Yao Xue, Zeng Fan-xu, Yao Lin, Yan Li-cheng, Wang Miao-maio, Wang Man-man, Hao Yu-lan, Zhang Yan-shu
Department of Toxicology, School of Public Health, Hebei United University, Tangshan, Hebei Province 063000, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2012 Feb;30(2):81-4.
To explore the effects of acrylamide on the permeability of blood cerebrospinal fluid barrier (BCB) and tight junction protein ZO-1 of choroid plexus in rats and to provide a theoretical basis for explaining the mechanism of nerve injury induced by acrylamide.
Thirty two male Sprague-Dawley rats were randomly divided into ACR and control groups. ACR group was exposed to 20 mg/kg ACR daily for 5 days a week by intraperitoneal injection (i.p.) for 4 weeks. Control group was exposed to normal saline. The neurobehavioral tests (including sensatory and motor functions) were performed every week. At the end of exposure, Evan blue (EB) and Sodium fluorescein (NaFI) content in rat CSF were detected for determining the BCB permeability, Real-time PCR was used to measure the expression levels of ZO-1 mRNA in the epithelium cells of choroid plexus, and laser scanning confocal microscope (LSCM) was utilized to observe the distribution of ZO-1 protein.
Neurobehavioral tests showed that the tail-flick latencies of ACR group were 27.77% and 53.71% as long as control group in the 3rd week and 4th week, respectively (P < 0.05). The hind lamb splay distances of ACR group were 131.76% and 153.77% as long as control group in the 3rd week and 4th week, respectively (P < 0.05). Evan blue (EB) and Sodium fluorescein (NaFI) content of ACR group were significantly higher than those of control group (P < 0.05). In the 4th week, the expression level of ZO-1 mRNA in ACR group was 0.21 +/- 0.07, which was significantly lower than that (0.31 +/- 0.11) in control group (P < 0.05). In the 4th week, the ZO-1 protein expression level of choroid plexus in ACR group was significantly lower than that in control group (P < 0.05).
Acrylamide could increased the BCB permeability of rats, which may be involved in the central nervous injury induced by ACR.
探讨丙烯酰胺对大鼠血脑脊液屏障（BCB）通透性及脉络丛紧密连接蛋白ZO-1的影响，为解释丙烯酰胺所致神经损伤机制提供理论依据。
将32只雄性Sprague-Dawley大鼠随机分为丙烯酰胺组（ACR组）和对照组。ACR组每周5天腹腔注射（i.p.）20mg/kg丙烯酰胺，共4周。对照组注射生理盐水。每周进行神经行为学测试（包括感觉和运动功能）。暴露结束时，检测大鼠脑脊液中伊文思蓝（EB）和荧光素钠（NaFI）含量以测定BCB通透性，采用实时荧光定量PCR检测脉络丛上皮细胞中ZO-1 mRNA表达水平，利用激光扫描共聚焦显微镜（LSCM）观察ZO-1蛋白分布。
神经行为学测试显示，ACR组在第3周和第4周的甩尾潜伏期分别为对照组的27.77%和53.71%（P<0.05）。ACR组在第3周和第4周的后肢撑开距离分别为对照组的131.76%和153.77%（P<0.05）。ACR组伊文思蓝（EB）和荧光素钠（NaFI）含量显著高于对照组（P<0.05）。第4周，ACR组ZO-1 mRNA表达水平为0.21±0.07，显著低于对照组（0.31±0.11）（P<0.05）。第4周，ACR组脉络丛ZO-1蛋白表达水平显著低于对照组（P<0.05）。
丙烯酰胺可增加大鼠BCB通透性，这可能与丙烯酰胺所致中枢神经损伤有关。
