来源于HIV-1 gp120 V3区的多肽诱导PC12细胞凋亡的初步研究

Initial study on polypeptide-induced PC12 cell apoptosis in the area of HIV-1 gp120

目的研究HIV-1 gp120 V3区多肽诱导神经细胞凋亡中的机制。方法体外培养大鼠肾上腺嗜铬细胞瘤细胞(PC12细胞),采用Annexin V联合细胞周期与细胞凋亡检测试剂盒(PI)法结合流式细胞术检测细胞的凋亡;获得细胞凋亡模型后,采用Western blotting研究不同浓度(0、100、200、400、800 nmol/L)来源于gp120的多肽处理细胞以及400 nmol/L多肽在不同时间(0、4、12、24、36、48 h)对PC12细胞PLK-1表达的影响。结果 HIV-1 gp120 V3区多肽诱导PC12细胞凋亡后,Polo样激酶1的表达降低,并呈现浓度-时间依赖性。结论 HIV-1 gp120 V3区多肽诱导PC12细胞凋亡与PLK-1有关。

Objective To study the mechanism of polypeptide-induced PC12 nervous cell apoptosis in the area of HIV-1gp120. Methods The adrenal gland chromaffin tumor cell（PC12） by cultivation in vitro was detected the apoptosis by Annexin V combined with PI and flow cytometry. Obtaining the model of cell apoptosis,it adopted Western blotting to inspect the polypeptide-disposed cells from gp120 with the concerntrations of 0,100,200,400 and 800 nmol/L and the influence on PC12 cells′ PLK-1 expression of 400 nmol/L polypeptide at the time of 4th,12 th,24th,36 th,48th hour. Results After the apoptosis of polypeptide-induced PC12 cells,The expression of polo-like kinases-1 was decreased and demonstrated dependence of concentrationtime. Conclusion The apoptosis of polypeptide-induced PC12 cells in the area of HIV-1 gp120 V3 is involved in PLK-1.