《中国康复理论与实践》

《中国康复理论与实践》

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丁苯酞注射液对局灶性脑缺血再灌注大鼠的脑保护作用及机制①

赵秀芹1，毛文静1，李世英1，张晋霞1，贺永贵1，余红2，刘斌1   

  1. 1.华北理工大学附属医院神经内科，河北唐山市063000；2.华北理工大学基础医学院，河北唐山市063000。
  • 出版日期:2016-01-25 发布日期:2016-05-23

Effect of Butylphthalide Injection on Neural Protection in Focal Cerebral Ischemia-reperfusion Rats

ZHAO Xiu-qin1, MAO Wen-jing1, LI Shi-ying1, ZHANG Jin-xia1, HE Yong-gui1, YU Hong2, LIU Bin1   

  1. 1. Department of Neurology, Hospital Affiliated to North China University of Science and Technology, Tangshan, Hebei 063000, China; 2. Basic Medical College of North China University of Science and Technology, Tangshan, Hebei 063000, China
  • Published:2016-01-25 Online:2016-05-23

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摘要： 目的探讨丁苯酞对局灶性脑缺血再灌注大鼠的脑保护机制。方法160 只雄性Sprague-Dawley 大鼠随机分为假手术组(Sham组, n=10)、缺血再灌注组(IR 组, n=50)、丁苯酞高剂量后处理组(高剂量组, n=50)、丁苯酞中剂量后处理组(中剂量组, n=25)和丁苯酞低剂量后处理组(低剂量组, n=25)。后4 组线栓法制作缺血2 h 再灌注模型。Sham组术后24 h 处死，其他各组分别于再灌注6 h、12 h、24 h、48 h、72 h 处死，5 只用于应用原位末端标记(TUNEL)法检测细胞凋亡，免疫组织化学染色法观察沉默信息调节因子2 相关酶1(SIRT1)及过氧化物酶体增殖物激活受体γ辅激活因子1α (PGC-1α)的表达。Sham组、IR 组及高剂量组另5 只用实时荧光定量PCR检测SIRT1 及PGC-1α的表达。结果与IR 组比较，丁苯酞各剂量组各时间点凋亡细胞数均显著减少(F>160.60,P<0.001)，SIRT1、PGC-1α阳性细胞数显著增多(F>87.20, P<0.001)。与低、中剂量组比较，高剂量组各时间点凋亡细胞数更少(P<0.05)，SIRT1、PGC-1α阳性细胞数更多(P<0.05)，低、中剂量组之间除再灌注6 h 外，也有显著性差异(P<0.05)。与IR 组比较，高剂量组各时间点SIRT1 及PGC-1α mRNA表达均明显增多(t>4.13, P<0.01)。结论丁苯酞能抑制大鼠脑缺血再灌注后细胞凋亡，可能与上调SIRT1 及PGC-1α的表达有关。

关键词: 脑缺血再灌注, 丁苯酞, 凋亡, 沉默信息调节因子2 相关酶1, 过氧化物酶体增殖物激活受体&gamma, 辅激活因子1&alpha

Abstract: Objective To observe the neural protection of 3-n-butylphthalide (NBP) injection in focal cerebral ischemia-reperfusion rats. Methods 160 male Sprague-Dawley rats were randomly divided into sham group (n=10), ischemia- reperfusion group (IR group, n=50), high-dose NBP treatment group (high-dose group, n=50), middle-dose NBP treatment group (middle-dose group, n=25) and low-dose NBP treatment group (low-dose group, n=25). The later 4 groups were occluded the middle cerebral artery for 2 hours and reperfused. The sham group was sacrificed 24 hours after operation, and the other groups at 6, 12, 24, 48 and 72 hours after reperfusion, in which 5 of them were stained with TdT mediated dUTP Nick End Labeling (TUNEL) to observe the neuronal apoptosis, and immunohistochemistry to observe the expression of silent information regulation 2 homolog 1 (SIRT1) and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α); the other 5 of sham group, IR group and high-dose group were observed with quantitative real-time PCR of SIRT1 and PGC-1α. Results Compared with the IR group, the number of apoptotic cells decreased and the SIRT1 and PGC-1α positive cells increased in all NBP groups at each time (F>160.60, P<0.001), and it was the least of apoptotic cells and most of SIRT1 and PGC-1α positive cells in the high-dose group (P<0.05), while there was significant difference between the low-dose group and the middle-dose group, excluding 6 hours after reperfusion (P<0.05). Compared with IR group, the expression of SIRT1 and PGC-1α mRNA increased in the high-dose group at each time (t> 4.13, P<0.01). Conclusion NBP can protect brain from apoptosis in focal cerebral ischemia-reperfusion rats, which may relate to more expression of SIRT1 and PGC-1α.

Key words: cerebral ischemia-reperfuson, Butylphthalide, apoptosis, silent information regulation 2 homolog 1, peroxisome proliferator- activated receptor &gamma, coactivator-1α