CAJ | 학술논문

目的探讨白藜芦醇甙(PD)对缺氧缺血性脑损伤(HIBD)新生大鼠空间学习记忆的影响及海马CA1区突触素表达的变化.方法 7日龄SD大鼠37只随机分为假手术组、HIBD自然恢复组和PD治疗组,采用经典的Rice方法制备缺氧缺血性脑损伤动物模型,分别在生后28 d(缺氧缺血后21 d)进行Morris水迷宫测试,评价其学习记忆能力,用免疫组织化学方法来观察各组大鼠海马CA1区突触素的变化.结果 HIBD后3周Morris测验,假手术组、HIBD自然恢复组和PD治疗组大鼠4 d的平均逃避潜伏期分别为(39.55±8.08)s、(52.37±8.03)s、(43.29±7.63)s,PD治疗组大鼠逃避潜伏期明显短于HIBD自然恢复组(P＜0.05),且3组大鼠在4 d内的逃避潜伏期均逐渐变短;3组大鼠穿过平台次数分别为(5.29±2.62)次、(2.36±1.80)次、(4.25±1.66)次,PD治疗组大鼠穿过平台次数显著多于HIBD自然恢复组(P＜0.05);3组大鼠在目标象限内游泳时间分别为(15.74±3.85)s、(10.63±3.66)s、(14.32±2.52)s,PD治疗组在目标象限内游泳时间明显多于HIBD自然恢复组(P＜0.05).3组大鼠海马CA1区突触素的平均密度值分别为0.1674±0.0111、0.261 2±0.0323和0.295 2±0.044 3,PD治疗组大鼠海马CA1区突触素表达明显多于HIBD自然恢复组(P＜0.05).结论白藜芦醇甙能减轻新生大鼠缺氧缺血引起的脑损伤,提高新生大鼠缺氧缺血后远期的学习记忆能力.这种保护作用与白藜芦醇甙能促进HIBD后神经元重塑的突触素表达有关.
목적 탐토백려호순대(PD)대결양결혈성뇌손상(HIBD)신생대서공간학습기억적영향급해마CA1구돌촉소표체적변화.방법 7일령SD대서37지수궤분위가수술조、HIBD자연회복조화PD치료조,채용경전적Rice방법제비결양결혈성뇌손상동물모형,분별재생후28 d(결양결혈후21 d)진행Morris수미궁측시,평개기학습기억능력,용면역조직화학방법래관찰각조대서해마CA1구돌촉소적변화.결과 HIBD후3주Morris측험,가수술조、HIBD자연회복조화PD치료조대서4 d적평균도피잠복기분별위(39.55±8.08)s、(52.37±8.03)s、(43.29±7.63)s,PD치료조대서도피잠복기명현단우HIBD자연회복조(P＜0.05),차3조대서재4 d내적도피잠복기균축점변단;3조대서천과평태차수분별위(5.29±2.62)차、(2.36±1.80)차、(4.25±1.66)차,PD치료조대서천과평태차수현저다우HIBD자연회복조(P＜0.05);3조대서재목표상한내유영시간분별위(15.74±3.85)s、(10.63±3.66)s、(14.32±2.52)s,PD치료조재목표상한내유영시간명현다우HIBD자연회복조(P＜0.05).3조대서해마CA1구돌촉소적평균밀도치분별위0.1674±0.0111、0.261 2±0.0323화0.295 2±0.044 3,PD치료조대서해마CA1구돌촉소표체명현다우HIBD자연회복조(P＜0.05).결론 백려호순대능감경신생대서결양결혈인기적뇌손상,제고신생대서결양결혈후원기적학습기억능력.저충보호작용여백려호순대능촉진HIBD후신경원중소적돌촉소표체유관.
Objective To explore the protective effects and possible mechanisms of Polydatin (PD)on hypoxic-ischemia brain injury(HIBD) in neonatal rat by means of spatial learning memory and the expression of synaptophysin in hippocampal CA1. Methods Thirty-seven neonatal SD rats were divided into 3 groups at random: normal sham-operated group( no hypoxia and ischemia); HIBD group( no medication) ;PD treatment group. 7-old-day rat' s model of HIBD was established by left carotid artery ligation and 2 h hypoxia. Morris water maze test was used to evaluate cognitive function in the rats after 28-day-old( 21-day later after HI). Immunohistochemical method was used to measure the expression of synaptophysin after the end of Morris water maze test. Results Morris water maze results showed that the mean escape latency of the shamgroup (SG) ,HIBD group (HIBD) and PD treatment group (PD) were (39. 55 ±8. 08) s, (52. 37 ±8.03) s and (43.29 ± 7. 63 ) s respectirely. For PD and SG, the mean escape latency was significantly shorter than the HIBD (P ＜0.05). After training,the mean escape latency in the three groups of rats was shortened gradually. The frequency of platform crossings were 5. 29 ±2.62、2. 36 ± 1.80、4. 25 ± 1. 66 in the SG,HIBD and PD respectirely. The frequency of platform crossings in PD was higher than that of HIBD ( P ＜ 0. 05 ). The swimming time in target quadrant were ( 15.74 ± 3.85) s, ( 10. 63 ± 3.66) s and ( 14. 32 ± 2. 52 ) s in SG, HIBD and PD respectirely. For HIBD ,the swimming time in target quadrant was significantly shorter comparing to SG and PD ( P ＜ 0. 05 ). The expression of synaptophys in hippocampal CA1 in PD ( 0. 295 2 ± 0. 044 3 )were evidently higher than that in the HIBD group (0.261 2 ±0.032 3) at 3 week after operation (P ＜0. 05). Conclusion Spatial learning memory deficits and the decrease of synaptophys in hippocampal CA1 could be induced by hypoxic-ischemia. Polydatin could improve the learning and memory ability in neonatal rats following hypoxic-ischemia brain damage. The mechanisms of improvement with Polydatin treatment is associated with the enhancement of expression of synaptophys.