中国药理学通报
中國藥理學通報
중국약이학통보
Chinese Pharmacological Bulletin
2015年
10期
1458-1462
,共5页
赵丕文%臧金凤%陶仕英%陈梦%牛建昭
趙丕文%臧金鳳%陶仕英%陳夢%牛建昭
조비문%장금봉%도사영%진몽%우건소
丹参酮IIA%乳腺癌%T47D细胞%细胞增殖%G蛋白偶联雌激素受体%雌激素受体%基因沉默
丹參酮IIA%乳腺癌%T47D細胞%細胞增殖%G蛋白偶聯雌激素受體%雌激素受體%基因沉默
단삼동IIA%유선암%T47D세포%세포증식%G단백우련자격소수체%자격소수체%기인침묵
tanshinone IIA%breast cancer%T47 D cell%cell proliferation%G protein-coupled estrogen re-ceptor%estrogen receptor%gene silence
目的:利用经典雌激素受体( estrogenic receptor,ER)和G蛋白偶联雌激素受体( G protein-coupled estrogen recep-tor, GPER)阳性乳腺癌T47D细胞,探索丹参酮IIA( Tanshi-none IIA)对细胞增殖活性的影响及其GPER介导与调节功能。方法以GPER激动剂G1和GPER拮抗剂G15为工具药干预,并应用 GPER SiRNA 转染构建 GPER 基因沉默的T47D细胞,利用MTT细胞增殖实验观察丹参酮IIA对T47D细胞增殖速率的影响及 GPER 的介导作用。利用 Western blot方法检测丹参酮IIA对T47D细胞GPER表达情况的影响。结果1×10-5 mol · L-1~1×10-7 mol · L-1丹参酮IIA能够明显抑制T47D细胞增殖,且该抑制作用可被G1拮抗,可被G15增强。丹参酮 IIA 作用于 GPER 基因沉默的T47D细胞,该细胞表现出更为明显的生长抑制效应。 West-ern blot测定结果表明,1×10-5 mol · L-1和1×10-6 mol · L-1丹参酮IIA可使 T47D 细胞 GPER 蛋白表达明显降低。结论丹参酮IIA具有抑制乳腺癌T47D细胞增殖的作用,该抑制作用可经GPER途径介导;且丹参酮IIA具有对靶细胞GPER表达的调节功能。
目的:利用經典雌激素受體( estrogenic receptor,ER)和G蛋白偶聯雌激素受體( G protein-coupled estrogen recep-tor, GPER)暘性乳腺癌T47D細胞,探索丹參酮IIA( Tanshi-none IIA)對細胞增殖活性的影響及其GPER介導與調節功能。方法以GPER激動劑G1和GPER拮抗劑G15為工具藥榦預,併應用 GPER SiRNA 轉染構建 GPER 基因沉默的T47D細胞,利用MTT細胞增殖實驗觀察丹參酮IIA對T47D細胞增殖速率的影響及 GPER 的介導作用。利用 Western blot方法檢測丹參酮IIA對T47D細胞GPER錶達情況的影響。結果1×10-5 mol · L-1~1×10-7 mol · L-1丹參酮IIA能夠明顯抑製T47D細胞增殖,且該抑製作用可被G1拮抗,可被G15增彊。丹參酮 IIA 作用于 GPER 基因沉默的T47D細胞,該細胞錶現齣更為明顯的生長抑製效應。 West-ern blot測定結果錶明,1×10-5 mol · L-1和1×10-6 mol · L-1丹參酮IIA可使 T47D 細胞 GPER 蛋白錶達明顯降低。結論丹參酮IIA具有抑製乳腺癌T47D細胞增殖的作用,該抑製作用可經GPER途徑介導;且丹參酮IIA具有對靶細胞GPER錶達的調節功能。
목적:이용경전자격소수체( estrogenic receptor,ER)화G단백우련자격소수체( G protein-coupled estrogen recep-tor, GPER)양성유선암T47D세포,탐색단삼동IIA( Tanshi-none IIA)대세포증식활성적영향급기GPER개도여조절공능。방법이GPER격동제G1화GPER길항제G15위공구약간예,병응용 GPER SiRNA 전염구건 GPER 기인침묵적T47D세포,이용MTT세포증식실험관찰단삼동IIA대T47D세포증식속솔적영향급 GPER 적개도작용。이용 Western blot방법검측단삼동IIA대T47D세포GPER표체정황적영향。결과1×10-5 mol · L-1~1×10-7 mol · L-1단삼동IIA능구명현억제T47D세포증식,차해억제작용가피G1길항,가피G15증강。단삼동 IIA 작용우 GPER 기인침묵적T47D세포,해세포표현출경위명현적생장억제효응。 West-ern blot측정결과표명,1×10-5 mol · L-1화1×10-6 mol · L-1단삼동IIA가사 T47D 세포 GPER 단백표체명현강저。결론단삼동IIA구유억제유선암T47D세포증식적작용,해억제작용가경GPER도경개도;차단삼동IIA구유대파세포GPER표체적조절공능。
Aim To explore the effects of tanshinone IIA on cell proliferation via G protein-coupled estrogen receptor inductive and regulative pathway in typical es-trogen receptor and G protein-coupled estrogen receptor positive T47D breast cancer cells. Methods The pro-liferation rate of T47 D cells influenced by tanshinone IIA was analyzed by MTT assay. G protein-coupled es-trogen receptor agonist G1 and GPER antagonist G15 were employed as tools. GPER SiRNA was applied to build GPER gene silence T47D cells. GPER expres-sion influenced by tanshinone IIA was measured by Western blot. Results The proliferation rates of T47D cells treated with 1 × 10 -5 mol·L-1 - 1 × 10 -7 mol· L-1 of tanshinone IIA were decreased significantly. Such effects could be attenuated by G1 or enhanced by G15 . Growth of GPER SiRNA transfected T47 D cells were significantly inhibited by 1 × 10 -5 mol·L-1 - 1 × 10 -7 mol·L-1 of tanshinone IIA treating. Result of Western blot showed that tanshinone IIA at 1 × 10 -5 mol· L-1 and 1 × 10 -6 mol · L-1 could induce de-crease of GPER protein expression in T47D cells. Conclusions Tanshinone IIA shows inhibitory effects on proliferation rate of T47 D breast cancer cells via GPER pathway. Tanshinone IIA could perform regula-tive function on GPER expression level in target cells.