国际儿科学杂志
國際兒科學雜誌
국제인과학잡지
INTERNATIONAL JOURNAL OF PEDIATRICS
2011年
1期
94-95,封3,封4
,共4页
曲云霞%李开花%何绘敏%王朝晖%徐立新
麯雲霞%李開花%何繪敏%王朝暉%徐立新
곡운하%리개화%하회민%왕조휘%서립신
白藜芦醇甙%缺氧缺血性脑损伤%细胞间黏附分子
白藜蘆醇甙%缺氧缺血性腦損傷%細胞間黏附分子
백려호순대%결양결혈성뇌손상%세포간점부분자
Hypoxic-ischemic brain damage%Polydatin%Intercellular cell adhesion molecule-1
目的 探讨白藜芦醇甙(PD)对缺氧缺血性脑损伤(HIBD)新生大鼠脑组织细胞间黏附分子(ICAM-1)表达的影响.方法 7日龄SD大鼠54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HIBD动物模型,用免疫组织化学方法观察各组大鼠脑皮质微血管内皮ICAM-1的表达.结果 假手术组少许脑实质中微血管显示阳性免疫染色.HIBD组缺氧缺血后6h ICAM-1 免疫染色阳性血管数明显增多,12h达高峰,24h ICAM-1表达仍然持续在较高水平;PD治疗组与HIBD组比较,缺氧缺血后6h、12h、24h脑微血管内皮ICAM-1表达明显减少(P<0.05或P<0.01).结论 在HIBD早期使用PD能降低脑微血管内皮ICAM-1的表达,抑制脑内炎症反应,对缺氧缺血后大脑具有神经保护作用.
目的 探討白藜蘆醇甙(PD)對缺氧缺血性腦損傷(HIBD)新生大鼠腦組織細胞間黏附分子(ICAM-1)錶達的影響.方法 7日齡SD大鼠54隻隨機分為假手術組、HIBD自然恢複組和PD治療組,採用經典的Rice方法製備HIBD動物模型,用免疫組織化學方法觀察各組大鼠腦皮質微血管內皮ICAM-1的錶達.結果 假手術組少許腦實質中微血管顯示暘性免疫染色.HIBD組缺氧缺血後6h ICAM-1 免疫染色暘性血管數明顯增多,12h達高峰,24h ICAM-1錶達仍然持續在較高水平;PD治療組與HIBD組比較,缺氧缺血後6h、12h、24h腦微血管內皮ICAM-1錶達明顯減少(P<0.05或P<0.01).結論 在HIBD早期使用PD能降低腦微血管內皮ICAM-1的錶達,抑製腦內炎癥反應,對缺氧缺血後大腦具有神經保護作用.
목적 탐토백려호순대(PD)대결양결혈성뇌손상(HIBD)신생대서뇌조직세포간점부분자(ICAM-1)표체적영향.방법 7일령SD대서54지수궤분위가수술조、HIBD자연회복조화PD치료조,채용경전적Rice방법제비HIBD동물모형,용면역조직화학방법관찰각조대서뇌피질미혈관내피ICAM-1적표체.결과 가수술조소허뇌실질중미혈관현시양성면역염색.HIBD조결양결혈후6h ICAM-1 면역염색양성혈관수명현증다,12h체고봉,24h ICAM-1표체잉연지속재교고수평;PD치료조여HIBD조비교,결양결혈후6h、12h、24h뇌미혈관내피ICAM-1표체명현감소(P<0.05혹P<0.01).결론 재HIBD조기사용PD능강저뇌미혈관내피ICAM-1적표체,억제뇌내염증반응,대결양결혈후대뇌구유신경보호작용.
Objective To investigate the protective effects and possible mechanisms of polydatin(PD) on hypoxic-ischemia brain damage(HIBD) in neonatal rat by means of the expression of intercellular cell adhesion molecule( ICAM)-1 in cortex. Methods Fifty-four SD rats were divided into 3 groups at random, shame group (no HIBD), HIBD group (no medication) ,and PD treatment group. 7day-old rat's HIBD model was established by Rice's method. ICAM-1 expression in brain after HIBD was measured in different time by Immunohistochemitry technique. Results In sham group, there were less brain microvessel immunostained positively. In HIBD group,the number of ICAM-1 immuno-positive staining blood vessels increased significantly after 6h, 12h reached peak point. ICAM-1 immunoreactive staining of blood vessels levels continued in the peak after 24h. In PD treatment group, ICAM-1 expression on brain microvascular endothelial decreased after HIBD 6h, 12h, 24h, which was significant compared with HIBD group( P < 0. 05 or P < 0. 01 separately). Conclusion The expression of ICAM-1 was involved in the procedure induced by hypoxic-ischemia. After HIBD, polydatin would downregulate ICAM-1 expression in cerebral microvascular endothelial, and inhibite the inflammatory response.