| Objective: By establishing rat models of transient focal ischemia-reperfusion, we investigate the rule and modulation mechanism of the expression of TNF-α, TGF-β1 and ICAM-1 through detecting their expression after different time of ischemia-reperfusion .We also explore the neuroprotective effects of Acanthopanax senticosus injection (ASI).Materials and methods: In this subject, the healthy adult rats of Wistar strain were selected as experimental study objects. The rats were divided randomly into four groups: sham operation group, ischemia-reperfusion group, treatment of ASI group and positive control group. The rat models of transient ischemia-reperfusion were established by occlusion the right middle cerebral artery (MCA), using an intraluminal filament method.The expression of TNF-α, TGF-β1 and ICAM-1 in cerebral ischemic territory after different time of ischemia-reperfusion were detected by immunohistochemistry way.Results: (1) Compared with sham operation group , the expressions of TNF-α, TGF-β1 and ICAM-1 in cerebral ischemic territory increased after cerebral ischemia(P<0.01). The level of TNF-a rose at 6h and peaked at 12h after ischemia- reperfusion. The eyeable expressions of TGF-β1 marked increase at 6h and the peak at 24-48h after ischemia-reperfusion. ICAM-1 expressions raised obviously at 12h and peaked at 24h after the cerebral ischemic -reperfusion.Then their level decreased gradually. (2)ASI may obviously reduce the expressions of TNF-a and ICAM-1, at the same time accelerate the level of TGF-pi. The expressions of ASI group had significant difference at the corresponding time point compared with model group (P<0.01 or P<0.05).Conclusion:(l)High expressions of TNF-α, TGF-β1 andICAM-1 may play a key role in the cerebral ischemic-reperfusion injury.(2) ASI may play its neuroprotective role by reduce the expressions of TNF-a and ICAM-1,and increase the expressions of TGF-pl.
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