Expressions Of NF-κB,ICAM-1 And VCAM-1 In Rat Models Of Transient Focal Ischemia-reperfusion And The Neuroprotective Effects Of β-Sodium Aescinate

Objective: By establishing rat models of transient focal ischemia-reperfusion, We investigate the rule and modulating mechanism of the expressions of NF- kB, ICAM-1 and VCAM-1 through detecting their expressions after different time of ischemia-reperfusion. We also explore the neuroprotective effects of β -Sodium Aescinate .Materials and methods: In experiment one, rat models of transient focal ischemia-reperfusion were established by occluding the right middle cerebral artery(MCA), using an intraluminal filament method. The expressions of NF-kB, ICAM-1 and VCAM-1 in cerebral ischemic territory after different time of ischemia-reperfusion were detected by immunohistochemistry way.In experiment two, 5mg/kg (3 -Sodium Aescinate was given peritoneally 24h, 1h before ischemia and at the right time of reperfusion, respectively. We analyzed the effects of |3 -Sodium Aescinate on brain by evaluating the infarct volume and the expressions of NF- k B, ICAM-1 and VCAM-1 through TTC staining and immunohistochemistry 24h and 48h after reperfusion.Results: (1) The expressions of NF- k B, IC AM-1 and VC AM-1 in ischemic territory increased after cerebral ischemia. NF- k B immunoreactivity peaked at 12 ~ 24h after reperfusion. ICAM-1 immunoreactivity peaked at 24h after reperfusion and VCAM-1 at 24 ~ 48h. All of them decreased gradually, but remained a higher level than normal 72h after reperfusion. (2) The expression of NF- k B positively...