[Effects and related mechanism of quercetin on thrombin-induced proliferation and migration of rat vascular smooth muscle cells].
Yu-Rong Jiang, Jian Ming Yang, Xiaowen Liu, Y Li, L Teng, Jiawang Ding, Qiutang Zeng, J Yang
Abstract
Yu-Rong Jiang, Jian Ming Yang, Xiaowen Liu, Y Li, L Teng, Jiawang Ding, Qiutang Zeng, J Yang
Abstract
OBJECTIVE: To investigate the effects and related mechanism of quercetin on thrombin-induced proliferation and migration of rat vascular smooth muscle cells(VSMCs). METHODS: 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. RESULTS: (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). CONCLUSION: 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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OBJECTIVE: To investigate the effects and related mechanism of quercetin on thrombin-induced proliferation and migration of rat vascular smooth muscle cells(VSMCs). METHODS: 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. RESULTS: (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). CONCLUSION: 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.
Key concepts: Thrombin, Quercetin, Vascular smooth muscle, Kinase, Western blot, p38 mitogen-activated protein kinases, Extracellular, Molecular biology