Studies of the mediators of the acute inflammatory response induced in rats in different sites by carrageenan and turpentine

Endocannabinoids inhibit release of nerve growth factor by inflammation-activated mast cells

“…For example, mast cells increase their number and are activated following allergen or bacterial lipopolysaccharide challenge [32], as well as in increasing post-traumatic or post-ischemic inflammatory events [33]. It is in fact common notion that a quantitative evaluation of the real damage consequent to application of noxious stimuli is reasonable after one day or more from damage [34]. For example, in nervous trauma, this is the consequence of the progressive recruiting of neurons to apoptotic phenomena, which are triggered with the traumatic event and eventually progress in following hours [33].…”

Local administration of transcription factor decoy oligonucleotides to nuclear factor-κB prevents carrageenin-induced inflammation in rat hind paw

“…40 The initial phase of edema (0-1 h) has been attributed to the release of histamine, 5-hydroxytriptamine and bradykinin. 2 In contrast, the second phase of swelling (1-6 h), which is inhibited by nonsteroidal anti-inflammatory drugs, has been correlated with the elevated production of PGs and NO following the induction of COX-2 and iNOS protein expression in activated leukocytes infiltrated into the carrageenin-injected rat paw. [2][3][4][5][6] Since the discovery of the involvement of iNOS and COX-2 in inflammation, [3][4][5][6][7][8][9][10] molecules endowed with the ability of interfering with the expression of these two enzymes have attracted great interest.…”

“…2 In contrast, the second phase of swelling (1-6 h), which is inhibited by nonsteroidal anti-inflammatory drugs, has been correlated with the elevated production of PGs and NO following the induction of COX-2 and iNOS protein expression in activated leukocytes infiltrated into the carrageenin-injected rat paw. [2][3][4][5][6] Since the discovery of the involvement of iNOS and COX-2 in inflammation, [3][4][5][6][7][8][9][10] molecules endowed with the ability of interfering with the expression of these two enzymes have attracted great interest. Moreover, a growing body of evidence has demonstrated that many of the clinically important antiinflammatory agents, including salicylates 41 and glucocorticoids, [42][43][44] share the ability to inhibit NF-B activation and therefore a large variety of inflammatory genes, amongst these COX-2 45,46 and iNOS.…”

“…1 Rat paw edema induced by carrageenin, an experimental model of acute inflammation, is characterized by an early phase (0-1 h) brought about by the release of histamine, 5-hydroxytriptamine and bradykinin followed by a late phase (1-6 h) mainly sustained by prostaglandins (PGs) and nitric oxide (NO). [2][3][4] It has been demonstrated that both PGs and NO released at inflammatory site are generated by the inducible isoforms of cyclooxygenase (COX-2) and nitric oxide synthase (iNOS), respectively. [3][4][5][6][7][8][9][10][11] The promoter region of COX-2 [12][13][14] and iNOS genes [15][16][17] has been cloned and sequenced.…”

Evidence for activation of the tissue kallikrein‐kinin system in nociceptive transmission and inflammatory responses of mice using a specific enzyme inhibitor

“…At doses e ective in nociception, TKI reduced the paw swelling induced by carrageenin with the e ect lasting for 5 h at the highest doses (41 mmol kg 71 , i.p., and 410 mmol kg 71 , s.c.). The e ect could also be related to inhibition of kinins release, which have been implicated as major proin¯ammatory mediators in addition to histamine and prostaglandins (Di Rosa et al, 1971;Hargreaves et al, 1988). In the same model, tissues kinins were shown to be maximal after 1 h injection of carrageenin and to induce the release of other mediators that interact in synergism producing the oedema.…”