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目的观察二十二碳六烯酸(DHA)对1-溴丙烷(1-BP)致大鼠学习能力损伤的拮抗作用。方法将48只健康成年SPF级雄性Wistar大鼠随机分为4组,即对照(玉米油)组、1-BP染毒组和低、高剂量DHA干预组,每组12只。1-BP染毒组和低、高剂量DHA干预组每天灌胃染毒800 mg/kg的1-BP;4 h后,低、高剂量DHA干预组分别灌胃染毒250、500mg/kg的DHA,每日1次,连续11 d。染毒第8~11天采用Morris水迷宫试验中的定位导航试验检测大鼠的学习能力。染毒结束后,检测大脑皮层匀浆中还原型谷胱甘肽(GSH)、丙二醛(MDA)含量及谷胱甘肽还原酶(GR)活力。采用Western blotting方法检测大脑皮层脑红蛋白(neuroglobin,Ngb)的表达。结果与对照组比较,1-BP染毒组大鼠游泳总路程和逃避潜伏期延长(P<0.05);与1-BP染毒组相比,各剂量DHA干预组大鼠的游泳路程和逃避潜伏期缩短(P<0.05)。与对照组比较,1-BP染毒组大鼠大脑皮层匀浆中GSH含量及GR活力均下降,而1-BP染毒组MDA含量及高剂量DHA干预组GSH含量均升高(P<0.05);与1-BP染毒组比较,各剂量DHA干预组大鼠大脑皮层匀浆中GSH含量及GR活力均升高,MDA含量均下降(P<0.05)。与对照组比较,1-BP染毒组和低剂量DHA干预组大鼠大脑皮层匀浆中Ngb蛋白的表达水平均下降,而高剂量DHA干预组Ngb蛋白的表达水平升高(P<0.05);与1-BP染毒组比较,各剂量DHA干预组大鼠大脑皮层匀浆中Ngb蛋白的表达水平均升高(P<0.05)。结论 DHA能够减轻1-BP导致的大鼠中枢神经系统氧化应激反应及由此引起的学习能力损伤,激活GR活力、增强Ngb表达可能是DHA的保护机制之一。
Objective To observe the antagonistic effect of docosahexaenoic acid (DHA) on learning ability impairment induced by 1-bromopropane (1-BP) in rats. Methods Forty-eight healthy adult male Sprague-Dawley (Wistar) male Wistar rats were randomly divided into 4 groups: control (corn oil), 1-BP and low and high dose DHA intervention groups, 12 rats in each group. 1-BP and 1-BP in low-dose and high-dose DHA groups were intragastrically administrated with 800 mg / kg 1-BP. After 4 h, low- and high-dose DHA intervention groups were given 250 and 500 mg / kg DHA, once daily for 11 days. From the 8th day to the 11th day of exposure, the learning ability of the rats was tested by the positioning and navigation test in the Morris water maze test. After the exposure, the contents of reduced glutathione (GSH), malondialdehyde (MDA) and glutathione reductase (GR) in the cerebral cortex homogenate were measured. Western blotting was used to detect the expression of neuroglobin (Ngb) in the cerebral cortex. Results Compared with the control group, the total swimming distance and escape latency of 1-BP-treated rats were longer than those of the control group (P <0.05). Compared with the 1-BP-treated rats, the swimming distance and escape latency Shortened (P <0.05). Compared with the control group, the content of GSH and the activity of GR in the cerebral cortex homogenate of 1-BP treatment group were decreased, while the content of GSH in 1-BP treatment group and GSH level in high-dose DHA intervention group were increased (P <0.05 ). Compared with 1-BP-treated group, GSH and GR activity in cerebral cortex homogenate of rats in each dose of DHA intervention group were increased, and MDA content decreased (P <0.05). Compared with the control group, the expression of Ngb protein in the cerebral cortex homogenate of 1-BP and low-dose DHA intervention groups decreased, while the expression level of Ngb protein in high-dose DHA intervention group increased (P <0.05) Compared with 1-BP group, the expression of Ngb protein in cerebral cortex homogenate of DHA intervention group was increased (P <0.05). Conclusion DHA can reduce the oxidative stress reaction induced by 1-BP in rat CNS and its impairment of learning ability. Activation of GR activity and enhancement of Ngb expression may be one of the protective mechanisms of DHA.