Cao Li Hua, Lee Yun Jung, Kang Dae Gill, Kim Jin Sook, Lee Ho Sub
Professional Graduate School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk, 570-749, Republic of Korea.
Vascul Pharmacol. 2009 May-Jun;50(5-6):200-7. doi: 10.1016/j.vph.2009.01.008.
Pro-inflammatory cytokines induce the injury of endothelial cells in response to increases of adhesion molecules, leading to vascular inflammation and the development of atherosclerosis. In this study, we evaluated an ethanol extract of Zanthoxylum schinifolium (EZS) to determine if it inhibits the expressions of cellular adhesion molecules in human umbilical vein endothelial cells (HUVEC). When pretreatment of HUVEC with EZS, EZS suppressed the expression levels of cell adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-), and E-selectin induced by TNF-alpha. The adhesion of HL-60 cells to TNF-alpha-induced endothelial cells was decreased significantly in a concentration-dependent manner. Furthermore, TNF-alpha-induced MCP-1 and IL-8 mRNA expression levels were also attenuated by pretreatment with EZS. In addition, EZS suppressed TNF-alpha-induced production of reactive oxygen species (ROS). EZS inhibited NF-kappaB activation and IkappaB-alpha phosphorylation induced by TNF-alpha, subsequent degradation of IkappaB-alpha. Finally, EZS inhibited TNF-alpha-induced p38 MAPK and c-Jun N-terminal kinase (JNK) phosphorylation. Taken together, these results demonstrate that EZS suppresses vascular inflammatory process, which may be closely related to the inhibition of ROS, JNK, p38 MAPK and NF-kappaB activation in HUVEC.
促炎细胞因子会因黏附分子增加而诱导内皮细胞损伤，导致血管炎症和动脉粥样硬化的发展。在本研究中，我们评估了竹叶椒乙醇提取物（EZS），以确定其是否能抑制人脐静脉内皮细胞（HUVEC）中细胞黏附分子的表达。用EZS预处理HUVEC时，EZS可抑制肿瘤坏死因子-α（TNF-α）诱导的血管细胞黏附分子-1（VCAM-1）、细胞间黏附分子-1（ICAM-）和E-选择素等细胞黏附分子的表达水平。HL-60细胞与TNF-α诱导的内皮细胞的黏附以浓度依赖的方式显著降低。此外，EZS预处理还可减弱TNF-α诱导的单核细胞趋化蛋白-1（MCP-1）和白细胞介素-8（IL-8）mRNA表达水平。此外，EZS可抑制TNF-α诱导的活性氧（ROS）生成。EZS可抑制TNF-α诱导的核因子-κB（NF-κB）激活以及IκB-α磷酸化，随后IκB-α降解。最后，EZS可抑制TNF-α诱导的p38丝裂原活化蛋白激酶（p38 MAPK）和c-Jun氨基末端激酶（JNK）磷酸化。综上所述，这些结果表明EZS可抑制血管炎症过程，这可能与抑制HUVEC中的ROS、JNK、p38 MAPK和NF-κB激活密切相关。
