CONTEXT: The effects of icariin, a chief constituent of ï¬avonoids from Epimedium brevicornum Maxim (Berberidaceae), on the levels of HIF-1α, HSP-60 and HSP-70 remain unknown. OBJECTIVE: To explore the effects of icariin on the levels of HSP-60, HIF-1α and HSP-70 neuron-specific enolase (NSE) and cell viability. MATERIALS AND METHODS: PC12 cells were treated with icariin (10(-7), 10(-6) or 10(-5â)mol/L) for 3âh (1âh before oxygen-glucose deprivation (OGD) plus 2âh OGD). HSP-60, HIF-1α, HSP-70 and NSE were measured using enzyme-linked immunosorbent assay (ELISA). Cell viability was determined by metabolic 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. RESULTS: After 2âh OGD, levels of HIF-1α, HSP-60, HSP-70 and NSE were increased significantly (HIF-1α: 33.3â±â1.9âng/L, HSP-60: 199â±â16âng/L, HSP-70: 195â±â17âng/L, NSE: 1487â±â125âng/L), and cell viability was significantly decreased (0.26â±â0.03), while icariin (10(-7), 10(-6), or 10(-5â)mol/L) significantly reduced the contents of HIF-1α, HSP-60, HSP-70 and NSE (HIF-1α: 14.1â±â1.4, 22.6â±â1.8, 15.7â±â2.1, HSP-60: 100â±â12, 89â±â6, 113â±â11, HSP-70: 139â±â9, 118â±â7, 95â±â9 and NSE: 1121â±â80, 1019â±â52, 731â±â88), and improved cell viability (0.36â±â0.03, 0.38â±â0.04, 0.37â±â0.03) in OGD-treated PC12 cells. DISCUSSION AND CONCLUSION: These results indicate that the protective mechanisms of icariin against OGD-induced injury may be related to down-regulating the expression of HIF-1α, HSP-60 and HSP-70.
The effects of icariin on the expression of HIF-1α, HSP-60 and HSP-70 in PC12 cells suffered from oxygen-glucose deprivation-induced injury.
淫羊藿苷对缺氧缺糖损伤的 PC12 细胞中 HIF-1α、HSP-60 和 HSP-70 表达的影响
阅读:6
作者:Mo Zhen-Tao, Li Wen-Na, Zhai Yu-Rong, Gao Shu-Ying
| 期刊: | Pharmaceutical Biology | 影响因子: | 4.800 |
| 时间: | 2017 | 起止号: | 2017 Dec;55(1):848-852 |
| doi: | 10.1080/13880209.2017.1281968 | 研究方向: | 细胞生物学 |
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
