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作 者:郭书真 李昌崇[1] 林立[1] Guo Shu-zhen;Li Chang-chong;Lin Li(Department of Endocrinology and Genetic Disease,The Second Affiliated Hospital,Yuying Children's Hospital of Wenzhou Medical University,Wenzhou 325000)
出 处:《中国抗生素杂志》2020年第1期87-91,共5页Chinese Journal of Antibiotics
基 金:浙江省自然科学青年基金项目(No.LQ17H010003);温州市公益性科技计划项目(No.Y20140668);国家自然科学青年基金项目(No.81700011);浙江省教育厅项目(No.Y201432837)
摘 要:目的观察人β-防御素2(hBD2)对肺炎链球菌(SP)感染人肺腺癌细胞(A549)细胞凋亡的影响。方法建立SP感染A549细胞模型,hBD2以10、20和30ng/mL的浓度梯度干预该模型,观察细胞形态变化,CCK-8法检测细胞活力,qRT-PCR检测细胞Bax、Bcl-2及caspase-3mRNA表达,免疫细胞化学法检测细胞Bax、Bcl-2蛋白的表达。结果SP感染引起A549细胞皱缩、空泡化,hBD2一定程度上保护细胞活力,抑制Bax表达,上调Bcl-2的表达。结论hBD2对SP感染的A549细胞凋亡具有保护作用。Objective To observe the effects of human beta defensin 2(hBD2)on apoptosis of human lung adenocarcinoma cell line(A549)infected by Streptococcus pneumoniae(SP).Methods The model of A549 cell infected by SP was established.hBD2 was used to intervene the model with the concentration gradient of 10,20 and 30ng/mL.The morphological changes of cells were observed.The cell viability was detected by the CCK-8 method.QRT-PCR was used to detect the expression of Bax,Bcl-2,and caspase-3 in mRNA level,and the expression of proteins Bax and Bcl-2 in A549 cells was detected by immunocytochemistry.Results SP infection caused A549 cells to collapse and vacuolate.hBD2,to a certain extent,protect cell viability,inhibit Bax expression,and up-regulate Bcl-2 expression.Conclusion hBD2 protects A549 cells infected by SP in the apoptosis pathway with a concentration dependent manner.
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