摘要
为了评价卷烟烟气的危害性,研究了巴豆醛导致人支气管上皮细胞BEAS-2B死亡机制。即采用MTT法检测细胞存活率,化学发光法检测胞内ATP含量,流式细胞仪检测细胞凋亡率,流式细胞仪结合免疫化学检测线粒体细胞色素c,化学发光法检测caspase-9,caspase-3/7。结果显示,巴豆醛诱导细胞凋亡,且随着剂量增大,细胞由凋亡转向坏死。巴豆醛导致胞内ATP水平迅速下降,导致细胞线粒体膜电位下降,导致细胞色素c由线粒体释放至胞浆,激活caspase-9和caspase-3/7。结论:巴豆醛诱导细胞凋亡,且caspase级联酶参与巴豆醛诱导的细胞凋亡。
In order to assess the health risk of cigarette smoke,crotonaldehydeinduced cell death and its mechanism in BEAS-2B cells were investigated.Cell survival rate,intracellular ATP level,apoptosis rate,cytochrome c released from mitochondria to cytoplasm,and caspase-9 and caspase-3/7 activities were determined by MTT,chemiluminescence,flow cytometry,flow cytometry combined with immunochemistry,and chemiluminescence methods,respectively.The results showed that crotonaldehyde induced cell apoptosis,and turned into necrosis along with the increase of crotonaldehyde dosage.Crotonaldehyde caused that intracellular ATP level declined rapidly,mitochondria membrane potential decreased,cytochrome c released from mitochondria to cytoplasm,and caspase-9 and caspase-3/7 were activated.It was concluded that crotonaldehyde induced and caspase mediated cell apoptosis.
出处
《烟草科技》
EI
CAS
北大核心
2011年第1期36-42,共7页
Tobacco Science & Technology