| Objective:To study the neuroprotection and mechanism of danxing- tongluotang(DX)on rats with focal cerebral ischemiareperfusion (I/R) injury.Methods:Forty-eight SD rats were divided randomly into six groups:control group, shamoperated + normal saline (NS); model group, cerebral I/R+NS; nimodipine group,I/R+nimodipine; low dose of DX group, I/R+ low dose of DX;midst dose of DX group, I/R+ midst dose of DX;large dose of DX group,I/R+ large dose of DX.The six groups were fed with NS, nimodipine ,low dose of DX ,midst dose of DX or large dose of DX for consecutive six days.Focal ischemia-reperfusion modle was made with suture-occlude method.Group of cerebral ischemia for 2 h then reperfusion 24h.The behaviors of rats were observed and the expressive levels of Fas-L and COX-2 of brain tissue during the cerebral ischemia-reperfusion..Results: After cerebral I/R,the express of Fas-L in Apoptosis gene of model group increased significantly, the express of Fas-L in nimodipine group and low dose of DX group and midst dose of DX group and large dose of DX group decreased obviously and was lower than that in model group (P<0.05), The large dose of DX group was significant difference between the activity of low dose of DX group and midst dose of DX group (P<0.05),but there was significant difference between nimodipine group (P>0.05). Expression of COX-2 in brain tissue of model group increased significantly as compared with that in nimodipine and DX groups (P<0.05); the expression of cox-2 in brain tissue of nimodipine and DX groups was decreased significantly as compared with that in model group(P<0.01); the level of large dose of DX group and nimodipine group were lower than that other DX groups.Conclusion:Danxingtongluotang may protect the ischemia-brain during reperfusion injury.Reducing the expression of Fas-L and COX-2 of brain tissue decrease damages in the ischemia-reperfusion injury of hippocampus structure have the neurotic protective effect.
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