[Effects and related mechanism of quercetin on thrombin-induced proliferation and migration of rat vascular smooth muscle cells].

凝血酶 槲皮素 血管平滑肌 激酶 免疫印迹 p38丝裂原活化蛋白激酶 细胞外 分子生物学 化学 内分泌学 内科学 蛋白激酶A 医学 生物 生物化学 血小板 平滑肌 抗氧化剂 基因
作者
Yu-Rong Jiang,Jian Yang,Xiaowen Liu,Ying Li,Lin Teng,Jiawang Ding,Qiutang Zeng
出处
期刊:PubMed 卷期号:44 (8): 696-9 被引量:1
标识
DOI:10.3760/cma.j.issn.0253-3758.2016.08.011
摘要

To investigate the effects and related mechanism of quercetin on thrombin-induced proliferation and migration of rat vascular smooth muscle cells(VSMCs).Third to fifth generation VSMCs were divided into three groups, including control group (with PBS on the base of medium DMEM), thrombin group (with 1 U/ml thrombin on the base of medium DMEM) and quercetin group (treated with 100 μmol/L quercetin before 1 U/ml thrombin on the base of medium DMEM). The proliferation and migration capacitities were tested by CCK-8 kit and transwell chamber, respectively. The protein level of phospho-extracellular signal regulated kinase 1/2 and phosphor-p38 were measured by Western blot.(1) According to the CCK-8 results, optical density value was significantly higher in thrombin group than that of control group(2.59±0.16 vs. 1.97±0.18, P<0.01), which could be significantly attenuated by pretreatment with quercetin(2.13±0.19, P<0.01), and there was no significant difference between quercetin group and control group(P>0.05). (2) The transwell results showed that the migrated VSMCs were significantly higher in thrombin group than in control group (1 337±162 vs. 99±26, P<0.01), which could be significantly reduced by pretreatment with quercetin (926±111, P<0.05), but still significantly higher than control group (P<0.01). (3) The protein expressions of phospho-extracellular signal regulated kinase 1/2 and phosphor-p38 were significantly upregulated in thrombin group compared to control group (both P<0.05), which could be significantly downregulated by pretreatment with quercetin (P<0.05).Quercetin can effectively attenuate thrombin-induced vascular smooth muscle cells proliferation and migration, possibly through inhibiting the phosphorylation of extracellular signal regulated kinase 1/2 and p38 pathway.
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