Involvement of heme oxygenase-1 induction in anti-vascular inflammation effects of Xanthoceras sorbifolia in human umbilical vein endothelial cells  

作　　者：Jung Joo Yoon Byung Hyuk Han Eun Sik Choi Seung Namgung Da Hye Jeong Song Nan Jin Yun Jung Lee Dae Gill Kang Ho Sub Lee 

机构地区：[1]College of Oriental Medicine and Professional Graduate School of Oriental Medicine, Wonkwang University [2]Hanbang Cardio-Renal Syndrome Research Center, Wonkwang University [3]Institute of Materia Medica, Taishan Medical University

出　　处：《Journal of Traditional Chinese Medicine》2018年第6期803-814,共12页中医杂志（英文版）

基　　金：Supported by the Natural Science Foundation of Shandong Province,China(No.ZR2015HM037);a National Research Foundation of Korea(NRF)Grant Funded by the Korean Government(No.NRF-2017R1A5A2015805)

摘　　要：OBJECTIVE: To define the effects of Xanthoceras sorbifolia(EXS) on vascular inflammation and the mechanisms in endothelial cells.METHODS: Vascular protective effects of an ethanol extract of seeds from EXS(1-50 μg/mL) against tumor necrosis factor-α(TNF-α)-induced vascularinflammation were examined in human umbilical vein endothelial cells(HUVECs).RESULTS: EXS significantly decreased TNF-α-induced expression of cell adhesion molecules, such as intracellular adhesion molecule-1, vascular cell adhesion molecule-1, and endothelial cell selectin,in a dose-dependent manner. Pre-treatment with EXS significantly inhibited translocation and transcriptional activity of nuclear factor-κB(NF-κB) increased by TNF-α. EXS also significantly inhibited formation of intracellular reactive oxygen species(ROS). Moreover, the vascular protective effects of EXS were linked to up-regulation of heme oxygenase-1(HO-1) and nuclear factor E2-related factor-2(Nrf-2) expression. EXS-induced HO-1 expression was significantly decreased in SnPP(HO-1 inhibitor)-and HO-1 siRNA-treated cells, whereas an increase was found in cobalt protoporphyrin IX(CoPP)(HO-1 inducer)-treated cells. In addition, pretreatment with EXS increased HO-1 and Nrf-2 expression under TNF-α stimulation with or without N-acetyl-L-cysteine. Furthermore, the inhibitory effects of EXS on TNF-α-induced vascular inflammation were partially reversed in SnPP-and of HO-1siRNA-treated cells but increased by CoPP.CONCLUSION: These results suggest that EXS may have important implications for prevention of vascular complications associated with vascular inflammation by inhibition of the NF-κB/ROS pathway and activation of the Nrf-2/HO-1 pathway.OBJECTIVE: To define the effects of Xanthoceras sorbifolia(EXS) on vascular inflammation and the mechanisms in endothelial cells.METHODS: Vascular protective effects of an ethanol extract of seeds from EXS(1-50 μg/mL) against tumor necrosis factor-α(TNF-α)-induced vascularinflammation were examined in human umbilical vein endothelial cells(HUVECs).RESULTS: EXS significantly decreased TNF-α-induced expression of cell adhesion molecules, such as intracellular adhesion molecule-1, vascular cell adhesion molecule-1, and endothelial cell selectin,in a dose-dependent manner. Pre-treatment with EXS significantly inhibited translocation and transcriptional activity of nuclear factor-κB(NF-κB) increased by TNF-α. EXS also significantly inhibited formation of intracellular reactive oxygen species(ROS). Moreover, the vascular protective effects of EXS were linked to up-regulation of heme oxygenase-1(HO-1) and nuclear factor E2-related factor-2(Nrf-2) expression. EXS-induced HO-1 expression was significantly decreased in SnPP(HO-1 inhibitor)-and HO-1 siRNA-treated cells, whereas an increase was found in cobalt protoporphyrin IX(CoPP)(HO-1 inducer)-treated cells. In addition, pretreatment with EXS increased HO-1 and Nrf-2 expression under TNF-α stimulation with or without N-acetyl-L-cysteine. Furthermore, the inhibitory effects of EXS on TNF-α-induced vascular inflammation were partially reversed in SnPP-and of HO-1siRNA-treated cells but increased by CoPP.CONCLUSION: These results suggest that EXS may have important implications for prevention of vascular complications associated with vascular inflammation by inhibition of the NF-κB/ROS pathway and activation of the Nrf-2/HO-1 pathway.

关 键 词：SAPINDACEAE Vascular disease inflammation Human UMBILICAL VEIN endothelial cells Cell adhesion molecules NF-KAPPA B HEME oxy-genase-1 

分 类 号：R[医药卫生]