Apoptosis of airway epithelial cells induced by corticosteroids

Larmonier et al. , found that curcumin attenuated lipopolysaccharide (LPS)-stimulated expression and secretion of macrophage inflammatory protein (MIP)-2, IL-1β, keratinocyte chemoattractant (KC), and MIP-1α in colonic epithelial cells (CECs) and in macrophages. Curcumin significantly inhibited PMN chemotaxis against MIP-2, KC, or against conditioned media from LPS-treated macrophages or CEC, a well as the IL-8-mediated chemotaxis of human neutrophils. Curcumin inhibited random neutrophil migration with no toxic effects, suggesting a direct effect on neutrophil chemokinesis. Curcumin inhibited PMN motility by the downregulation of PI3K activity, AKT phosphorylation, and F-actin polymerization [ 37 ]. Epstein also demonstrated reduced p38 MAPK activation and IL-1β, enhanced IL-10 and dose-dependent suppression of MMP-3 in CMF in curcumin-treated mucosal biopsies [ 38 ]. Curcumin has been shown to attenuate colitis in the dinitrobenzenesulfonic acid (DNB)-induced murine model of colitis with a reduction in MPO activity, IL-1β expression, and reduction of p38 MAPK. Binion et al. , found curcumin may inhibit VEGF-mediated angiogenesis in human intestinal microvascular endothelial cells via down regulation of the COX-2 and MAPK [ 39 , 40 ]. Curcumin also inhibited the expression of VCAM-1 in HIMECs through the block of p38 MAPK, Akt, and NF-κB. Thus curcumin may represent a novel therapeutic agent targeting endothelial activation in IBD [ 41 , 42 ]. Curcumin showed a protective effects on 2,4,6-trinitrobenzenesulphonic acid-induced colitis in mice. Curcumin also reduced NO and O 2 levels, which were associated with the effective expression of Th1 and Th2 cytokines and inducible NO synthase. NF-κB activation in colonic mucosa was also suppressed in the curcumin-treated mice [ 43 ].

Overperfuson and underperfusion should not be confused with hypoperfusion and hyperperfusion, which relate to the perfusion level relative to a tissue's current need to meet its metabolic needs. For example, hypoperfusion can be caused when an artery or arteriole that supplies blood to a volume of tissue becomes blocked by an embolus , causing either no blood or at least not enough blood to reach the tissue. Hyperperfusion can be caused by inflammation , producing hyperemia of a body part. Malperfusion, also called poor perfusion, is any type of incorrect perfusion. There is no official or formal dividing line between hypoperfusion and ischemia ; sometimes the latter term refers to zero perfusion, but often it refers to any hypoperfusion that is bad enough to cause necrosis .

Apoptosis of airway epithelial cells induced by corticosteroids

apoptosis of airway epithelial cells induced by corticosteroids

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