Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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. The aim of this study was to investigate the anti-inflammatory and analgesic potential of CML-1. The animals used in this study were administered either vehicle or CML-1 (30, 100, 300 and 600 mg/kg) orally. The vascular permeability induced by acetic acid was significantly reduced by CML-1 in all doses. The swelling of the rat's hind paw induced by carrageenan was significantly inhibited by CML-1 in doses of 100, 300 and 600 mg/kg. In the case of rheumatoid arthritis induced by complete Freund's adjuvant in rats, the treatment with CML-1 at a dose level of 300 mg/kg inhibited edema. CML-1 at a dose level of 600 mg/kg inhibited acetic acid-induced writhing syndrome, however it did not have any anti-nociceptive action in the Randall-Selitto assay or the hot plate test. Our findings suggest that CML-1 has a potent anti-inflammatory activity.
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PMID:Anti-inflammatory activity of CML-1: an herbal formulation. 1584 31

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.
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PMID:CML-1 inhibits TNF-alpha-induced NF-kappaB activation and adhesion molecule expression in endothelial cells through inhibition of IkBalpha kinase. 1692 Feb 99