实用药物与临床
實用藥物與臨床
실용약물여림상
PRACTICAL PHARMACY AND CLINICAL REMEDIES
2014年
5期
528-531
,共4页
苦参碱%前列腺癌%细胞凋亡%Cyclin D1%ERK1/2
苦參堿%前列腺癌%細胞凋亡%Cyclin D1%ERK1/2
고삼감%전렬선암%세포조망%Cyclin D1%ERK1/2
Matrine%Prostate cancer%Apoptosis%Cyclin D1%ERK1/2
目的:研究苦参碱( MR)对人前列腺癌PC-3M细胞周期与凋亡的影响。方法稳定培养PC-3M细胞株系,经0(空白组)、30、60、120μM浓度MR给药72 h后,应用四甲基偶氮唑盐( MTT)法检测MR对PC-3M抑制率,碘化丙啶(PI)染色检测细胞形态学的变化,免疫组织化学法检测细胞周期蛋白D1(Cyclin D1)表达,Western blot法检测细胞外调节蛋白激酶1/2(ERK1/2)磷酸化蛋白水平。结果与空白组比较,MR给药后有效抑制PC-3M的细胞增殖(P<0.01),并促进癌细胞凋亡。同时,MR能显著减少Cyclin D1的表达以及下调内源性p-ERK1/2水平(P<0.01)。结论苦参碱可发挥有效的抗癌作用,推测其机制为抑制癌症细胞增殖并介导细胞凋亡,以及抑制内源性ERK1/2/Cyclin D1通路。
目的:研究苦參堿( MR)對人前列腺癌PC-3M細胞週期與凋亡的影響。方法穩定培養PC-3M細胞株繫,經0(空白組)、30、60、120μM濃度MR給藥72 h後,應用四甲基偶氮唑鹽( MTT)法檢測MR對PC-3M抑製率,碘化丙啶(PI)染色檢測細胞形態學的變化,免疫組織化學法檢測細胞週期蛋白D1(Cyclin D1)錶達,Western blot法檢測細胞外調節蛋白激酶1/2(ERK1/2)燐痠化蛋白水平。結果與空白組比較,MR給藥後有效抑製PC-3M的細胞增殖(P<0.01),併促進癌細胞凋亡。同時,MR能顯著減少Cyclin D1的錶達以及下調內源性p-ERK1/2水平(P<0.01)。結論苦參堿可髮揮有效的抗癌作用,推測其機製為抑製癌癥細胞增殖併介導細胞凋亡,以及抑製內源性ERK1/2/Cyclin D1通路。
목적:연구고삼감( MR)대인전렬선암PC-3M세포주기여조망적영향。방법은정배양PC-3M세포주계,경0(공백조)、30、60、120μM농도MR급약72 h후,응용사갑기우담서염( MTT)법검측MR대PC-3M억제솔,전화병정(PI)염색검측세포형태학적변화,면역조직화학법검측세포주기단백D1(Cyclin D1)표체,Western blot법검측세포외조절단백격매1/2(ERK1/2)린산화단백수평。결과여공백조비교,MR급약후유효억제PC-3M적세포증식(P<0.01),병촉진암세포조망。동시,MR능현저감소Cyclin D1적표체이급하조내원성p-ERK1/2수평(P<0.01)。결론고삼감가발휘유효적항암작용,추측기궤제위억제암증세포증식병개도세포조망,이급억제내원성ERK1/2/Cyclin D1통로。
Objective To assess the effect of matrine on cell cycle and apoptosis of human prostate cancer PC-3M. Methods Stably cultured PC-3M cell lines was treated MR 0 (blank group),30,60,120 μM concentrations,re-spectively,for 72 h. MTT assay was employed for MR-mediated inhibition rate of PC-3M. Propidium iodide (PI) stai-ning was used to observe morphological changes. Cyclin D1 expression was analyzed by immunohistochemistry, the phosphorylated level of extracellular regulated kinase1/2 was tested via Western blot assay. Results Compared with the blank group,MR administration led to the effective anti-proliferation of PC-3M cells (P<0. 01),and promoted ap-optosis in tumour cells (P<0. 01). Meanwhile,MR administration also distinctly reduced the Cyclin D1 expression and down-regulated endogenous p-ERK1/2 level ( P <0. 01 ) . Conclusion Overall, matrine plays the pronounced anti-cancer effect,which the mechanism is linked to the suppression of cancer cell proliferation and mediation of apoptosis, as well as the inhibition of endogenous ERK1/2/Cyclin D1 pathway.