RESUMO
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.
RESUMO
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.