YS 49, 1-(α-naphtylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, regulates angiotensin II-stimulated ROS production, JNK phosphorylation and vascular smooth muscle cell proliferation via the induction of heme oxygenase-1

Neferine inhibits angiotensin II-stimulated proliferation in vascular smooth muscle cells through heme oxygenase-1

“…CO is one of the products of heme degradation. The antiproliferative effect of YS 49 on VSMC is reversed by pretreatment with hemoglobin, a CO scavenger [38] . Cdk-2 is a key regulator of both G 1 and S phase cell progression.…”

Activation of PPAR-γ by Carbon Monoxide from CORM-2 Leads to the Inhibition of iNOS but not COX-2 Expression in LPS-Stimulated Macrophages

“…CO inhibits LPS-induced production of cytokines both in vitro and in vivo, and consequently exhibits important cytoprotective function and antiinflammatory properties that are beneficial for the resolution of acute inflammation [1,2]. Therefore CO releasing molecules (CORMs) are now being used as very useful pharmacological tools for investigation of CO effect [4,5,[12][13][14][15][16][17][18]. Several previous reports have clearly shown the involvement of PPAR-γ in the anti-inflammatory properties of CO [21,22].…”

“…On the other hand, prostaglandins (PGs) are also potent pro-inflammatory mediators derived from arachidonic acid metabolism by COX, and play an important role in modulating a number of pathological conditions including inflammatory responses. Carbon monoxide (CO) is one of the main metabolites of heme degradation by heme oxygenase (HO)-1 [3][4][5][6][7]. Its anti-inflammatory, anti-apoptotic, cytoprotective, and vasodilatory properties are well documented in different experimental models [7].…”

Cytotoxic response in human lung epithelial cells and ion characteristics of urban-air particles from Torino, a northern Italian city

“…The epidemiological associations are well established between PM mass concentrations and increased human mortality and morbidity (Brook et al 2010 , Pope andDockery 2006 ). Currently, the hypothesis that long-term exposure to air pollution can produce human morbidity and mortality is unanimously accepted, and epidemiological evidence suggests an increased risk of lung cancer for people living in urban areas (Nerriere et al 2005, Sun et al 2008 ). Long-term exposure to air pollution PM increases the risk of lung cancer, respiratory diseases and arteriosclerosis, whereas short-term exposure can exacerbate several forms of respiratory diseases, i.e.…”

“…Terzano et al 2010. Under physiological conditions, the normal production of reactive oxygen species (ROS) is counteracted by antioxidant scavengers and enzymes, which include both enzymes and non-enzymatic scavengers (de Kok et al 2006 ;Garcon et al 2006 ;Sun et al 2008 ). However, under abnormal conditions, excessive levels of ROS exceed the detoxification capacity of the antioxidant defences, thereby causing a change in the redox status of the cell (Jomova and Valko 2011 ;Lonkar and Dedon 2011 ;Ziech et al 2011 ).…”