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- Title
落新妇苷对永生化人角质形成细胞 HaCaT 增殖、凋亡的影响及机制探讨.
- Authors
张春红; 杨帆; 张欢欢; 张春敏; 韩长玉; 杜锡贤; 范玉
- Abstract
Objective To observe the effects of astilbin on the cell proliferation and apoptosis of human keratinocyte cell line HaCaT and to investigate the mechanism. Methods HaCaT cells in the logarithmic phase were selected. The observation group was incubated with different concentrations of astilbin, and theblank control group was cultured with DMEM solution for 24 hours. The proliferation and apoptosis of HaCaT cells were respectively measured by MTT and flow cytometry (FCM). HaCaT cells in the logarithmic phase were selected. The observation group was cultured with different concentrations of astilbin +20 ngmL INF-γ, the model group was cultured with 20 ngmL INF-γ and the blank control group was cultured with DMEM solution for 24 hours. Real-time fuorogenetic quantitative PCR ( FQ-PCR) was employed to detect the expression of nuclear transcription factor-κB p65 (NF-κB pκ65),osteopontin (OPN) and vascular endothelial growth factor (VEGF) mRNA. Results When the concentrations of astilbin were 25,50,100,200,400 μg/mL,the proliferation inhibition rates of HaCaT cells were 3. 06%,26. 53%,40. 82%,26. 53% and 61.22% . When the concentrations of astilbin were 50,100,200 μg/mL,the early apoptosis rates of HaCaT cells in the observation group were 3. 26%,8. 24% and 3. 26%,respectively. Compared with the blank control group (1.33% ),significant difference was found in the early apoptosis rate (all P <0. 05) . Compared with the blank control group, the expression of NF-κB p65 , OPN and VEGF mRNA was increased in the model control group ( all P < 0. 01) . Compared with the model control group, the expression of NF-κB p65, OPN and VEGF mRNA was gradually decreased with the increased concentrations of astilbin (all P<0.05).Conclusion Astilbin can inhibit the proliferation and induce the apoptosis of HaCaT cells, whose mechanism may be associated with the inhibition of VEGF,NF-κB p65 and OPN mRNA expression.
- Publication
Shandong Medical Journal, 2015, Vol 55, Issue 46, p20
- ISSN
1002-266X
- Publication type
Article
- DOI
10.3969/j.issn.1002-266X.2015.46.007