黄芩苷对凝血酶诱导的人脐静脉内皮细胞损伤的保护作用。
Baicalin Protects against Thrombin-Induced Cell Injury in Human Umbilical Vein Endothelial Cells.
机构信息
Department of Geriatrics, Southern Hospital of the Second Hospital of Shandong University, Jinan 250033, China.
Intensive Care Unit, Qianfoshan Hospital, Shandong University, Jinan 250014, China.
出版信息
Biomed Res Int. 2019 Aug 6;2019:2187306. doi: 10.1155/2019/2187306. eCollection 2019.
Thrombin plays a pivotal role in the pathogenesis of atherosclerosis. Baicalin, an active flavonoid compound, was shown to attenuate the development of atherosclerosis, but the mechanism remains elusive. In the present study, the role and mechanism of baicalin in thrombin-induced cell injury was investigated in human umbilical vein endothelial cells (HUVECs). Our results showed that baicalin significantly reduced thrombin-induced apoptosis of HUVECs. Additional experiments showed that baicalin inhibited thrombin-induced NF-B activation and PAR-1 expression. In addition, baicalin decreased thrombin-induced PAR-1 expression by inhibiting ERK pathway. These results indicated that baicalin has protective effects on thrombin-induced cell injury in HUVECs possibly through inhibition of PAR-1 expression and its downstream NF-B activation, which was mediated by ERK1/2 activation.
凝血酶在动脉粥样硬化的发病机制中起着关键作用。黄芩素是一种具有生物活性的黄酮类化合物,已被证明能减轻动脉粥样硬化的发展,但作用机制尚不清楚。在本研究中,研究了黄芩素在凝血酶诱导的人脐静脉内皮细胞(HUVEC)损伤中的作用及其机制。结果表明,黄芩素能显著减轻凝血酶诱导的 HUVEC 凋亡。进一步的实验表明,黄芩素抑制凝血酶诱导的 NF-B 激活和 PAR-1 表达。此外,黄芩素通过抑制 ERK 通路降低凝血酶诱导的 PAR-1 表达。这些结果表明,黄芩素对凝血酶诱导的 HUVEC 损伤具有保护作用,可能是通过抑制 PAR-1 表达及其下游 NF-B 激活,而这是由 ERK1/2 激活介导的。