Glossogyne tenuifolia Extract Inhibits TNF-α-Induced Expression of Adhesion Molecules in Human Umbilical Vein Endothelial Cells via Blocking the NF-kB Signaling Pathway

Molecules

Hsia-Fen Hsu¹  Thung-Lip Lee²  Kwan-Lih Hsu²  Wei-Kung Tseng²  Chau-Chung Wu³  Yu-Feng Wei⁴  Chin-Feng Hsuan⁵  Jer-Yiing Houng⁵ 

[1] Department of Nutrition, I-Shou University, Kaohsiung 82445, Taiwan;Division of Cardiology, Department of Internal Medicine, E-Da Hospital/I-Shou University, Kaohsiung 82445, Taiwan;Division of Cardiology, Department of Internal Medicine, National Taiwan University Hospital, Taipei 10002, Taiwan;Division of Pulmonary Medicine, Department of Internal Medicine,E-Da Hospital/I-Shou University, Kaohsiung 82445, Taiwan;Institute of Biotechnology and Chemical Engineering, I-Shou University, Kaohsiung 84001,Taiwan;

关键词: Glossogyne tenuifolia;    luteolin;    luteolin-7-glucoside;    adhesion molecule;    nuclear factor-kB;   

DOI  :  10.3390/molecules200916908

来源: DOAJ

【 摘 要 】

Chronic inflammation plays a pivotal role in the development of atherosclerosis, where the pro-inflammatory cytokine-induced expression of endothelial adhesion molecules and the recruitment of monocytes are the crucial events leading to its pathogenesis. Glossogyne tenuifolia ethanol extract (GTE) is shown to have potent anti-inflammatory and antioxidant activities. We evaluated the effects of GTE and its major components, luteolin (lut), luteolin-7-glucoside (lut-7-g), and oleanolic acid (OA) on TNF-α-induced expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs). The results demonstrated that GTE, lut, and lut-7-g attenuated the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in TNF-α-activated HUVECs, and inhibited the adhesion of monocytes to TNF-α-activated HUVECs. The TNF-α-induced mRNA expression of ICAM-1 and VCAM-1 was also suppressed, revealing their inhibitory effects at the transcriptional level. Furthermore, GTE, lut, and lut-7-g blocked the TNF-α-induced degradation of nuclear factor-kB inhibitor (IkB), an indicator of the activation of nuclear factor-kB (NF-kB). In summary, GTE and its bioactive components were effective in preventing the adhesion of monocytes to cytokine-activated endothelium by the inhibition of expression of adhesion molecules, which in turn is mediated through blocking the activation and nuclear translocation of NF-kB. The current results reveal the therapeutic potential of GTE in atherosclerosis.

【 授权许可】

Unknown