天津医药
天津醫藥
천진의약
Tianjin Medical Journal
2015年
11期
1267-1270
,共4页
刘方康%牛琼%王爱丽%贾兴芳%胡营滨%刘成霞
劉方康%牛瓊%王愛麗%賈興芳%鬍營濱%劉成霞
류방강%우경%왕애려%가흥방%호영빈%류성하
甘草%胃肿瘤%基质金属蛋白酶9%异甘草素%侵袭%PI3K/Akt%蛋白激酶B%磷酸化蛋白激酶B
甘草%胃腫瘤%基質金屬蛋白酶9%異甘草素%侵襲%PI3K/Akt%蛋白激酶B%燐痠化蛋白激酶B
감초%위종류%기질금속단백매9%이감초소%침습%PI3K/Akt%단백격매B%린산화단백격매B
glycyrrhiza uralensis%stomach neoplasms%matrix metalloproteinase 9%isoliquiritigenin%invasive ability%PI3K/Akt%Akt%P-Akt
目的：探讨异甘草素（isoliquiritigenin）对人胃癌SGC7901细胞侵袭能力的影响及其可能的分子机制。方法取对数生长期人胃癌SGC7901细胞，分为对照组（正常细胞培养液），异甘草素实验组(异甘草素溶于细胞培养液，浓度分别为10、25、50、100μmol/L)，每组4个复孔。培养24、48、72 h后采用MTT法检测异甘草素对细胞生长的抑制情况，摸索后续实验药物浓度和作用时间；采用Transwell小室侵袭实验检测各组细胞的侵袭能力；Western blotting法检测基质金属蛋白酶-9（MMP-9）、蛋白激酶B（Akt）和磷酸化Akt（P-Akt）的表达。结果10μmol/L异甘草素不能抑制胃癌细胞株SGC7901的生长，而25、50、100μmol/L异甘草素可明显抑制其生长，且呈时间和浓度依赖性，24、48、72 h半数抑制浓度（IC50）分别为52.48、44.49、32.50μmol/L，故选定后续实验药物浓度为25、50、100μmol/L，作用时间为24 h。与对照组穿膜细胞数（个：209.75±9.29）相比，25μmol/L组（138.50±10.15）、50μmol/L组（89.50±16.56）、100μmol/L组（45.00±8.08）逐渐降低（F=267.948，P<0.05）。各组间Akt蛋白水平差异无统计学意义（F=1.492）；随异甘草素浓度的增加，P-Akt、MMP-9蛋白水平逐渐降低（F分别为359.219、431.324，均P<0.05）。结论异甘草素能够抑制SGC7901细胞侵袭能力，其机制可能与下调PI3K/Akt信号转导通路蛋白及其下游的MMP-9蛋白表达有关。
目的：探討異甘草素（isoliquiritigenin）對人胃癌SGC7901細胞侵襲能力的影響及其可能的分子機製。方法取對數生長期人胃癌SGC7901細胞，分為對照組（正常細胞培養液），異甘草素實驗組(異甘草素溶于細胞培養液，濃度分彆為10、25、50、100μmol/L)，每組4箇複孔。培養24、48、72 h後採用MTT法檢測異甘草素對細胞生長的抑製情況，摸索後續實驗藥物濃度和作用時間；採用Transwell小室侵襲實驗檢測各組細胞的侵襲能力；Western blotting法檢測基質金屬蛋白酶-9（MMP-9）、蛋白激酶B（Akt）和燐痠化Akt（P-Akt）的錶達。結果10μmol/L異甘草素不能抑製胃癌細胞株SGC7901的生長，而25、50、100μmol/L異甘草素可明顯抑製其生長，且呈時間和濃度依賴性，24、48、72 h半數抑製濃度（IC50）分彆為52.48、44.49、32.50μmol/L，故選定後續實驗藥物濃度為25、50、100μmol/L，作用時間為24 h。與對照組穿膜細胞數（箇：209.75±9.29）相比，25μmol/L組（138.50±10.15）、50μmol/L組（89.50±16.56）、100μmol/L組（45.00±8.08）逐漸降低（F=267.948，P<0.05）。各組間Akt蛋白水平差異無統計學意義（F=1.492）；隨異甘草素濃度的增加，P-Akt、MMP-9蛋白水平逐漸降低（F分彆為359.219、431.324，均P<0.05）。結論異甘草素能夠抑製SGC7901細胞侵襲能力，其機製可能與下調PI3K/Akt信號轉導通路蛋白及其下遊的MMP-9蛋白錶達有關。
목적：탐토이감초소（isoliquiritigenin）대인위암SGC7901세포침습능력적영향급기가능적분자궤제。방법취대수생장기인위암SGC7901세포，분위대조조（정상세포배양액），이감초소실험조(이감초소용우세포배양액，농도분별위10、25、50、100μmol/L)，매조4개복공。배양24、48、72 h후채용MTT법검측이감초소대세포생장적억제정황，모색후속실험약물농도화작용시간；채용Transwell소실침습실험검측각조세포적침습능력；Western blotting법검측기질금속단백매-9（MMP-9）、단백격매B（Akt）화린산화Akt（P-Akt）적표체。결과10μmol/L이감초소불능억제위암세포주SGC7901적생장，이25、50、100μmol/L이감초소가명현억제기생장，차정시간화농도의뢰성，24、48、72 h반수억제농도（IC50）분별위52.48、44.49、32.50μmol/L，고선정후속실험약물농도위25、50、100μmol/L，작용시간위24 h。여대조조천막세포수（개：209.75±9.29）상비，25μmol/L조（138.50±10.15）、50μmol/L조（89.50±16.56）、100μmol/L조（45.00±8.08）축점강저（F=267.948，P<0.05）。각조간Akt단백수평차이무통계학의의（F=1.492）；수이감초소농도적증가，P-Akt、MMP-9단백수평축점강저（F분별위359.219、431.324，균P<0.05）。결론이감초소능구억제SGC7901세포침습능력，기궤제가능여하조PI3K/Akt신호전도통로단백급기하유적MMP-9단백표체유관。
