元义[1]
机构地区:[1]重庆医科大学超声影像学研究所附属第二医院超声科,重庆市400010
出 处:《中国超声医学杂志》2006年第4期241-243,共3页Chinese Journal of Ultrasound in Medicine
基 金:国家自然科学基金重点(No.30430230);面上项目(No.30370402)
摘 要:目的研究自制“表活显”(self-made surfactant fluorocarbon-filled microbubbles,SFCMB)结合磷脂酰丝氨酸(phospha-tidylserine,PS)后对白细胞的靶向性作用机制。方法流式细胞仪测定白细胞激活前和激活后与SFCMB-PS的结合情况,补体和β2整合素中的Mac-1缺乏时激活的白细胞与SFCMB-PS的结合情况。结果未激活的白细胞与微泡的结合率为(5.27±0.75)%,激活的白细胞与微泡的结合率为(39.67±6.83)%,结合率明显提高(P<0.01);补体和β2整合素中的Mac-1缺乏时,两者的结合明显受到抑制,结合率降到(12.27±1.66)%(P<0.01)和(10.90±2.40)%(P<0.01)。结论SFCMB-PS是通过β2整合素中的Mac-1和补体介导途径与激活的白细胞结合并进入细胞内的。Objective To study the mechanism of self-made surfactant fluorocarbon-filled microbubbles (SFCMB) combined with phosphatidylserine (PS) targeted to activate leukocytes. Methods Flow cytometry detected the attachment of SFCMB-PS targeted to incubated inte inactivated or activated leukocytes and to serous incubated into β2-integrin Mac-1 or complement-deficit leucocytes. Results Flow cytometry results revealed that the conjugation rates of SFCMB-PS to inactivated and activated leukocytes were 5.27±0. 75%, vs 39.67±6.83%, P〈 0. 01 ; the conjugation rates of serous complement and β2-integrin Mac-1 deficit were obviously inhibited and decreased to 12. 27± 1.66% and 10. 90±2.40% respectively. Both rates vs 39.67±6.83% were P〈0. 01. Conclusions The mechanism of SFCMB-PS targeted to activated leukocytes is due to β2-integrin Mac-1 and complement inducement.
分 类 号:R445.1[医药卫生—影像医学与核医学]
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