Bax α高表达PC12细胞系的建立及(-)黄皮酰胺抗细胞凋亡作用机制的研究

CONSTRUCTION OF BAXα HIGH EXPRESSING PC-12 CELL LINE AND THE MECHANISMS OF (-)CLAUSENAMIDE IN INHIBITING APOPTOSIS

摘要: 目的　用Bax α高表达的PC12细胞研究了(-)黄皮酰胺的抗细胞凋亡作用。方法　先将Bax α cDNA从原核载体pBluescript SK克隆到真核载体pcDNA3。用脂质体转染的方法将pcDNA3-Bax α导入PC12细胞。以6-羟基多巴胺（6-OHDA）诱导Bax α高表达PC12细胞的凋亡。结果　(-)黄皮酰胺（0.1～10 μmol.L^-1）可使细胞凋亡率显著降低。结论　(-)黄皮酰胺可以抑制细胞凋亡，对神经退行性病变有一定应用前景。

Abstract: AIM　PC12 cells with high expression of Baxα were used to study the antiapoptotic effects of (-)clausenamide.METHODS　The Baxα cDNA was first subcloned from pBluescript SK to eukaryotic vector pcDNA3. The pcDNA3-Baxα was transformed into PC12 cells. PC12 cells with high expression of Baxα were subjected to neurotoxin 6-hydroxydopamine 100 μmol.L^-1 to induce apoptosis.RESULTS　The Baxα expressing PC-12 cells has a higher apoptosis percentage compared with the vector transfected controls(49.96% vs 32.9%). (-)Clausenamide(0.1～10 μmol*L^-1) was shown to significantly decrease the apoptotic cells measured by flowcytometry method. (-)Clausenamide(0.1～1.0 μmol.L^-1) also improved the compromised mitochondrial membrane potential. CONCLUSION　These findings suggest that (-)clausenamide may save the cells from apoptosis and provide a clue to the therapy of neurodegenerative diseases.