Objective To investigate the effects of isoliquiritigenin on the invasive ability of human gastric carcinoma SGC7901 cells, and its molecular mechanisms thereof. Methods The logarithmic phase human gastric carcinoma SGC7901 cells were divided into control group (normal cell culture fluid) and isoliquiritigenin group (isoliquiritigenin solu?ble in cell culture fluid, the concentrations were 10, 25, 50 and 100 μmol/L respectively). Each group had four repeated holes. The proliferation of SGC7901 cells were detected with MTT assay after 24 h, 48 h and 72 h of culture. The experimen?tal drug concentration and action time were researched for the subsequent experiments. The in vitro invasion abilities of SGC7901 cells were assessed with Transwell test. The expression levels of MMP9, Akt and P-Akt were detected by Western blot assay. Results The proliferation of SGC7901 cells were inhibited by 10μmol/L isoliquiritigenin, which can be signifi?cantly inhibited by 25, 50 and 100μmol/L isoliquiritigenin in a concentration-dependent and time-dependent manner. The half inhibitory concentrations (IC50) of 24, 48 and 72 h were 52.48, 44.49 and 32.50μmol/L, respectively. Therefore, the 25, 50 and 100μmol/L isoliquiritigenin were selected as the subsequent experimental drug concentration, and 24 h was used as the action time. Compared with the control group (209.75±9.29), the membrane cell number of 25μmol/L (138.50±10.15), 50μmol/L (89.50 ± 16.56) and 100μmol/L (45.00 ± 8.08) decreased gradually (F=267.948,P<0.05). There was no signifi?cant difference in the expression level of Akt protein between four groups (F=1.492). The expression levels of P-Akt and MMP9 were gradually decreased with the increase of the isoliquirigenin concentration (F=359.219 and 431.324,P<0.05). Conclusion Isoliquiritigenin can obviously inhibit invasion ability of SGC7901 cells, which may be related to the down reg?ulation of the signal transduction pathway protein PI3K/Akt and the down steam protein MMP9.
