CAJ | 학술논문

目的探讨流感病毒(H1 N1)感染血管平滑肌细胞后,血管平滑肌细胞的数量、增殖率、凋亡率及分泌相关细胞因子的变化,从细胞水平探讨流感病毒感染在动脉粥样硬化形成中的作用以及可能的机制.方法分别通过细胞计数试验、流式细胞术和酶联免疫吸附试验,检测未感染病毒的细胞(对照组)和病毒感染后细胞(实验组),在不同时段(0h、6h、12h、24h、48 h)血管平滑肌细胞增殖率、凋亡率和分泌IL-6、sFas、血小板衍生生长因子(platelet-derived growth factor,PDGF)的变化情况.结果实验组0h血管平滑肌细胞增殖率和凋亡率分别为10.39％和0.44％；6 h后细胞增殖率(12.68％)和凋亡率(0.73％)均增加；12 h增殖率达到高峰(18.01％),凋亡率反而降低(0.14％)；24 h后增殖率下降(12.89％),凋亡率明显增加(1.09％)；48 h增殖率进一步降低(7.07％),凋亡率达到高峰(4.61％).各时期的细胞增殖率和凋亡率与0h比较,差异具有统计学意义(P＜0.05).细胞数量、IL-6、sFas、PDGF均在感染12～18 h达到分泌高峰,随后下降.实验组每个时间点的细胞数量,细胞因子的分泌量与0h比较,差异均有统计学意义(P＜0.05).结论流感病毒感染血管平滑肌细胞后,使平滑肌细胞增殖、凋亡发生紊乱,由此提示流感病毒感染可能参与动脉粥样硬化的形成和发展,同时细胞因子在其中发挥重要的作用.
목적 탐토류감병독(H1 N1)감염혈관평활기세포후,혈관평활기세포적수량、증식솔、조망솔급분비상관세포인자적변화,종세포수평탐토류감병독감염재동맥죽양경화형성중적작용이급가능적궤제.방법 분별통과세포계수시험、류식세포술화매련면역흡부시험,검측미감염병독적세포(대조조)화병독감염후세포(실험조),재불동시단(0h、6h、12h、24h、48 h)혈관평활기세포증식솔、조망솔화분비IL-6、sFas、혈소판연생생장인자(platelet-derived growth factor,PDGF)적변화정황.결과 실험조0h혈관평활기세포증식솔화조망솔분별위10.39％화0.44％；6 h후세포증식솔(12.68％)화조망솔(0.73％)균증가；12 h증식솔체도고봉(18.01％),조망솔반이강저(0.14％)；24 h후증식솔하강(12.89％),조망솔명현증가(1.09％)；48 h증식솔진일보강저(7.07％),조망솔체도고봉(4.61％).각시기적세포증식솔화조망솔여0h비교,차이구유통계학의의(P＜0.05).세포수량、IL-6、sFas、PDGF균재감염12～18 h체도분비고봉,수후하강.실험조매개시간점적세포수량,세포인자적분비량여0h비교,차이균유통계학의의(P＜0.05).결론 류감병독감염혈관평활기세포후,사평활기세포증식、조망발생문란,유차제시류감병독감염가능삼여동맥죽양경화적형성화발전,동시세포인자재기중발휘중요적작용.
Objective To research the influenza virus infection on rat vascular smooth cells number,proliferation,apoptosis,the amount of IL-6,sFas,platelet-derived growth factor(PDGF) and the mechanism of atherosclerosis.Methods Flow cytometry,enzyme-linked immunosorbent assay and cell count experiments were used to detect these indicators at 0 h,6 h,12 h,24 h,48 h.Results After influenza virus infected at 0 h,proliferation,apoptosis condition were 10.39％,0.44％,respectively; at 6 h,proliferation,apoptosis respectively increased to 12.68％,0.73％ ; proliferation reached the peak at 12 h (18.01％),instead apoptosis decreased to 0.14％ ; at 24 h,proliferation decreased to 12.89％ and apoptosis markedly increased to 1.09％ ; at 48 h,proliferation further reduced to 7.07％ and apoptosis reached the peak(4.61％).The number of cells and the cytokine secretion were statistically significant to control group (P＜0.05).Conclusion Influenza virus infection might lead to change of cell proliferation and apoptosis and involve the atherosclerosis form and development,and cytokines played an important role in them.