中国药业
中國藥業
중국약업
CHINA PHARMACEUTICALS
2014年
21期
18-19
,共2页
罗英豪%赖翔宇%王霞%尹偲偲
囉英豪%賴翔宇%王霞%尹偲偲
라영호%뢰상우%왕하%윤시시
P38MARK信号传导通路%人参多糖%K562细胞%凋亡
P38MARK信號傳導通路%人參多糖%K562細胞%凋亡
P38MARK신호전도통로%인삼다당%K562세포%조망
P38MARKsignal transfer pathway%ginseng polysaccharide%K562 cells%apoptosis
目的：探讨人参多糖诱导白血病细胞K562凋亡的机制。方法取对数生长期的K562细胞，调整密度为5×105个/mL，对照组予以常规培养；人参多糖( GPS )组加入400 mg/L GPS。采用流式细胞仪（MTT法）检测GPS对K562细胞增殖的影响；免疫细胞化学方法检测细胞中P－P38蛋白定位及表达量的变化。Western blotting检测细胞中P38及P－P38蛋白的变化。结果 GPS对K562细胞在体外有明显的增殖抑制作用，在100~800 mg/L质量浓度范围内，其抑制作用呈浓度依赖性，在400 mg/L时达到细胞的半数抑制率，且在48 h时抑制率达到高峰；免疫细胞化学显示，P－P38蛋白主要分布在胞浆，与对照组相比，P－P38蛋白表达明显增强，且向胞核转移。Western blotting检测结果显示P38总蛋白无明显变化（ P>0.05）；P－P38蛋白有增加趋势，且在作用48 h后增加明显（ P<0.05）。结论 GPS能促进K562细胞凋亡，其促凋亡机制可能是通过P38MAPK信号传导通路实现的。
目的：探討人參多糖誘導白血病細胞K562凋亡的機製。方法取對數生長期的K562細胞，調整密度為5×105箇/mL，對照組予以常規培養；人參多糖( GPS )組加入400 mg/L GPS。採用流式細胞儀（MTT法）檢測GPS對K562細胞增殖的影響；免疫細胞化學方法檢測細胞中P－P38蛋白定位及錶達量的變化。Western blotting檢測細胞中P38及P－P38蛋白的變化。結果 GPS對K562細胞在體外有明顯的增殖抑製作用，在100~800 mg/L質量濃度範圍內，其抑製作用呈濃度依賴性，在400 mg/L時達到細胞的半數抑製率，且在48 h時抑製率達到高峰；免疫細胞化學顯示，P－P38蛋白主要分佈在胞漿，與對照組相比，P－P38蛋白錶達明顯增彊，且嚮胞覈轉移。Western blotting檢測結果顯示P38總蛋白無明顯變化（ P>0.05）；P－P38蛋白有增加趨勢，且在作用48 h後增加明顯（ P<0.05）。結論 GPS能促進K562細胞凋亡，其促凋亡機製可能是通過P38MAPK信號傳導通路實現的。
목적：탐토인삼다당유도백혈병세포K562조망적궤제。방법취대수생장기적K562세포，조정밀도위5×105개/mL，대조조여이상규배양；인삼다당( GPS )조가입400 mg/L GPS。채용류식세포의（MTT법）검측GPS대K562세포증식적영향；면역세포화학방법검측세포중P－P38단백정위급표체량적변화。Western blotting검측세포중P38급P－P38단백적변화。결과 GPS대K562세포재체외유명현적증식억제작용，재100~800 mg/L질량농도범위내，기억제작용정농도의뢰성，재400 mg/L시체도세포적반수억제솔，차재48 h시억제솔체도고봉；면역세포화학현시，P－P38단백주요분포재포장，여대조조상비，P－P38단백표체명현증강，차향포핵전이。Western blotting검측결과현시P38총단백무명현변화（ P>0.05）；P－P38단백유증가추세，차재작용48 h후증가명현（ P<0.05）。결론 GPS능촉진K562세포조망，기촉조망궤제가능시통과P38MAPK신호전도통로실현적。
Objective To investigate the mechanism of ginseng polysaccharide ( GPS ) inducing apoptosis of human leukemia K562 cells. Methods The density of K562 cells with logarithmic phase was regulated to 5 × 105/mL. The blank control group was performed the routine culture;the GPS group was added with 400 mg/L GPS. The effects of GPS on the proliferation of K562 cells were determined by MTT assay;the localization and expression quantity change of P38 were detected by the immunohistochemistry method and the P-P38 protein change was detected by Western blot. Results GPS significantly inhibited the K562 cells proliferation in vitro in a dose dependent manner during the concentration range of 100-800 mg/L, which at the concentration of 400 mg/L reached the cellular half number inhibiting rate and the inhibiting rate reached its peak at 48 h;the immunocytochemistry results showed that P-P38 was main-ly distributed in cytoplasm, compared with the blank group, the P-P38 expression was significantly enhanced and shifted to the nucle-ar. The Western blot results showed that the total protein of P38 had no significant changes ( P>0. 05 );P-P38 had an increasing trend and was increased significantly after 48 h action ( P<0. 05 ) . Conclusion GPS promotes the apoptosis of K562 cells, its mechanism may be realized by the P38MAPK signal transduction pathway.
