中国骨质疏松杂志
中國骨質疏鬆雜誌
중국골질소송잡지
CHINESE JOURNAL OF OSTEOPOROSIS
2009年
7期
506-512
,共7页
张燕燕%朱国英%顾淑珠%陈晓
張燕燕%硃國英%顧淑珠%陳曉
장연연%주국영%고숙주%진효
Genistein%乳腺癌细胞%成骨细胞%增殖%分化%矿化结节
Genistein%乳腺癌細胞%成骨細胞%增殖%分化%礦化結節
Genistein%유선암세포%성골세포%증식%분화%광화결절
Genistein%Breast cancer cells%Osteoblast%Proliferation%Differentiation%Bone nodule formation
目的 探讨Genistein对乳腺癌细胞致成骨细胞(osteoblast, OB)增殖、分化和矿化功能的影响,观察Genistein在乳腺癌骨转移的病理条件下是否能调节OB生物学功能.方法 源于大鼠颅盖骨的原代OB与50%来自人源性乳腺癌细胞系MDA-MB-231或MCF-7的条件培养基(conditioned medium,CM)共同培养,并加入5×10-7 mol/L (G7)、5×10-8 mol/L (G8)或5×10-9mol/L (G9) 的Genistein进行干预.MTT法观察其对OB增殖的影响;PNPP偶氮法观察其对OB碱性磷酸酶(alkaline phosphatase, ALP)活性的影响;茜素红S(ARS)进行矿化结节染色并计算面积以观察其对OB矿化能力的影响.结果 MDA-MB-231和MCF-7细胞条件培养基可显著抑制OB的增殖.用Genistein干预1 d、3 d和5 d后,OB增值率可有不同程度的提高,差异有统计学意义(P<0.05).此外,乳腺癌细胞条件培养基可明显下调OB的ALP活性,而用不同浓度的Genistein干预后,OB的ALP活性分别较MDA-MB-231和MCF-7细胞条件培养基组增加22.7%、32.4%、63.5%和27.7%、32.0%、58.3%(P<0.05).Genistein还可改善乳腺癌细胞条件培养基对OB矿化能力的抑制,增加OB形成的矿化结节面积.结论 在乳腺癌骨转移的病理条件下,Genistein可促进OB的增殖、分化和矿化能力,改善乳腺癌细胞对OB生物学功能的抑制作用.
目的 探討Genistein對乳腺癌細胞緻成骨細胞(osteoblast, OB)增殖、分化和礦化功能的影響,觀察Genistein在乳腺癌骨轉移的病理條件下是否能調節OB生物學功能.方法 源于大鼠顱蓋骨的原代OB與50%來自人源性乳腺癌細胞繫MDA-MB-231或MCF-7的條件培養基(conditioned medium,CM)共同培養,併加入5×10-7 mol/L (G7)、5×10-8 mol/L (G8)或5×10-9mol/L (G9) 的Genistein進行榦預.MTT法觀察其對OB增殖的影響;PNPP偶氮法觀察其對OB堿性燐痠酶(alkaline phosphatase, ALP)活性的影響;茜素紅S(ARS)進行礦化結節染色併計算麵積以觀察其對OB礦化能力的影響.結果 MDA-MB-231和MCF-7細胞條件培養基可顯著抑製OB的增殖.用Genistein榦預1 d、3 d和5 d後,OB增值率可有不同程度的提高,差異有統計學意義(P<0.05).此外,乳腺癌細胞條件培養基可明顯下調OB的ALP活性,而用不同濃度的Genistein榦預後,OB的ALP活性分彆較MDA-MB-231和MCF-7細胞條件培養基組增加22.7%、32.4%、63.5%和27.7%、32.0%、58.3%(P<0.05).Genistein還可改善乳腺癌細胞條件培養基對OB礦化能力的抑製,增加OB形成的礦化結節麵積.結論 在乳腺癌骨轉移的病理條件下,Genistein可促進OB的增殖、分化和礦化能力,改善乳腺癌細胞對OB生物學功能的抑製作用.
목적 탐토Genistein대유선암세포치성골세포(osteoblast, OB)증식、분화화광화공능적영향,관찰Genistein재유선암골전이적병리조건하시부능조절OB생물학공능.방법 원우대서로개골적원대OB여50%래자인원성유선암세포계MDA-MB-231혹MCF-7적조건배양기(conditioned medium,CM)공동배양,병가입5×10-7 mol/L (G7)、5×10-8 mol/L (G8)혹5×10-9mol/L (G9) 적Genistein진행간예.MTT법관찰기대OB증식적영향;PNPP우담법관찰기대OB감성린산매(alkaline phosphatase, ALP)활성적영향;천소홍S(ARS)진행광화결절염색병계산면적이관찰기대OB광화능력적영향.결과 MDA-MB-231화MCF-7세포조건배양기가현저억제OB적증식.용Genistein간예1 d、3 d화5 d후,OB증치솔가유불동정도적제고,차이유통계학의의(P<0.05).차외,유선암세포조건배양기가명현하조OB적ALP활성,이용불동농도적Genistein간예후,OB적ALP활성분별교MDA-MB-231화MCF-7세포조건배양기조증가22.7%、32.4%、63.5%화27.7%、32.0%、58.3%(P<0.05).Genistein환가개선유선암세포조건배양기대OB광화능력적억제,증가OB형성적광화결절면적.결론 재유선암골전이적병리조건하,Genistein가촉진OB적증식、분화화광화능력,개선유선암세포대OB생물학공능적억제작용.
Objective To investigate the effects of Genistein on changes of osteoblastic proliferation, differentiation and mineralization induced by breast cancer cells, and in order to observe whether Genistein regulates osteoblastic biological function in pathological condition with bone metastasis. Methods The osteoblasts harvested from calvaria of Sprague Dawley rats were cultured with 50% conditioned medium collected from two types of human breast cancer lines: MDA-MB-231 and MCF-7, and treated with different concentrations of Genistein: 5×10-7mol/L (G7)、5×10-8mol/L (G8)、5×10-9mol/L (G9). Then the proliferation was analyzed by MTT method, the alkaline phosphatase (ALP) activity was assessed by the p-nitrophenyl phosphate (PNPP) method,and the area of bone nodule formation was observed by alizarin red S (ARS) staining and measured to analyze the mineralization ability. Results Conditioned medium from MDA-MB-231 or MCF-7 significantly suppressed osteoblastic proliferation, while the proliferation on day 1, day 3 and day 5 was improved in the different extents when osteoblasts were treated with Genistein. Otherwise, conditioned medium significantly inhibited ALP activity on day 3, while compared with conditioned medium group, different concentrations of Genistein could increase the ALP activity of osteoblasts by 22.7%、32.4%、63.5% and 27.7%、32.0%、58.3%, respectively. Genistein also increased the area of bone nodule formation and improved osteoblastic mineralization ability inhibited by conditioned medium. Conclusion In pathological condition with bone metastasis, Genistein could promoto osteoblastic proliferation, differentiation and mineralization, improve osteoblastic biological function inhibited by breast cancer cells.
