PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21679760-6 2011 RESULTS: Sinomenine was found to significantly inhibit TNF-alpha induced cell surface expression of vascular cell adhesion molecule (VCAM)-1 and release of inflammatory cytokine and chemokine IL-6, CCL2 and CXCL8 from both normal and RA-FLS (all p<0.05). sinomenine 9-19 tumor necrosis factor Homo sapiens 55-64 21679760-7 2011 Moreover, the suppression of sinomenine on TNF-alpha induced VCAM-1 expression and IL-6 release of RA-FLS was significantly higher than that of normal FLS (p<0.05). sinomenine 29-39 tumor necrosis factor Homo sapiens 43-52 21679760-9 2011 Further investigations showed that sinomenine and LMS could significantly suppress TNF-alpha-induced phosphorylation of inhibitor kappaBalpha and extracellular signal-regulated protein kinase, the central signaling molecules mediating TNF-alpha-induced VCAM-1 expression and chemokine production. sinomenine 35-45 tumor necrosis factor Homo sapiens 83-92 21679760-9 2011 Further investigations showed that sinomenine and LMS could significantly suppress TNF-alpha-induced phosphorylation of inhibitor kappaBalpha and extracellular signal-regulated protein kinase, the central signaling molecules mediating TNF-alpha-induced VCAM-1 expression and chemokine production. sinomenine 35-45 tumor necrosis factor Homo sapiens 235-244 21679760-10 2011 CONCLUSION: Our results therefore provide a new insight into the differential anti-inflammatory activities of sinomenine and LMS through the suppression of TNF-alpha-activated FLS by modulating distinct intracellular signaling pathways in RA. sinomenine 110-120 tumor necrosis factor Homo sapiens 156-165 17869461-0 2007 Sinomenine suppresses TNF-alpha-induced VCAM-1 expression in human umbilical vein endothelial cells. sinomenine 0-10 tumor necrosis factor Homo sapiens 22-31 17869461-13 2007 Our preliminary data indicates that SN has an inhibitory effect in vitro on TNF-alpha-induced VCAM-1 expression at both mRNA level and protein level in HUVECs, and suggests that SN may be a novel method of immunotherapy for rheumatic carditis or rheumatic heart disease. sinomenine 36-38 tumor necrosis factor Homo sapiens 76-85