中国实用医刊
中國實用醫刊
중국실용의간
CENTRAL PLAINS MEDICAL JOURNAL
2013年
4期
1-3
,共3页
五味子多糖%乳腺癌%MCF-7细胞%Bcl-2蛋白%Bax蛋白
五味子多糖%乳腺癌%MCF-7細胞%Bcl-2蛋白%Bax蛋白
오미자다당%유선암%MCF-7세포%Bcl-2단백%Bax단백
Schizandrm chinensis polysaccharide%Human breast cancer%MCF-7 cells%Bcl-2%Bax
目的 研究五味子多糖对人乳腺癌MCF-7细胞株的生长抑制作用及其机制.方法 将40只成年雄性Wistar大鼠分为对照组、药物低剂量组、中剂量组和高剂量组四组,每组10只.其中药物中、低、高剂量组分别给予50、100和200 mg/kg剂量五味子多糖灌胃,对照组给予等体积生理盐水灌胃,连续灌胃7d后分别提取血清.乳腺癌MCF-7细胞分为药物组、阴性对照组和空白组.药物组分别加入各剂量组的含药血清,阴性对照组加入对照组大鼠的纯化血清,空白组为10％小牛血清的DMEM培养液,MTT法检测细胞的增殖情况,蛋白免疫印迹(Western blotting)检测细胞Bcl-2和Bax的表达.结果 阴性对照组细胞生长抑制率为(2.94±0.03)％,低、中、高不同药物浓度组细胞生长抑制率分别为(13.25±1.42)％、(32.50±0.76)％、(43.09±0.84)％.低剂量组与阴性对照组相比差异有统计学意义(P＜0.05),中高剂量组与阴性对照组相比差异有统计学意义(P＜0.01),且具有浓度依赖关系.Western blotting检测,低、中、高不同药物浓度组Bcl-2蛋白表达明显低于阴性对照组和空白组；低、中、高不同药物浓度组Bax蛋白表达明显高于阴性对照组和空白组.结论 五味子多糖能有效抑制乳腺癌MCF-7细胞株的增殖,并降低细胞株Bcl-2蛋白表达,增强Bax蛋白表达,五味子多糖对乳腺癌MCF-7细胞株的生长抑制作用机制与诱发细胞凋亡有关.
目的 研究五味子多糖對人乳腺癌MCF-7細胞株的生長抑製作用及其機製.方法 將40隻成年雄性Wistar大鼠分為對照組、藥物低劑量組、中劑量組和高劑量組四組,每組10隻.其中藥物中、低、高劑量組分彆給予50、100和200 mg/kg劑量五味子多糖灌胃,對照組給予等體積生理鹽水灌胃,連續灌胃7d後分彆提取血清.乳腺癌MCF-7細胞分為藥物組、陰性對照組和空白組.藥物組分彆加入各劑量組的含藥血清,陰性對照組加入對照組大鼠的純化血清,空白組為10％小牛血清的DMEM培養液,MTT法檢測細胞的增殖情況,蛋白免疫印跡(Western blotting)檢測細胞Bcl-2和Bax的錶達.結果 陰性對照組細胞生長抑製率為(2.94±0.03)％,低、中、高不同藥物濃度組細胞生長抑製率分彆為(13.25±1.42)％、(32.50±0.76)％、(43.09±0.84)％.低劑量組與陰性對照組相比差異有統計學意義(P＜0.05),中高劑量組與陰性對照組相比差異有統計學意義(P＜0.01),且具有濃度依賴關繫.Western blotting檢測,低、中、高不同藥物濃度組Bcl-2蛋白錶達明顯低于陰性對照組和空白組；低、中、高不同藥物濃度組Bax蛋白錶達明顯高于陰性對照組和空白組.結論 五味子多糖能有效抑製乳腺癌MCF-7細胞株的增殖,併降低細胞株Bcl-2蛋白錶達,增彊Bax蛋白錶達,五味子多糖對乳腺癌MCF-7細胞株的生長抑製作用機製與誘髮細胞凋亡有關.
목적 연구오미자다당대인유선암MCF-7세포주적생장억제작용급기궤제.방법 장40지성년웅성Wistar대서분위대조조、약물저제량조、중제량조화고제량조사조,매조10지.기중약물중、저、고제량조분별급여50、100화200 mg/kg제량오미자다당관위,대조조급여등체적생리염수관위,련속관위7d후분별제취혈청.유선암MCF-7세포분위약물조、음성대조조화공백조.약물조분별가입각제량조적함약혈청,음성대조조가입대조조대서적순화혈청,공백조위10％소우혈청적DMEM배양액,MTT법검측세포적증식정황,단백면역인적(Western blotting)검측세포Bcl-2화Bax적표체.결과 음성대조조세포생장억제솔위(2.94±0.03)％,저、중、고불동약물농도조세포생장억제솔분별위(13.25±1.42)％、(32.50±0.76)％、(43.09±0.84)％.저제량조여음성대조조상비차이유통계학의의(P＜0.05),중고제량조여음성대조조상비차이유통계학의의(P＜0.01),차구유농도의뢰관계.Western blotting검측,저、중、고불동약물농도조Bcl-2단백표체명현저우음성대조조화공백조；저、중、고불동약물농도조Bax단백표체명현고우음성대조조화공백조.결론 오미자다당능유효억제유선암MCF-7세포주적증식,병강저세포주Bcl-2단백표체,증강Bax단백표체,오미자다당대유선암MCF-7세포주적생장억제작용궤제여유발세포조망유관.
Objective To research the inhibitory effect of the polysaccharide from schisandra chinensis on human breast cancer MCF-7 cells and its mechanism.Methods Forty adult male Wistar rats were divided into low dose group,middle dose group,high dose group and control group with 10 rats in each group.The rats in drug group were given the polysaccharide from schisandra chinensis pured for different doses (50,100 and 200 mg/kg) by gavage.The rats in control group were given 0.9％ NaCl by gavage.The serum was obtained after continuous intragastric administration 7 days.The MCF-7 cells were divided into drug group,negative group and control group.The cells in drug group were cultivated in medium containing the rat serum including low,medium and high dose drugs.The cells in negative group were cultivated in serum from the rats in control group.The cells in control group were cultivated in DMEM medium containing 10％ calf serum.The proliferation of human breast cancer MCF-7 cells was detected by MTT assay.The expression of Bcl-2 and Bax was determined by Western blotting.Results The MTT results showed that the inhibitory rate of cell growth in negative group was (2.94 ± 0.03) ％.The inhibitory rates in low,medium and high dose drug groups were (13.25 ± 1.42) ％,(32.50 ±0.76) ％ and (43.09 ± 0.84) ％ respectively.The difference between low dose drug group and negative group was significant (P ＜ 0.05).The differences between medium,high dose drug group and negative group were also significant (P ＜ 0.01) in a concentration dependent manner.The expressions of Bcl-2 in low,medium and high dose drug groups were lower than those in negative group and control group.The expressions of Bax in low,medium and high dose drug groups were higher than those in negative group and control group.Conclusions Polysaccharide from schisandra chinensis can inhibit the Bcl-2 expression and can promote Bax expression in human breast cancer MCF-7 cells and induce apoptosis of MCF-7 cells and inhibit cell proliferarion.
