国际流行病学传染病学杂志
國際流行病學傳染病學雜誌
국제류행병학전염병학잡지
INTERNATIONAL JOURNAL OF EPIDEMIOLOGY AND INFECTIOUS DISEASE
2010年
6期
375-378
,共4页
张文杰%李朝霞%田淑菊%龚晏萱%毛维武%屈延
張文傑%李朝霞%田淑菊%龔晏萱%毛維武%屈延
장문걸%리조하%전숙국%공안훤%모유무%굴연
肝肿瘤%普伐他汀%增殖%侵袭
肝腫瘤%普伐他汀%增殖%侵襲
간종류%보벌타정%증식%침습
Liver neoplasms%Pravastatin%Proliferation%Invasion
目的 观察普伐他汀(Pra)抑制肝癌细胞株HepG2增殖及侵袭、运动的作用及机制.方法 培养HepG2细胞,以四甲基偶氮唑蓝(MTT)比色法测定不同浓度Pra对HepG2细胞增殖的抑制效应,并与对照组作比较.以Matrigel侵袭实验和迁移实验检测Pra对HepG2细胞的侵袭、运动能力的影响;p38活性试剂盒测定p38活性;Western印迹法测定磷酸化p38(p-p38)、丝裂原活化蛋白激酶磷酸酶1(MKP-1)、RhoC及基质金属蛋白酶2(MMP-2)表达.结果 MTT比色法及Matrigel侵袭和迁移实验显示,Pra明显抑制HepG2细胞增殖及侵袭、运动能力;Pra可抑制p38活性,并抑制p-p38、RhoC及MMP-2表达,同时上调MKP-1表达.以0.01 g/LPra组为例,其抑制HepG2细胞增殖率为(89.51±9.55)%,对照组为100.00%(F=19.76,P＜0.05);对p38活性的影响:0.01g/L Pra组为p38活性为(87.45±8.22)%,对照组为100.00%(F=22.29,P＜0.05).结论 Pra通过抑制p38活性及p-p38表达、提高MKP-1表达,抑制肝癌HepG2细胞株增殖,并通过下调RhoC及MMP-2表达,抑制其侵袭、运动能力.
目的 觀察普伐他汀(Pra)抑製肝癌細胞株HepG2增殖及侵襲、運動的作用及機製.方法 培養HepG2細胞,以四甲基偶氮唑藍(MTT)比色法測定不同濃度Pra對HepG2細胞增殖的抑製效應,併與對照組作比較.以Matrigel侵襲實驗和遷移實驗檢測Pra對HepG2細胞的侵襲、運動能力的影響;p38活性試劑盒測定p38活性;Western印跡法測定燐痠化p38(p-p38)、絲裂原活化蛋白激酶燐痠酶1(MKP-1)、RhoC及基質金屬蛋白酶2(MMP-2)錶達.結果 MTT比色法及Matrigel侵襲和遷移實驗顯示,Pra明顯抑製HepG2細胞增殖及侵襲、運動能力;Pra可抑製p38活性,併抑製p-p38、RhoC及MMP-2錶達,同時上調MKP-1錶達.以0.01 g/LPra組為例,其抑製HepG2細胞增殖率為(89.51±9.55)%,對照組為100.00%(F=19.76,P＜0.05);對p38活性的影響:0.01g/L Pra組為p38活性為(87.45±8.22)%,對照組為100.00%(F=22.29,P＜0.05).結論 Pra通過抑製p38活性及p-p38錶達、提高MKP-1錶達,抑製肝癌HepG2細胞株增殖,併通過下調RhoC及MMP-2錶達,抑製其侵襲、運動能力.
목적 관찰보벌타정(Pra)억제간암세포주HepG2증식급침습、운동적작용급궤제.방법 배양HepG2세포,이사갑기우담서람(MTT)비색법측정불동농도Pra대HepG2세포증식적억제효응,병여대조조작비교.이Matrigel침습실험화천이실험검측Pra대HepG2세포적침습、운동능력적영향;p38활성시제합측정p38활성;Western인적법측정린산화p38(p-p38)、사렬원활화단백격매린산매1(MKP-1)、RhoC급기질금속단백매2(MMP-2)표체.결과 MTT비색법급Matrigel침습화천이실험현시,Pra명현억제HepG2세포증식급침습、운동능력;Pra가억제p38활성,병억제p-p38、RhoC급MMP-2표체,동시상조MKP-1표체.이0.01 g/LPra조위례,기억제HepG2세포증식솔위(89.51±9.55)%,대조조위100.00%(F=19.76,P＜0.05);대p38활성적영향:0.01g/L Pra조위p38활성위(87.45±8.22)%,대조조위100.00%(F=22.29,P＜0.05).결론 Pra통과억제p38활성급p-p38표체、제고MKP-1표체,억제간암HepG2세포주증식,병통과하조RhoC급MMP-2표체,억제기침습、운동능력.
Objective To observe the effects of pravastatin on the proliferation and invasion of human heptocarcinoma cell line HepG2. Methods The effects of different levels of pravastatin on the proliferation of HepG2 cells were observed by MTT assay; boyden chamber for invasion and motility assays, p38 activity was measured by immuno-precipitation, the expressions of p-p38, MKP-1, RhoC and MMP-2 were analyzed by Western blot. Results Pravastatin depressed the proliferation of HepG2 cells. The intracellular p38 activity and expressions of p-p38, RhoC and MMP-2 were decreased, while MKP-1 expression was elevated by different concentrations of pravastatin. As the pravastatin group in 0.01 g/L for example, the rate of elepressing HepG2 proliferation was(89.51 ± 9.55)%, and the rate in control group was 100.00% ( F = 19.76, P ＜ 0.05 ); p38 activity was( 87.45 ± 8.22) % in 0.01 g/L pravastatin group and in control group was 100.00% ( F = 22.29, P ＜ 0.05). Conclusions Pravastatin can depress the proliferation of HepG2 cell line with inhibiting activity and expression of p-p38. Meanwhile, pravastatin can depress the invasion and motility of HepG2 cells with inhibiting RhoC and MMP-2 expressions.
