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挤压伤大鼠血清对血管内皮细胞凋亡的作用及机制探讨
引用本文:Liu SP,Luo B,Li ZH,Liu XS. 挤压伤大鼠血清对血管内皮细胞凋亡的作用及机制探讨[J]. 法医学杂志, 2007, 23(6): 409-410,413
作者姓名:Liu SP  Luo B  Li ZH  Liu XS
作者单位:中山大学中山医学院法医病理学教研室,广东,广州,510080
基金项目:广东省自然科学基金资助项目(05300606)
摘    要:目的观察挤压伤大鼠血清对血管内皮细胞凋亡的影响及可能机制。方法培养小牛主动脉内皮细胞,观察挤压伤大鼠血清对培养的血管内皮细胞凋亡及胞内钙浓度的影响,并检测血浆内皮素-1(endothelin-1,ET-1)及心钠素(atrial natriuretic peptide,ANP)的含量。结果与正常大鼠血清相比,挤压伤大鼠血清致细胞的凋亡百分数由(8.26±1.75)%降为(2.75±0.90)%,胞内钙浓度由(96.98±3.95)nmol/L增加到(118.79±3.22)nmol/L,挤压伤大鼠血浆内皮素-1和心钠素含量显著增高。结论肢体挤压伤大鼠血清可抑制血管内皮细胞的凋亡,此效应可能与内皮素-1和心钠素诱发胞内钙浓度增加有关。

关 键 词:挤压  损伤  血管内皮细胞  凋亡
文章编号:1004-5619(2007)06-0409-02
修稿时间:2007-01-29

Effects of serum from crush injury rats on vascular endothelial cell apoptosis and their potential mechanism
Liu Shui-Ping,Luo Bin,Li Zhao-Hui,Liu Xiao-Shan. Effects of serum from crush injury rats on vascular endothelial cell apoptosis and their potential mechanism[J]. Journal of Forensic Medicine, 2007, 23(6): 409-410,413
Authors:Liu Shui-Ping  Luo Bin  Li Zhao-Hui  Liu Xiao-Shan
Affiliation:Department of Forensic Pathology, Zhongshan Medical School of Sun Yat-sen University, Guangzhou, China. liushp@mail.sysu.edu.cn
Abstract:OBJECTIVE: To investigate the effects of serum from crush injury rats on vascular endothelial cell apoptosis and their potential mechanism. METHODS: Bovine aorta endothelial cells were cultured in vitro and the effects of serum from crush injury rats on cell apoptosis and intracellular calcium concentration ([Ca2+]i) were observed. Meanwhile, the levels of rat blood plasma endothelin-1 (ET-1) and atrial natriuretic peptide(ANP) were measured. RESULTS: Compared with normal rat serum treatment, the cell apoptosis rate decreased from (8.26+/-1.75)% to (2.75+/-0.90)%, while the concentration of [Ca2+]i increased from (96.98+/-3.95) to (118.79+/-3.22) nmol/L in serum from crush injury rats, respectively. The concentration of ET-1 and ANP increased significantly in crush injury rat serum. CONCLUSION: Serum from crush injury rats could inhibit apoptosis of the vascular endothelial cells. These effects may be related to increased level of [Ca2+]i mediated by ET-1 and ANP.
Keywords:crush  injury  vascular endothelial cell  apoptosis
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