解放军医药杂志
解放軍醫藥雜誌
해방군의약잡지
MEDICAL&PHARMACEUTICAL JOURNAL OF CHINESE PEOPLE'S LIBERATION ARMY
2015年
4期
20-23
,共4页
周曙%蔡涛%覃兴贵%赵蕾蕾%薛李
週曙%蔡濤%覃興貴%趙蕾蕾%薛李
주서%채도%담흥귀%조뢰뢰%설리
黄芩苷%Hep G2细胞%细胞凋亡%c-Jun 氨基末端激酶
黃芩苷%Hep G2細胞%細胞凋亡%c-Jun 氨基末耑激酶
황금감%Hep G2세포%세포조망%c-Jun 안기말단격매
Baicalin%Hep G2 cell%Apoptosis%C- jun n-terminal kinase
目的:探讨黄芩苷对人肝癌 HepG2细胞生长的抑制作用及其对 c-Jun 氨基末端激酶(JNK)信号通路的影响。方法50、100、150μg/ ml 的黄芩苷分别与人肝癌 HepG2细胞共同培养24、48和72 h,MTT 测定细胞生长抑制率;采用 Western blotting 方法检测黄芩苷处理72 h 后 HepG2细胞 JNK 和 p-JNK 的表达变化并观察 JNK 抑制剂对细胞凋亡的影响。结果黄芩苷对人肝癌 HepG2细胞增殖抑制作用呈时间依赖性,黄芩苷浓度低于100μg/ ml 其对细胞的抑制作用随浓度升高而增强,超过100μg/ ml 其对细胞的抑制作用不再增强。在黄芩苷处理后 HepG2细胞 p-JNK 蛋白表达上调,使用 JNK 抑制剂后,能阻断 JNK 蛋白的磷酸化,并且降低黄芩苷诱导细胞凋亡的能力。结论黄芩苷通过激活 JNK 信号通路诱导人肝癌 HepG2细胞凋亡。
目的:探討黃芩苷對人肝癌 HepG2細胞生長的抑製作用及其對 c-Jun 氨基末耑激酶(JNK)信號通路的影響。方法50、100、150μg/ ml 的黃芩苷分彆與人肝癌 HepG2細胞共同培養24、48和72 h,MTT 測定細胞生長抑製率;採用 Western blotting 方法檢測黃芩苷處理72 h 後 HepG2細胞 JNK 和 p-JNK 的錶達變化併觀察 JNK 抑製劑對細胞凋亡的影響。結果黃芩苷對人肝癌 HepG2細胞增殖抑製作用呈時間依賴性,黃芩苷濃度低于100μg/ ml 其對細胞的抑製作用隨濃度升高而增彊,超過100μg/ ml 其對細胞的抑製作用不再增彊。在黃芩苷處理後 HepG2細胞 p-JNK 蛋白錶達上調,使用 JNK 抑製劑後,能阻斷 JNK 蛋白的燐痠化,併且降低黃芩苷誘導細胞凋亡的能力。結論黃芩苷通過激活 JNK 信號通路誘導人肝癌 HepG2細胞凋亡。
목적:탐토황금감대인간암 HepG2세포생장적억제작용급기대 c-Jun 안기말단격매(JNK)신호통로적영향。방법50、100、150μg/ ml 적황금감분별여인간암 HepG2세포공동배양24、48화72 h,MTT 측정세포생장억제솔;채용 Western blotting 방법검측황금감처리72 h 후 HepG2세포 JNK 화 p-JNK 적표체변화병관찰 JNK 억제제대세포조망적영향。결과황금감대인간암 HepG2세포증식억제작용정시간의뢰성,황금감농도저우100μg/ ml 기대세포적억제작용수농도승고이증강,초과100μg/ ml 기대세포적억제작용불재증강。재황금감처리후 HepG2세포 p-JNK 단백표체상조,사용 JNK 억제제후,능조단 JNK 단백적린산화,병차강저황금감유도세포조망적능력。결론황금감통과격활 JNK 신호통로유도인간암 HepG2세포조망。
Objective To study the effects of Baicalin on inhibiting the proliferation of HepG2 cells and c- jun n-terminal kinase (JNK) signaling pathway in patients with hepatic cancer. Methods The 50, 100 and 150 μg/ ml of Baicalin were respectively cultured with HepG2 cells for 24 h, 48 h and 72 h, and then the inhibitory rate of cell prolifer-ation was detected using MTT assay. The changes of HepG2 cells and expressions of JNK and p-JNK after Baicalin treat-ment were detected using Western blotting, and the effect of JNK inhibitor on apoptosis was observed. Results The in-hibitory effect of Baicalin on the proliferation of HepG2 cells of patients with hepatic cancer was time dependence, and the inhibitory effect of Baicalin concentration was lower than 100 μg/ ml on cell proliferation enhanced with the increased con-centration, while the inhibitory effect of Baicalin concentration more than 100 μg/ ml was not enhanced. The p-JNK pro-tein expression in HepG2 cells was increased after Baicalin treatment. After use of JNK inhibitor, the phosphorylation of JNK protein was blocked, and apoptotic ability induced by Baicalin was reduced. Conclusion Baicalin can induce HepG2 apoptosis by activating JNK signaling pathways in patients with hepatic cancer.