中国生化药物杂志
中國生化藥物雜誌
중국생화약물잡지
CHINESE JOURNAL OF BIOCHEMICAL PHARMACEUTICS
2014年
3期
37-39,43
,共4页
胡军%胡名松%曾慰%刘翔%郑达扬%高文奎
鬍軍%鬍名鬆%曾慰%劉翔%鄭達颺%高文奎
호군%호명송%증위%류상%정체양%고문규
异硫氰酸苯乙酯%肺肿瘤,细胞系%磷酸酯酶与张力蛋白同源物%凋亡
異硫氰痠苯乙酯%肺腫瘤,細胞繫%燐痠酯酶與張力蛋白同源物%凋亡
이류청산분을지%폐종류,세포계%린산지매여장력단백동원물%조망
phenethyl isothiocyanate%lung neoplasm%cell line%phosphatase and tensin homologue%apoptosis
目的:研究异硫氰酸苯乙酯(phenethyl isothiocyanate,PEITC)抑制肺癌细胞NCI-H446生长的机制。方法体外培养肺癌NCI-H446细胞,并分为对照组和PEITC处理组。对照组细胞给予0.1%二甲基亚砜处理,PEITC组分别用10μmol/L、30μmol/L和50μmol/L PEITC作用24 h,噻唑蓝法和流式细胞术分别检测细胞的增殖与凋亡;Western blot检测Akt磷酸化、细胞内活性caspase-3和caspase-9的表达以及胞浆中细胞色素C的含量;Real time PCR检测磷酸酯酶与张力蛋白同源物(phosphatase and tensin homologue, PTEN)mRNA水平。结果 PEITC可显著抑制肺癌NCI-H446细胞增殖(P<0.05),并诱导其凋亡。PEITC处理后,肺癌细胞内活性caspase-3和caspase-9含量显著高于对照组(P<0.05);同时,PEITC 处理后,肺癌细胞质中细胞色素C 含量明显增高(P<0.05)。PEITC也能抑制NCI-H446细胞中Akt的磷酸化水平。此外,PEITC处理后,可明显诱导肺癌细胞内PTEN表达的增加(P<0.05),其中50μmol/L PEITC处理后,PTEN mRNA含量增高了4.6倍。结论 PEITC能抑制NCI-H446肺癌细胞生长,其机制可能通过上调PETN表达,从而抑制PI3K/Akt的活性有关。
目的:研究異硫氰痠苯乙酯(phenethyl isothiocyanate,PEITC)抑製肺癌細胞NCI-H446生長的機製。方法體外培養肺癌NCI-H446細胞,併分為對照組和PEITC處理組。對照組細胞給予0.1%二甲基亞砜處理,PEITC組分彆用10μmol/L、30μmol/L和50μmol/L PEITC作用24 h,噻唑藍法和流式細胞術分彆檢測細胞的增殖與凋亡;Western blot檢測Akt燐痠化、細胞內活性caspase-3和caspase-9的錶達以及胞漿中細胞色素C的含量;Real time PCR檢測燐痠酯酶與張力蛋白同源物(phosphatase and tensin homologue, PTEN)mRNA水平。結果 PEITC可顯著抑製肺癌NCI-H446細胞增殖(P<0.05),併誘導其凋亡。PEITC處理後,肺癌細胞內活性caspase-3和caspase-9含量顯著高于對照組(P<0.05);同時,PEITC 處理後,肺癌細胞質中細胞色素C 含量明顯增高(P<0.05)。PEITC也能抑製NCI-H446細胞中Akt的燐痠化水平。此外,PEITC處理後,可明顯誘導肺癌細胞內PTEN錶達的增加(P<0.05),其中50μmol/L PEITC處理後,PTEN mRNA含量增高瞭4.6倍。結論 PEITC能抑製NCI-H446肺癌細胞生長,其機製可能通過上調PETN錶達,從而抑製PI3K/Akt的活性有關。
목적:연구이류청산분을지(phenethyl isothiocyanate,PEITC)억제폐암세포NCI-H446생장적궤제。방법체외배양폐암NCI-H446세포,병분위대조조화PEITC처리조。대조조세포급여0.1%이갑기아풍처리,PEITC조분별용10μmol/L、30μmol/L화50μmol/L PEITC작용24 h,새서람법화류식세포술분별검측세포적증식여조망;Western blot검측Akt린산화、세포내활성caspase-3화caspase-9적표체이급포장중세포색소C적함량;Real time PCR검측린산지매여장력단백동원물(phosphatase and tensin homologue, PTEN)mRNA수평。결과 PEITC가현저억제폐암NCI-H446세포증식(P<0.05),병유도기조망。PEITC처리후,폐암세포내활성caspase-3화caspase-9함량현저고우대조조(P<0.05);동시,PEITC 처리후,폐암세포질중세포색소C 함량명현증고(P<0.05)。PEITC야능억제NCI-H446세포중Akt적린산화수평。차외,PEITC처리후,가명현유도폐암세포내PTEN표체적증가(P<0.05),기중50μmol/L PEITC처리후,PTEN mRNA함량증고료4.6배。결론 PEITC능억제NCI-H446폐암세포생장,기궤제가능통과상조PETN표체,종이억제PI3K/Akt적활성유관。
Objective To investigate the anti-proliferation mechanisms of Phenethyl isothiocyanate (PEITC)in human lung cancer cells line NCI-H446. Methods Human lung cancer cell line NCI-H446 was cultured in vitro,and treated with 10,30,50μmol/L PEITC for 24 h respectively. Cell viability and apoptosis were analyzed by methylthiazolyldiphenyl-tetrazolium bromide (MTT)assay and flow cytometry,respectively. Phosphorylation of Akt,activation of caspase-3 and caspase-9 in NCI-H446 cells,and production of cytochrome C in cytoplasm were detected by Western blot. Expression of phosphatase and tensin homologue (PTEN)was detected by real-time PCR. Results PEITC significantly reduced NCI-H446 cells proliferation in dose-dependent manner (P<0.05 ),and apoptosis was also inducted after PEITC administration. PEITC also markedly induced expression of caspase-3 and caspase-9,as compared with control group. And the level of cytochrome C in the cytoplasm was also increased after treatment with PEITC.Furthermore,PEITC treatment significantly increased the mRNA level of PTEN in NCI-H446 cells. Conclusion PEITC may be used as a potential anti-lung cancer agent by regulationg PI3K/AKT pathway and increasing PETN expression.