中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2014年
7期
1293-1297
,共5页
西罗莫司%顺铂%自噬%细胞凋亡
西囉莫司%順鉑%自噬%細胞凋亡
서라막사%순박%자서%세포조망
Sirolimus%Cisplatin%Autophagy%Apoptosis
目的：研究雷帕霉素联合顺铂诱导肝癌细胞凋亡、自噬及其对细胞侵袭转移能力的影响。方法将雷帕霉素以及顺铂分别或联合作用于HepG-2细胞，采用MTT法检测HepG-2细胞增殖抑制情况，采用透射电镜、流式细胞仪检测HepG-2细胞凋亡，采用MDC染色、转染pGFP-LC3检测细胞自噬，用Transwell小室测定HepG-2细胞对细胞外基质的侵袭力。结果与对照组相比，单独应用雷帕霉素组未出现明显的细胞凋亡情况；单独应用顺铂组细胞凋亡情况较明显，凋亡率达到（21.27±3.65）%；顺铂联合应用雷帕霉素组细胞凋亡率最高，达到（43.33±5.64）%。雷帕霉素组、顺铂组和顺铂联合应用雷帕霉素组HepG-2细胞均出现点状的自噬泡，顺铂联合应用雷帕霉素组自噬泡数量显著高于雷帕霉素组和顺铂组。雷帕霉素组、顺铂组和顺铂联合应用雷帕霉素组对HepG-2细胞侵袭抑制率分别为（19.2±5.1）%、（47.8±4.1）%和（78.0±2.4）%。结论顺铂可直接诱导HepG-2细胞凋亡，雷帕霉素本身不诱导HepG-2细胞凋亡，但其可显著促进顺铂诱导的HepG-2细胞凋亡；同时顺铂和雷帕霉素均可直接诱导HepG-2细胞自噬，但两者联合应用促进HepG-2细胞自噬情况非常明显。体外侵袭实验结果表明顺铂联合应用雷帕霉素可显著降低HepG-2细胞的体外侵袭能力。
目的：研究雷帕黴素聯閤順鉑誘導肝癌細胞凋亡、自噬及其對細胞侵襲轉移能力的影響。方法將雷帕黴素以及順鉑分彆或聯閤作用于HepG-2細胞，採用MTT法檢測HepG-2細胞增殖抑製情況，採用透射電鏡、流式細胞儀檢測HepG-2細胞凋亡，採用MDC染色、轉染pGFP-LC3檢測細胞自噬，用Transwell小室測定HepG-2細胞對細胞外基質的侵襲力。結果與對照組相比，單獨應用雷帕黴素組未齣現明顯的細胞凋亡情況；單獨應用順鉑組細胞凋亡情況較明顯，凋亡率達到（21.27±3.65）%；順鉑聯閤應用雷帕黴素組細胞凋亡率最高，達到（43.33±5.64）%。雷帕黴素組、順鉑組和順鉑聯閤應用雷帕黴素組HepG-2細胞均齣現點狀的自噬泡，順鉑聯閤應用雷帕黴素組自噬泡數量顯著高于雷帕黴素組和順鉑組。雷帕黴素組、順鉑組和順鉑聯閤應用雷帕黴素組對HepG-2細胞侵襲抑製率分彆為（19.2±5.1）%、（47.8±4.1）%和（78.0±2.4）%。結論順鉑可直接誘導HepG-2細胞凋亡，雷帕黴素本身不誘導HepG-2細胞凋亡，但其可顯著促進順鉑誘導的HepG-2細胞凋亡；同時順鉑和雷帕黴素均可直接誘導HepG-2細胞自噬，但兩者聯閤應用促進HepG-2細胞自噬情況非常明顯。體外侵襲實驗結果錶明順鉑聯閤應用雷帕黴素可顯著降低HepG-2細胞的體外侵襲能力。
목적：연구뢰파매소연합순박유도간암세포조망、자서급기대세포침습전이능력적영향。방법장뢰파매소이급순박분별혹연합작용우HepG-2세포，채용MTT법검측HepG-2세포증식억제정황，채용투사전경、류식세포의검측HepG-2세포조망，채용MDC염색、전염pGFP-LC3검측세포자서，용Transwell소실측정HepG-2세포대세포외기질적침습력。결과여대조조상비，단독응용뢰파매소조미출현명현적세포조망정황；단독응용순박조세포조망정황교명현，조망솔체도（21.27±3.65）%；순박연합응용뢰파매소조세포조망솔최고，체도（43.33±5.64）%。뢰파매소조、순박조화순박연합응용뢰파매소조HepG-2세포균출현점상적자서포，순박연합응용뢰파매소조자서포수량현저고우뢰파매소조화순박조。뢰파매소조、순박조화순박연합응용뢰파매소조대HepG-2세포침습억제솔분별위（19.2±5.1）%、（47.8±4.1）%화（78.0±2.4）%。결론순박가직접유도HepG-2세포조망，뢰파매소본신불유도HepG-2세포조망，단기가현저촉진순박유도적HepG-2세포조망；동시순박화뢰파매소균가직접유도HepG-2세포자서，단량자연합응용촉진HepG-2세포자서정황비상명현。체외침습실험결과표명순박연합응용뢰파매소가현저강저HepG-2세포적체외침습능력。
Objective To observe the cell apoptosis, autophagy and invasion of rapamycin combined with cisplatin in hepatoma carcinoma cell. Methods Rapamycin and cisplatin were mixed with HepG-2 cells, the cell apoptosis was detected by transmission electron microscopy and flow cytometry,the cell autophagy was detected by MDC stain and transfected pGFP-LC3. Matrigel-transwell chamber method was used to evaluate the cell abilities of metastasis and chemotaxis. Results Compared with the control group, rapamycin group does not appear obvious apoptosis. The apoptosis rate of cisplatin alone group reaches to (21.27±3.65)%. The apoptosis rate of cisplatin combinated with rapamycin group is the highest, which reaches to (43.33±5.64)%. Punctate of autophagic vacuoles were detected in rapamycin group, cisplatin group and cisplatin combinated with rapamycin group. Autophagic vacuoles in cisplatin combinated with rapamycin group were significantly higher than rapamycin hormone group and cisplatin group. The HepG-2 cell invasion inhibition rate was (19.2±5.1)%, (47.8±4.1)% and (78.0±2.4)% in rapamycin group, cisplatin group and cisplatin combinated with rapamycin group. Conclusions Cisplatin can directly induce HepG-2 cell apoptosis, rapamycin itself does not induce HepG-2 cell apoptosis, but it can significantly promote apoptosis in HepG-2 cell induced by cisplatin. Meanwhile cisplatin and rapamycin can directly induce HepG-2 cell autophagy, but both combined to promote HepG-2 cell autophagy more obviously. In vitro invasion essay showed that cisplatin combinated with rapamycin can inhibit the invasion and metastasis of HepG-2 cell.
