中国男科学杂志
中國男科學雜誌
중국남과학잡지
CHINESE JOURNAL OF ANDROLOGY
2014年
1期
13-17
,共5页
刘艳波%孙媛媛%徐杰%焦桥%费聪聪%赵晓晖%芦丽莉%董妍%赵雪俭
劉豔波%孫媛媛%徐傑%焦橋%費聰聰%趙曉暉%蘆麗莉%董妍%趙雪儉
류염파%손원원%서걸%초교%비총총%조효휘%호려리%동연%조설검
前列腺癌%甲基硒酸%细胞凋亡%stat3转录因子
前列腺癌%甲基硒痠%細胞凋亡%stat3轉錄因子
전렬선암%갑기서산%세포조망%stat3전록인자
prostatic neoplasms%methylseleninic acid%apoptosis%stat3 transcription factor
目的：探讨甲基硒酸（methylseleninic acid，MSA）对前列腺癌Lncap细胞促凋亡效应，并初步探讨发生机制。方法将体外培养的Lncap细胞分为4组，即空白对照组（mock），MSA低剂量组（1.25μM）、中剂量组（2.50μM）和高剂量组（5.00μM），MSA分别作用24h、48h和72h，倒置显微镜下观察细胞形态，SRB法检测细胞增殖情况；流式细胞术检测细胞周期及凋亡；免疫荧光及免疫细胞化学法检测细胞内stat3的表达。结果光镜及SRB实验结果显示：随MSA剂量增加及作用时间延长，Lncap细胞生长受到明显抑制；流式细胞术结果表明：MSA呈剂量及时间依赖关系促进细胞凋亡，并使细胞周期分布发生改变，多数细胞被阻滞于G0~G1期；免疫荧光及免疫组织化学结果发现：与对照组相比，MSA可明显抑制细胞内stat3表达。结论 MSA抑制细胞增殖并促进细胞凋亡，其发生机制可能与降低stat3表达，进而抑制下游增殖基因表达有关。
目的：探討甲基硒痠（methylseleninic acid，MSA）對前列腺癌Lncap細胞促凋亡效應，併初步探討髮生機製。方法將體外培養的Lncap細胞分為4組，即空白對照組（mock），MSA低劑量組（1.25μM）、中劑量組（2.50μM）和高劑量組（5.00μM），MSA分彆作用24h、48h和72h，倒置顯微鏡下觀察細胞形態，SRB法檢測細胞增殖情況；流式細胞術檢測細胞週期及凋亡；免疫熒光及免疫細胞化學法檢測細胞內stat3的錶達。結果光鏡及SRB實驗結果顯示：隨MSA劑量增加及作用時間延長，Lncap細胞生長受到明顯抑製；流式細胞術結果錶明：MSA呈劑量及時間依賴關繫促進細胞凋亡，併使細胞週期分佈髮生改變，多數細胞被阻滯于G0~G1期；免疫熒光及免疫組織化學結果髮現：與對照組相比，MSA可明顯抑製細胞內stat3錶達。結論 MSA抑製細胞增殖併促進細胞凋亡，其髮生機製可能與降低stat3錶達，進而抑製下遊增殖基因錶達有關。
목적：탐토갑기서산（methylseleninic acid，MSA）대전렬선암Lncap세포촉조망효응，병초보탐토발생궤제。방법장체외배양적Lncap세포분위4조，즉공백대조조（mock），MSA저제량조（1.25μM）、중제량조（2.50μM）화고제량조（5.00μM），MSA분별작용24h、48h화72h，도치현미경하관찰세포형태，SRB법검측세포증식정황；류식세포술검측세포주기급조망；면역형광급면역세포화학법검측세포내stat3적표체。결과광경급SRB실험결과현시：수MSA제량증가급작용시간연장，Lncap세포생장수도명현억제；류식세포술결과표명：MSA정제량급시간의뢰관계촉진세포조망，병사세포주기분포발생개변，다수세포피조체우G0~G1기；면역형광급면역조직화학결과발현：여대조조상비，MSA가명현억제세포내stat3표체。결론 MSA억제세포증식병촉진세포조망，기발생궤제가능여강저stat3표체，진이억제하유증식기인표체유관。
Objective To investigate the proapoptotic effects of methylseleninic acid (MSA) on prostatic cancer Lncap cells and explore its mechanism. Methods The treated Lncap cells were divided into four groups such as the control group (mock), MSA low-dose group (1.25μM), middle dose group (2.50μM) and high dose group (5.00μM) respectively. Cell morphology was observed with microscope at the time of 24h, 48h and 72h after treatment. Cell proliferation was detected by SRB assay. Cell cycle and apoptosis was measured by flow cytometry. Stat3 expression was detected by immunofluorescence and immunocytochemical analysis. Results Light microscopy observation and SRB results indicated that the growth of Lncap cells were inhibited obviously with MSA dose and time dependent effect. Flow cytometry analysis showed that MSA promoted LNCap cells apoptosis with dose and time dependent effect and changed the cell cycle distribution. The majority of cells were arrested in G0-G1 phase. Immunofluorescence and immunohistochemistry results showed MSA could inhibit the expression of intracellular stat3 compared with that of the control group. Conclusion MSA might inhibit cell proliferation and induce apoptosis, and its mechanism was associated with decreased stat3 expression.
