摘要
目的探讨微波辐照诱导心肌细胞凋亡的分子病理机制。方法以功率密度峰值为950mW/cm2的脉冲微波辐照心肌细胞0,30,60,120s后,采用倒置显微镜观察心肌细胞形态,流式细胞仪及原位末端标记方法检测心肌细胞凋亡率,免疫组织化学方法检测多种凋亡相关基因表达的变化。结果辐照后心肌细胞呈现出典型的细胞凋亡形态。辐照60s后6,24h,心肌细胞凋亡率分别为(36.76±5.31)和(26.44±3.94),与对照组(2.36±0.87)比较,差异有统计学意义(P<0.01)。原位末端标记结果表明,心肌细胞凋亡率与辐照剂量呈正相关。凋亡促进基因Bax、P53、双向调控基因c-myc表达显著增强(P<0.01),凋亡抑制基因Bcl-2表达一过性增强,随后明显降低(P<0.01)。结论心肌细胞是微波辐照损伤的敏感细胞,微波辐照可诱导心肌细胞凋亡,并存在剂量效应关系。Bcl-2/Bax、P53、c-myc参与微波辐照诱导的心肌细胞凋亡并发挥重要调控作用。
Objective To study the molecular pathologic mechanism of myocardial cell apoptosis irradiated by microwave. Methods Myocardial cells irradiated by pulse microwave at power density 950mW/cm^2. The irradiation time was 0, 30, 60,120s respectively. Then morphologic changes of cells were observed by inversion microscope, and the apoptosis rate was examined by flow cytometer and the method of TUNEL, and expression changes of many relevant apoptosis genes were investigated by immunohistochemical method. Results Myocardial cells appeared representative apoptosis image after irradiation. Apoptosis rates were ( 36.76 ± 5.31 ) and ( 26.44 ± 3.94 ) respectively at 6 h and 24 h after irradiation. There was marked statistical discrepancy compared with control group [ (2.36 ± 0.87 ). (P 〈 0.01 ). The results of TUNEL indicated the dosage-effect relationship between apoptosis and irradiation dosage. The expression of Bax, P53, and c-myc enhanced obviously ( P 〈 0.01 ), and Bcl-2 enhanced transitorily, and then reduced obviously ( P 〈 0.01 ). Conclusion Myocardial cells were sus- ceptive to microwave irradiation. The irradiation could induce apoptosis of myocardial cells, which appeared the dosage-effect relationship. Bcl-2/bax, p53 and c-myc were concerned with apoptosis and played important roles.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2007年第10期1167-1168,共2页
Chinese Journal of Public Health
基金
广东省自然科学基金项目(04300712)
关键词
微波
心肌细胞
凋亡
机制
microwave
myocardial cell
apoptosis
mechanism