医学研究生学报
醫學研究生學報
의학연구생학보
JOURNAL OF MEDICAL POSTGRADUATE
2014年
10期
1016-1019
,共4页
朱国华%张琦%戴海萍%沈群
硃國華%張琦%戴海萍%瀋群
주국화%장기%대해평%침군
姜黄素%RPMI8226细胞%丝裂原活化蛋白激酶家族%基质金属蛋白酶家族
薑黃素%RPMI8226細胞%絲裂原活化蛋白激酶傢族%基質金屬蛋白酶傢族
강황소%RPMI8226세포%사렬원활화단백격매가족%기질금속단백매가족
Curcumin%RPMI8226 cell%Mitogen activated protein kinase%Matrix metalloproteinases
目的：姜黄素（Curcumin， Cur）对多种肿瘤细胞均具有明确的抑制增殖、诱导凋亡与部分分化、抑制迁移等方面作用。文中研究Cur体外抑制人多发性骨髓瘤细胞RPMI8226增殖时丝裂原活化蛋白激酶（ mitogen actived protein kinase ， MAPKs）及基质金属蛋白酶（ matrix metalloproteinases ， MMPs）家族成员的表达，探讨Cur的抗肿瘤分子机制。方法以不同浓度Cur 作用 RPMI8226细胞不同时间， MTT检测细胞增殖抑制率，流式细胞术检测细胞周期变化， Western blot 检测MAPKs家族成员的表达，明胶酶谱法检测细胞培养上清中MMPs的活性。结果 Cur呈时间-剂量依赖性抑制RPMI8226细胞增殖，使细胞阻滞于G2/M期[（12．72±0．68）％vs （4．79±0．15）％]。以6．25μmol/L、12．50μmol/L及25．00μmol/L Cur分别处理RPMI8226细胞，细胞内JNK和p-JNK的表达均呈药物浓度依赖性上升（P＜0．01），而ERK1/2及P38 MAPK的表达与阴性对照组相比无明显改变（ P＞0．05）。另各Cur处理组的细胞培养上清中MMP-2及MMP-9的活性，随着Cur药物浓度的上升而逐渐下降（P＜0．01）。结论一定浓度的Cur不仅可能激活MAPKs家族中的JNK信号通路，体外诱导RPMI8226细胞的凋亡，且还可能通过抑制MMPs的活性，影响RPMI8226细胞的浸润与转移。
目的：薑黃素（Curcumin， Cur）對多種腫瘤細胞均具有明確的抑製增殖、誘導凋亡與部分分化、抑製遷移等方麵作用。文中研究Cur體外抑製人多髮性骨髓瘤細胞RPMI8226增殖時絲裂原活化蛋白激酶（ mitogen actived protein kinase ， MAPKs）及基質金屬蛋白酶（ matrix metalloproteinases ， MMPs）傢族成員的錶達，探討Cur的抗腫瘤分子機製。方法以不同濃度Cur 作用 RPMI8226細胞不同時間， MTT檢測細胞增殖抑製率，流式細胞術檢測細胞週期變化， Western blot 檢測MAPKs傢族成員的錶達，明膠酶譜法檢測細胞培養上清中MMPs的活性。結果 Cur呈時間-劑量依賴性抑製RPMI8226細胞增殖，使細胞阻滯于G2/M期[（12．72±0．68）％vs （4．79±0．15）％]。以6．25μmol/L、12．50μmol/L及25．00μmol/L Cur分彆處理RPMI8226細胞，細胞內JNK和p-JNK的錶達均呈藥物濃度依賴性上升（P＜0．01），而ERK1/2及P38 MAPK的錶達與陰性對照組相比無明顯改變（ P＞0．05）。另各Cur處理組的細胞培養上清中MMP-2及MMP-9的活性，隨著Cur藥物濃度的上升而逐漸下降（P＜0．01）。結論一定濃度的Cur不僅可能激活MAPKs傢族中的JNK信號通路，體外誘導RPMI8226細胞的凋亡，且還可能通過抑製MMPs的活性，影響RPMI8226細胞的浸潤與轉移。
목적：강황소（Curcumin， Cur）대다충종류세포균구유명학적억제증식、유도조망여부분분화、억제천이등방면작용。문중연구Cur체외억제인다발성골수류세포RPMI8226증식시사렬원활화단백격매（ mitogen actived protein kinase ， MAPKs）급기질금속단백매（ matrix metalloproteinases ， MMPs）가족성원적표체，탐토Cur적항종류분자궤제。방법이불동농도Cur 작용 RPMI8226세포불동시간， MTT검측세포증식억제솔，류식세포술검측세포주기변화， Western blot 검측MAPKs가족성원적표체，명효매보법검측세포배양상청중MMPs적활성。결과 Cur정시간-제량의뢰성억제RPMI8226세포증식，사세포조체우G2/M기[（12．72±0．68）％vs （4．79±0．15）％]。이6．25μmol/L、12．50μmol/L급25．00μmol/L Cur분별처리RPMI8226세포，세포내JNK화p-JNK적표체균정약물농도의뢰성상승（P＜0．01），이ERK1/2급P38 MAPK적표체여음성대조조상비무명현개변（ P＞0．05）。령각Cur처리조적세포배양상청중MMP-2급MMP-9적활성，수착Cur약물농도적상승이축점하강（P＜0．01）。결론일정농도적Cur불부가능격활MAPKs가족중적JNK신호통로，체외유도RPMI8226세포적조망，차환가능통과억제MMPs적활성，영향RPMI8226세포적침윤여전이。
Objective curcumin can suppress the proliferation , induce apoptosis and partial differentiation , and inhibit the migration of many kinds of tumor cells .The aim of this study was to investigate the expressions of mitogen-activated protein kinase (MAPKs) and matrix metalloproteinases (MMPs) when the proliferation of human multiple myeloma RPMI8226 cells was inhibited by curcumin in vitro, and to reveal the antitumor molecular mechanism of curcumin . Methods RPMI8226 cells were treated with various concentrations of curcumin for different periods of times .The inhibitory rate of curcumin on cell proliferation was detected by MTT assay , the cell cycle analyzed by flow cytometry , the protein levels of MAPKs measured by Western blot , and the activity of MMPs analyzed by Gelatin zymography . Results Curcumin inhibited the proliferation of RPMI 8226 cells in a time-and dose-dependent manner , and the cell cycle was arrested in the G 2/M phase ([12.72 ±0.68]%vs [4.79 ±0.15]%).The expressions of JNK and p-JNK showed a con-centration-dependent increase in the RPMI8226 cells treated with curcumin at 6.25, 12.50, and 25.00 μmol/L, respectively (P<0.01) , but the expressions of ERK 1/2 and P38 MAPK did not change significantly compared with the control group (P>0.05).In addition, the activities of MMP-2 and MMP-9 were decreased in a dose-depend-ent manner in the supernatant of RPMI8226 cells ( P <0.01). Conclusion A certain concentration of curcumin could not only acti-vate the JNK signalling pathway of the MAPKs family and induce the apoptosis of RPMI8226 cells, but also inhibit the activity of MMPs and influence the invasion and metastasis of RPMI 8226 cells.
