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Effect of Naoxinkang tablet on apoptosis-related gene Caspase-3 expression in rats with cerebral ischemia reperfusion injury
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DOI   10.11656/j.issn.1672-1519.2009.03.25
Key Words   Naoxinkang tablet;cerebral ischemia;reperfusion injury;Apoptosis;Caspase-3
Author NameAffiliation
SU Yun-ming Heilongjiang University of TCM, Haerbin 150040, China 
LI Huan Heilongjiang University of TCM, Haerbin 150040, China 
ZHANG Xue-hui Heilongjiang University of TCM, Haerbin 150040, China 
孟妍 Heilongjiang University of TCM, Haerbin 150040, China 
李卉 Heilongjiang University of TCM, Haerbin 150040, China 
Abstract
    [Objective] To observe the protective effect of Naoxinkang(improving the function of brain and heart) tablet on cerebral ischemia reperfusion injury in rats and furthermore explore the effect mechanism in treating cerebral ischemia in rats. [Methods] Wistarmale rats were randomly divided into seven groups:the high,middle,low dosage of Naoxinkang group,Nimodipine group,ginkgo leaf tablet group,model group and sham-operated group. The incomplete cerebral occlusion of middle cerebral artery in rats was induced with fishing line(MCAO). The effect of Naoxinkang tablet on protein expression of cysteiny aspartate specific protease-3(Caspase-3) was determined with immunohistochemical process at 24h,48h and 72h after cerebral ischemia,and the effect of Naoxinkang tablet on the change of ethology and pathomorphology due to nerve injury of rats with MCAO before and after treatment were also observed. [Results] Naoxinkang tablet could obviously improve pathomorphology of cerebral ischemia,inhibit the expression Caspase-3. The best therapeutic effect was observed in high dose group of Naoxinkang tablet,and the better therapeutic effect was also got with longer treatment course. [Conclusion] Naoxinkang tablet has certain time-effect and dose-effect relationship in protecting effect on cerebral ischemia. The mechanism of Naoxinkang tablet against cerebral ischemia is related to anti-inflammatory action,inhibition of cell apoptosis and affecting the related gene expression interrelated with cell apoptosis.

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