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CML-1 inhibits TNF-alpha-induced NF-kappaB activation and adhesion molecule expression in endothelial cells through inhibition of IkBalpha kinase.
J Ethnopharmacol. 2007 Jan 03; 109(1):78-86.JE

Abstract

CML-1 is a purified extract from a mixture of 13 oriental herbs (Achyranthis Radix, Angelicae Gigantis Radix, Cinnamomi Cortex Spissus, Eucommiae Cortex, Glycyrrhizae Radix, Hoelen, Lycii Fructus, Paeoniae Radix, Rehmanniae Radix Preparata and Atractylodis Rhizoma, Zingiberis Rhizoma, Zizyphi Semen, Acori Graminei Rhizoma) that have been widely used for the treatment of inflammatory diseases in Asia. Since our previous study has been shown to have the anti-inflammatory activity of CML-1 in vivo and the upregulation of adhesion molecules in response to numerous inducing factors is associated with inflammation, this study examined the effect of CML-1 on the expression of adhesion molecules induced by TNF-alpha in cultured human umbilical vein endothelial cells (HUVECs). Preincubation of HUVECs for 20h with CML-1 (1-100mug/ml) dose-dependently inhibited TNF-alpha (10ng/ml)-induced adhesion of THP-1 monocytic cells, as well as mRNA and protein expression of E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). CML-1 was also shown to inhibit NK-kB activation induced by TNF-alpha. Furthermore, CML-1 inhibited TNF-alpha-induced IkB kinase activation, subsequent degradation of IkBalpha, and nuclear translocation of NK-kB. Evidence presented in this report demonstrated that CML-1 inhibited the adhesive capacity of HUVEC and the TNF-alpha-mediated induction of E-selectin, ICAM-1 and VCAM-1 in HUVEC by inhibiting the IkB/NF-kB signaling pathway at the level of IkB kinase, which may explain the ability of CML-1 to suppress inflammation and modulate the immune response.

Authors+Show Affiliations

College of Pharmacy, Sungkyunkwan University, Suwon City, Kyunggi-do 440-746, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16920299

Citation

Mo, Seong-Ji, et al. "CML-1 Inhibits TNF-alpha-induced NF-kappaB Activation and Adhesion Molecule Expression in Endothelial Cells Through Inhibition of IkBalpha Kinase." Journal of Ethnopharmacology, vol. 109, no. 1, 2007, pp. 78-86.
Mo SJ, Son EW, Lee SR, et al. CML-1 inhibits TNF-alpha-induced NF-kappaB activation and adhesion molecule expression in endothelial cells through inhibition of IkBalpha kinase. J Ethnopharmacol. 2007;109(1):78-86.
Mo, S. J., Son, E. W., Lee, S. R., Lee, S. M., Shin, D. H., & Pyo, S. (2007). CML-1 inhibits TNF-alpha-induced NF-kappaB activation and adhesion molecule expression in endothelial cells through inhibition of IkBalpha kinase. Journal of Ethnopharmacology, 109(1), 78-86.
Mo SJ, et al. CML-1 Inhibits TNF-alpha-induced NF-kappaB Activation and Adhesion Molecule Expression in Endothelial Cells Through Inhibition of IkBalpha Kinase. J Ethnopharmacol. 2007 Jan 3;109(1):78-86. PubMed PMID: 16920299.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - CML-1 inhibits TNF-alpha-induced NF-kappaB activation and adhesion molecule expression in endothelial cells through inhibition of IkBalpha kinase. AU - Mo,Seong-Ji, AU - Son,Eun-Wha, AU - Lee,Sung-Ryul, AU - Lee,Sun-Mee, AU - Shin,Dae-Hee, AU - Pyo,Suhkneung, Y1 - 2006/07/11/ PY - 2005/11/05/received PY - 2006/06/19/revised PY - 2006/07/05/accepted PY - 2006/8/22/pubmed PY - 2007/4/14/medline PY - 2006/8/22/entrez SP - 78 EP - 86 JF - Journal of ethnopharmacology JO - J Ethnopharmacol VL - 109 IS - 1 N2 - CML-1 is a purified extract from a mixture of 13 oriental herbs (Achyranthis Radix, Angelicae Gigantis Radix, Cinnamomi Cortex Spissus, Eucommiae Cortex, Glycyrrhizae Radix, Hoelen, Lycii Fructus, Paeoniae Radix, Rehmanniae Radix Preparata and Atractylodis Rhizoma, Zingiberis Rhizoma, Zizyphi Semen, Acori Graminei Rhizoma) that have been widely used for the treatment of inflammatory diseases in Asia. Since our previous study has been shown to have the anti-inflammatory activity of CML-1 in vivo and the upregulation of adhesion molecules in response to numerous inducing factors is associated with inflammation, this study examined the effect of CML-1 on the expression of adhesion molecules induced by TNF-alpha in cultured human umbilical vein endothelial cells (HUVECs). Preincubation of HUVECs for 20h with CML-1 (1-100mug/ml) dose-dependently inhibited TNF-alpha (10ng/ml)-induced adhesion of THP-1 monocytic cells, as well as mRNA and protein expression of E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). CML-1 was also shown to inhibit NK-kB activation induced by TNF-alpha. Furthermore, CML-1 inhibited TNF-alpha-induced IkB kinase activation, subsequent degradation of IkBalpha, and nuclear translocation of NK-kB. Evidence presented in this report demonstrated that CML-1 inhibited the adhesive capacity of HUVEC and the TNF-alpha-mediated induction of E-selectin, ICAM-1 and VCAM-1 in HUVEC by inhibiting the IkB/NF-kB signaling pathway at the level of IkB kinase, which may explain the ability of CML-1 to suppress inflammation and modulate the immune response. SN - 0378-8741 UR - https://www.unboundmedicine.com/medline/citation/16920299/CML_1_inhibits_TNF_alpha_induced_NF_kappaB_activation_and_adhesion_molecule_expression_in_endothelial_cells_through_inhibition_of_IkBalpha_kinase_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0378-8741(06)00343-6 DB - PRIME DP - Unbound Medicine ER -