南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2015年
5期
619-624
,共6页
邵建立%李志忠%焦根龙%孙国栋%周志刚
邵建立%李誌忠%焦根龍%孫國棟%週誌剛
소건립%리지충%초근룡%손국동%주지강
灵芝酸A%人骨肉瘤%增殖%凋亡
靈芝痠A%人骨肉瘤%增殖%凋亡
령지산A%인골육류%증식%조망
ganoderic acid A%human osteosarcoma cells%proliferation%apoptosis%invasion
目的:探讨灵芝酸A对骨肉瘤细胞增殖、凋亡和迁移的影响。方法体外培养人骨肉瘤HOS和mg-63细胞与0.1、0.25和0.5 mmol/L的灵芝酸A孵育,采用CCK8检测HOS和MG-63细胞的增殖,流式细胞仪检测细胞凋亡,Transwell检测细胞的迁移和侵袭。Western blot检测细胞中p-STAT3、STAT3、p-p38、p38和NF-ΚB1蛋白的表达变化。结果灵芝酸A能够显著抑制人类骨肉瘤HOS和MG-63细胞的增殖,促进细胞凋亡以及抑制细胞迁移,并且这种效应存在剂量依赖性。与0.5 mmol/L灵芝酸A孵育能够显著降低HOS和MG-63细胞中STAT3的磷酸化水平,增加p38磷酸化水平,同时增加NF-κB1的表达水平。结论灵芝酸A能够杀死人类骨肉瘤HOS和MG-63细胞,可以作为抗骨肉瘤的药物进行开发。
目的:探討靈芝痠A對骨肉瘤細胞增殖、凋亡和遷移的影響。方法體外培養人骨肉瘤HOS和mg-63細胞與0.1、0.25和0.5 mmol/L的靈芝痠A孵育,採用CCK8檢測HOS和MG-63細胞的增殖,流式細胞儀檢測細胞凋亡,Transwell檢測細胞的遷移和侵襲。Western blot檢測細胞中p-STAT3、STAT3、p-p38、p38和NF-ΚB1蛋白的錶達變化。結果靈芝痠A能夠顯著抑製人類骨肉瘤HOS和MG-63細胞的增殖,促進細胞凋亡以及抑製細胞遷移,併且這種效應存在劑量依賴性。與0.5 mmol/L靈芝痠A孵育能夠顯著降低HOS和MG-63細胞中STAT3的燐痠化水平,增加p38燐痠化水平,同時增加NF-κB1的錶達水平。結論靈芝痠A能夠殺死人類骨肉瘤HOS和MG-63細胞,可以作為抗骨肉瘤的藥物進行開髮。
목적:탐토령지산A대골육류세포증식、조망화천이적영향。방법체외배양인골육류HOS화mg-63세포여0.1、0.25화0.5 mmol/L적령지산A부육,채용CCK8검측HOS화MG-63세포적증식,류식세포의검측세포조망,Transwell검측세포적천이화침습。Western blot검측세포중p-STAT3、STAT3、p-p38、p38화NF-ΚB1단백적표체변화。결과령지산A능구현저억제인류골육류HOS화MG-63세포적증식,촉진세포조망이급억제세포천이,병차저충효응존재제량의뢰성。여0.5 mmol/L령지산A부육능구현저강저HOS화MG-63세포중STAT3적린산화수평,증가p38린산화수평,동시증가NF-κB1적표체수평。결론령지산A능구살사인류골육류HOS화MG-63세포,가이작위항골육류적약물진행개발。
Objective To investigate the effect of ganoderic acid A (GA-A) on the biological behaviors of human osteosarcoma cells in vitro. Methods MG63 and HOS cells were treated with 0.1, 0.25, and 0.5 mmol/L GA-A, and the changes in cell proliferation, apoptosis and migration were evaluated using MTT assay, flow cytometry, and Transwell assay, respectively. The expressions of STAT3, p38, and NF-κB1 in the cells were analyzed by Western blotting. Results GA-A effectively inhibited the proliferation of human osteosarcoma HOS and MG-63 cells in a dose-dependent manner, and induced obvious cell apoptosis in both cells. Treatment with 0.5 mmol/L GA-A also resulted in significant inhibition of the invasion of both cells. The results of Western blotting showed that GA-A down-regulated the expression level of phosphorylated STAT3 and increased the phosphorylation level of p38 and NF-κB1 expression in both cells. Conclusion GA-A can induce proliferation inhibition, apoptosis and suppression of invasion in human osteosarcoma HOS and MG-63 cells.