摘要
目的观察坐骨神经损伤(SNI)后小鼠脑环氧合酶COX-1和2的表达变化。方法①对小鼠施行SNI,分别于SNI前和SNI后1、12 h和1、3、7、14、30、60 d等9个时间点采用热板法测定小鼠的热痛阈。②于SNI前和SNI后1、12h和1、3、7、14、30、60 d等9个时间点分别取脑,放射免疫分析测定脑组织PGF1α(COX-1催化产物)和PGE2(COX-2催化产物)的浓度,RT-PCR和W estern b lot法分别测定COX-1和COX-2 mRNA和蛋白的水平。结果SNI后小鼠热痛阈明显下降(P<0.05)。SNI后14 d PGF1α的浓度明显增高(P<0.05),而PGE2的浓度在3 d时即明显升高(P<0.05)。早期COX-1 mRNA和蛋白的表达均无明显增强,在14 d时才增高,这一增高持续至SNI后60 d(均P<0.05);而COX-2的表达在早期即明显增高,但增高到1 d即开始下降。结论SNI后早期COX-2表达增强,可能与疼痛的维持有关;而后期COX-1表达增强,可能与疼痛的发生有关。
Aim To observe the expression of cyclooxygenase COX-1 and 2 in brain after spared nerve injury （SNI）. Methods Pain thresholds by hot-plate test were determined before, 1 h, d, 30 dand60d to evaluate the after SNI. change of 12h, 1d, 3 d,7 d, 14 Three methods were used brain COX expression after SNI, radioimmunoassay for measurement of PGF1α（catalyzed by COX-1 ） and PGE2 （ catalyzed by COX- 2）, RT-PCR for mRNA and Western blotting for protein. Time points for assay were before SNI, 1 h, 12 h, 1 d, 3 d, 7 d, 14 d, 30 d and 60 d after SNI. Resuits Pain thresholds of mice decreased significantly during the period of 60 d after SNI （ all P 〈 0. 05 ）. The concentration of PGF1α in brain increased significantly at 14 d after SNI while the increase of PGE2 concentration appeared at 3 d after SNI（all P 〈0.05）. The levels of brain COX-1 mRNA and protein didn＇t increasesignificantly until 14 d after SNI, while that of COX-2 increased significantly and rapidly after SNI and reached peak at the time point of 1 d. Conclusion Brain COX-1 is involved in the late phase of neuropathie pain and may play a role in the persistenee of pain, while brain COX-2 is involved in the early phase of neuropathic pain and may play a role in the pain origination.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2006年第1期97-101,共5页
Chinese Pharmacological Bulletin
