Search for New Compounds with Anti-Inflammatory Activity Among 1,2,4-Triazole Derivatives.

Compounds containing the 1,2,4-triazole moiety in their structure exhibit broad biological activities. Many of these compounds demonstrate anti-inflammatory activity in vitro through various mechanisms, such as inhibiting COX-1/COX-2 and LOX, modulating pro-inflammatory cytokine levels, or having effects on other specific enzymes. Some also display activities in vivo.

Integrative pathway dissection of molecular mechanisms of moxLDL-induced vascular smooth muscle phenotype transformation.

Background: Atherosclerosis (AT) is a chronic inflammatory disease characterized by the accumulation of inflammatory cells, lipoproteins and fibrous tissue in the walls of arteries. AT is the primary cause of heart attacks and stroke and is the leading cause of death in Western countries. To date, the pathogenesis of AT is not well-defined.

Microarray analysis of ox-LDL (oxidized low-density lipoprotein)-regulated genes in human coronary artery smooth muscle cells.

Recent studies suggest that circulating LDL (low-density lipoproteins) play a central role in the pathogenesis of atherosclerosis, and the oxidized form (ox-LDL) is highly atherogenic. Deposits of ox-LDL have been found in atherosclerotic plaques, and ox-LDL has been shown to promote monocyte recruitment, foam cell formation and the transition of quiescent and contractile vascular SMCs (smooth muscle cells) to the migratory and proliferative phenotype. SMC phenotype transition and hyperplasia are the pivotal events in the pathogenesis of atherosclerosis.

mRNA differential display identification of vascular smooth muscle early response genes regulated by PDGF.

The modulation of vascular smooth muscle cells (VSMCs) from the quiescent phenotype to the proliferative and migratory phenotype is a critical event in the pathogenesis of atherosclerosis. To-date several growth factors, including platelet-derived growth factor, PDGF, have been shown to induce VSMC proliferation and migration. To further understand the mechanism of PDGF-induced VSMC activation, quiescent human coronary artery SMC were treated with PDGF, and the genes that displayed transcriptional changes within 3 and 8 h were identified using differential display RT-PCR, real-time PCR, nucleotide sequencing and bioinformatics.

Expression of gC1q-R/p33 and its major ligands in human atherosclerotic lesions.

A growing body of evidence supports the hypothesis that atherosclerosis has an inflammatory component, and that immune mechanisms, including complement activation, are likely to be involved. gC1q-R/p33 (gC1q-R) is a multifunctional and multicompartmental cellular protein, which is postulated to play a role in inflammation and thrombosis by interacting with C1q and high molecular weight kininogen (HK). To examine the expression of gC1q-R and its major ligands, C1q and HK, in human atherosclerotic lesions, sections of carotid arteries removed during endarterectomy and coronary arteries obtained at autopsy were stained with specific polyclonal or monoclonal antibodies.