中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (15): 2780-2784.doi: 10.3969/j.issn.1673-8225.2012.15.026

• 组织构建细胞学实验 cytology experiments in tissue construction • 上一篇    下一篇

过氧化物酶体增殖物激活受体γ激动剂对大鼠脊髓损伤后细胞自噬的影响★

黄  晨，陈  练，施  勤，杨惠林   

  1. 苏州大学附属第一医院骨科，江苏省苏州市   215006
  • 收稿日期:2011-11-30 修回日期:2012-01-21 出版日期:2012-04-08 发布日期:2012-04-08
  • 通讯作者: 杨惠林，教授，博士，苏州大学附属第一医院骨科，江苏省苏州市 215006
  • 作者简介:黄晨★，女，1985年生，山东省济南市人，汉族，2008年纽卡斯尔大学毕业，硕士，研究实习员，主要从事脊髓基础研究。Huangchen131@hotmail.com

Effect of peroxisome proliferator activated receptor gamma agonists on cell autophagy after spinal cord injury in rats 

Huang Chen, Chen Lian, Shi Qin, Yang Hui-lin   

  1. Department of Orthopaedics, First Affiliated Hospital of Soochow University, Suzhou  215006, Jiangsu Province, China
  • Received:2011-11-30 Revised:2012-01-21 Online:2012-04-08 Published:2012-04-08
  • Contact: Yang Hui-lin, Doctor, Professor, Department of Orthopaedics, First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China
  • About author:Huang Chen★, Master, Department of Orthopaedics, First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China Huangchen131@hotmail.com

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摘要：

背景：过氧化物酶体增殖物激活受体γ受体激动剂具有抗炎和抑制神经凋亡保护作用，能在一定程度上保护脊髓神经元，对脊髓损伤后细胞自噬应激调控等产生影响。
目的：观察过氧化物酶体增殖物激活受体γ对大鼠脊髓损伤后细胞自噬的影响。
方法：将60只SD大鼠分为3组，正常对照组仅做椎板切除，不损伤脊髓，腹腔注射生理盐水；其余大鼠以改良Allen法制作大鼠脊髓损伤模型，过氧化物酶体增殖物激活受体γ组腹腔注射罗格列酮；脊髓损伤组不做处理。损伤后1，3，7，       14 d为时间点并取材，对脊髓损伤区分别进行免疫组织化学法检测，并以Western Blot法检测Beclin 1/Bcl-2的表达变化，同时采用BBB评分方法观察神经功能恢复情况。
结果与结论：大鼠脊髓损伤后第3~14天，过氧化物酶体增殖物激活受体γ组BBB 评分显著高于脊髓损伤组(P < 0.05)。脊髓损伤组和过氧化物酶体增殖物激活受体γ组均见自噬相关阳性细胞表达，过氧化物酶体增殖物激活受体γ组细胞自噬程度相对降低，Beclin 1表达较脊髓损伤组降低(P < 0.05)，Bcl-2表达较脊髓损伤组明显增加(P < 0.05)，神经功能增强(P < 0.05)。提示过氧化物酶体增殖物激活受体γ激动剂在一定程度上降低大鼠脊髓损伤后细胞自噬，对细胞凋亡产生拮抗作用，并在一定程度上可促进神经功能的恢复。
关键词：过氧化物酶体增殖物激活受体γ；脊髓损伤；自噬；大鼠；神经功能
缩略语注释：PPARγ：Peroxisome proliferator activated receptor，过氧化物酶体增殖物激活受体γ
doi:10.3969/j.issn.1673-8225.2012.15.026

关键词: 过氧化物酶体增殖物激活受体&gamma, 脊髓损伤, 自噬, 大鼠, 神经功能

Abstract:

BACKGROUND: Peroxisome proliferator activated receptor γ (PPARγ) agonists have significant anti-inflammatory effects and present as the important mediator in protecting neurons and regulating cell autopagy after spinal cord injury.
OBJECTIVE: To investigate the effect of PPAR γ agonists on the cell autophagy following spinal cord injury in rats．
METHODS: Sixty SD rats were selected, and they were evenly divided into three groups: normal control group, PPARγ agonists group, and spinal cord injury group. Rats in the normal control group did not suffer from spinal cord injury and only received vertebrae plate resection followed by intraperitoneal injection of normal saline injection. Spinal cord injury models were prepared in the PPARγ agonists group and spinal cord injury groups using the improved Allen method. Meanwhile, PPARγ agonists group were intraperitoneally injected with rosiglitazone, and the spinal cord injury group received no treatment. Sample collection of the three groups was performed for immunohistochemical analysis at 1, 3, 7, 14 days after spinal cord injury. Beclin 1 and Bcl-2 expression was detected with the western blotting method, and the neurological function recovery of the spinal cord was also evaluated by Basso, Beattie and Bresnahan score．
RESULTS AND CONCLUSION: Basso, Beattie and Bresnahan score in the PPARγ agonists group was significantly higher than that in the spinal cord injury group at 3-14 days after spinal cord injury (P < 0.05). The positive cells related to autophagy were found in the spinal cord injury and PPARγ agonists groups, and the degree of autophagy was relatively decreased in the PPARγ agonists group (P < 0.05). Compared with the spinal cord injury group, beclin 1 expression was decreased and Bcl-2 expression was increased as well as the neurological function was improved in the PPARγ agonists group (P < 0.05). These findings suggest that PPARγ agonists can decrease cell autophagy to some extent and have an antagonistic on apoptosis to promote the recovery of neurological function to some extent.

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