摘要
目的:使用熊果酸(ursolic acid,UA)干预大鼠血管平滑肌细胞(vascular smooth muscle cell,VSMC),观察对信号转导与转录激活因子3(signal transduction and activator of transcription 3,STAT3)磷酸化蛋白(P-STAT3)表达的影响,观察其对VSMC增殖和迁移能力的影响,并探讨可能的机制。方法:应用不同浓度的UA干预VSMC,采用MTT法检测各组细胞的增殖情况,采用划痕实验观察各组细胞的迁移能力变化,采用Western Blot法检测各组细胞P-STAT3及T-STAT3蛋白的表达改变。结果:10μmol/L或25μmol/L UA可下调VSMC中P-STAT3蛋白的表达;UA可显著抑制细胞的增殖率,当药物浓度为10μmol/L或25μmol/L时,与对照组比较,差异有统计学意义(P<0.05),且25μmol/L组与10μmol/L组组间比较,差异有统计学意义(P<0.05);划痕实验结果显示药物干预后的细胞迁移能力受到抑制。结论:UA可能通过下调P-STAT3表达抑制VSMC的增殖及迁移能力。
Objective： To observe the effect of ursolic acid （UA） on the protein expression of phospho- rylated signal transducer and activator of transcription 3 （ P-STAT3 ） , and the effect on proliferation and migera- tion of rat vascular smooth muscle ceils （ VSMCs）, and explore the possible mechanism. Methods ： VSMCs were treated with different concentrations of UA （0, 10, 25 umol/L） for 24h. The inhibition of UA on the pro- liferation of VSMCs was measured by MTY assay, scratch wound assay was used to detect the influence of UA on migration of VSMCs, and the expressing of total STAT3 （T-STAT3） and phosphorylated STAT3 （P-STAT3） of VSMCs were detected by Western blot. Results： P-STAT3 expression could be downregulated by UA at con- centration of 10 i.umol/L or 25 i.umol/L; the proliferation of VSMCs was significantly inhibited by UA at the con- centration of 10 umol/L or 25 Ixmol/L （ P 〈0.05 vs. control）, and there was a statistical significant difference between 10 umol/L and 25 umol/L of UA （P 〈 0. 05 ） ; meanwhile, the ability of migration of VSMCs was sup- pressed by UA. Conclusion ： UA suppressed the proliferation and migration of VSMCs, which may be related to the downregulating the expressing of P-STAT3.
出处
《心肺血管病杂志》
CAS
2013年第5期624-627,共4页
Journal of Cardiovascular and Pulmonary Diseases
基金
国家自然科学基金(NO:30870641
NO:81001005)
关键词
熊果酸
血管平滑肌细胞
信号转导与转录激活因子3
增殖
迁移
Ursolic acid
Vascular smooth muscle cells
Signal transduction and activator of tran-scription 3
Proliferation
Migration
