LI Sheng-Ying, Sun- Juan, Niu-Bing-Han, Yan-Fu-Lin, Dan-Ge-Qin. Effect of lactuside B on the expression of bcl-2 and bax mRNA and their protein in rats’ cerebral cortex after cerebral ischemia-reperfusion injuryJ. 药学学报, 2011,46(11): 1314-1320.
Citation: LI Sheng-Ying, Sun- Juan, Niu-Bing-Han, Yan-Fu-Lin, Dan-Ge-Qin. Effect of lactuside B on the expression of bcl-2 and bax mRNA and their protein in rats’ cerebral cortex after cerebral ischemia-reperfusion injuryJ. 药学学报, 2011,46(11): 1314-1320.

Effect of lactuside B on the expression of bcl-2 and bax mRNA and their protein in rats’ cerebral cortex after cerebral ischemia-reperfusion injury

  • This study is to investigate the effect of the major chemical composition in rhizome of Pterocypsela elata, lactuside B, on expression of bcl-2, bax mRNA and their protein in rats’ cerebral cortex after cerebral ischemia-reperfusion injury.  First, middle cerebral artery ischemia-reperfusion injury model was established, and each group was treated with the corresponding medicines.  Animals were separately sacrificed at 24 h and 72 h.  The brain infarct volumes were detected by TTC dye, bcl-2 and bax mRNA expression was checked by RT-PCR, and the proteins of bcl-2 and bax were explored by two-step immunohistochemistry in cerebral cortex of rats.  Lactuside B can reduce brain infarct volume of cerebral cortex of rats, increase the expression of bcl-2 mRNA and decrease that of bax mRNA.  Moreover, the ratio of bcl-2 to bax mRNA is higher in 12.5 and 25 mg·kg−1 dose group, respectively, which is significantly different from that of model group (P < 0.05 or P < 0.01).  Generally, either 12.5 or 25 mg·kg−1 dose group is better than positive control medicine nimodipine (P < 0.05 or P < 0.01).  In addition, the expression of bcl-2 and bax protein is consistent with their gene expression.  Infarct volume and the ratio of bcl-2 to bax mRNA expression are significantly different (P < 0.05 or P < 0.01) between 72 h and 24 h group.  The results demonstrated that lactuside B could play a good role in resisting cerebral ischemia by upregulating the expression of bcl-2 mRNA and protein and downregulating that of bax mRNA and protein.

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