Baicalin Protects against Thrombin-Induced Cell Injury in Human Umbilical Vein Endothelial Cells.
Anna ZhangYunfeng HouChao SunYing PuYu SunYuan ZhangYang ShenQingbo ZhouPublished in: BioMed research international (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-κB 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-κB activation, which was mediated by ERK1/2 activation.
Keyphrases
- high glucose
- endothelial cells
- signaling pathway
- diabetic rats
- oxidative stress
- induced apoptosis
- poor prognosis
- drug induced
- single cell
- pi k akt
- cardiovascular disease
- cell proliferation
- cell therapy
- endoplasmic reticulum stress
- stem cells
- type diabetes
- binding protein
- mesenchymal stem cells
- long non coding rna
- nuclear factor
- high resolution
- toll like receptor
- high speed