大鼠椎间盘累积损伤性炎症反应中大麻素水解酶——FAAH、NAAA表达及意义的初步研究
A preliminary study of the expression and significance of CB hydrolyses FAAH and NAAA in bone and disc inflammation due to cumulative damage in rats
  
DOI:10.3969/j.issn.1006-7108.2015.06.009
中文关键词:  骨骼椎间盘炎症反应  累积性损伤  大麻素  N-乙酰基乙醇胺水解酸性酰胺酶  脂肪酸酰胺水解酶  动物实验研究
英文关键词:Bone and disc inflammation  Cumulative damage  Cannabinoids  FAAH  NAAA  Animal experimental study
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作者单位
梁峰* 刘振宁 谭树森 贾长青 柏树令 中国医科大学附属盛京医院脊柱关节骨科沈阳 110004 
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中文摘要:
      目的 本研究试图通过检测大麻素(CB)的两种主要水解酶——N-乙酰基乙醇胺水解酸性酰胺酶(NAAA)、脂肪酸酰胺水解酶(FAAH)在鼠累积损伤性椎间盘炎症反应过程中的表达来初步揭示其中大麻素的参与过程及作用机制。方法 清洁级Wistar大鼠随即分成实验组与对照组,根据Jill A. Ulrich制作方法准备实验组,以切皮后即缝合为对照组,在术后第3、7、10天,实验组与对照组每次各取6只,取出相应椎间盘,进行形态学观察,应用Real Time-PCR技术检测 FAAH、NAAA的表达水平。结果 与对照组相比,实验10d组可见刺伤所致纤维环断裂,髓核内出血。在椎间盘累积性损伤7d时, NAAA和FAAH表达含量分别约为对照组的3倍,并形成高峰;而在损伤10d后,其表达量呈减少趋势。结论 作为水解酶的底物CB类物质在第7天时候表达含量呈低谷,而随着时间的延长逐渐增高。CB类物质参与了炎症反应的发展过程,从而抑制骨骼椎间盘的退变。
英文摘要:
      Objective To reveal the function of CB during disc inflammation due to cumulative damage through detecting the expression level of the key hydrolyses of CB FAAH and NAAA. Methods Wister rats were randomly divided into two groups. Rats in the experimental group were prepared according to Jill A. Ulrich's method. Control group followed skin cut and close method. Six rats were collected from each group at the 3nd, 7th, and 10th day after the operation. The corresponding intervertebral disc was removed. Morphology was observed. The expression levels of FAAH and NAAA were detected using real-time PCR method. Results Compared to the control group, the rupture and nucleus bleeding were observed in 10 days in experimental group. At the 7th day after cumulative damage to the disc, NAAA and FAAH expression levels reached a peak at approximately 3 times over the control group. The expression decreased after 10 days of the injury. Conclusion As a substrate for the hydrolysis enzyme, CB expresses at a bottom level at the 7th day postoperatively, but it gradually increases over the later time. CB is involved in the inflammative reaction and leads to the inhibition of th disc degeneration.
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