|1.||Bueno, Lionel: 3 articles (08/2007 - 04/2003)|
|2.||Fioramonti, Jean: 3 articles (08/2007 - 04/2003)|
|3.||Henry, Peter J: 2 articles (12/2012 - 04/2005)|
|4.||Lohman, Rink-Jan: 2 articles (02/2012 - 10/2009)|
|5.||Salvador-Cartier, Christel: 2 articles (08/2007 - 08/2004)|
|6.||Cenac, Nicolas: 2 articles (08/2004 - 04/2003)|
|7.||Garcia-Villar, Rafael: 2 articles (08/2004 - 04/2003)|
|8.||Ferrier, Laurent: 2 articles (08/2004 - 04/2003)|
|9.||Vergnolle, Nathalie: 2 articles (08/2004 - 04/2003)|
|10.||Howitt, Lauren: 1 article (04/2014)|
12/01/2012 - "In summary, SLIGRL protected mice from IAV infection independently of PAR(2) and independently of direct inhibition of IAV attachment or replication, potentially through the activation of endogenous antiviral pathways within the mouse respiratory tract."
12/01/2012 - "Inhibitory influence of the hexapeptidic sequence SLIGRL on influenza A virus infection in mice."
06/01/2007 - "In addition, in a separate study in BALB/c mice, two immunological hallmarks of parasite infection, IgE- and IL-10-expressing lymphocytes, were shown to be augmented after the coadministration of the classic antigen ovalbumin with the PAR(2)-activating peptide SLIGRL (single letter amino acid sequence) but not the inactive reverse peptide LRGILS. "
08/01/2004 - "Thus, at the lower dose, SLIGRL increased colonic permeability without causing inflammation. "
08/01/2004 - "We evaluated the effects of intracolonic infusion of PAR(2)-activating peptide, SLIGRL, on colonic paracellular permeability and inflammation at two different doses, 5 and 100 microg per mouse, in an attempt to discriminate between both PAR(2)-mediated effects. "
08/01/2004 - "Moreover, SLIGRL at a dose that does not produce inflammation increases permeability via calmodulin activation, which binds and activates MLCK. "
04/15/2003 - "Thus, intracolonic infusion to mice of the PAR-2-activating peptide, SLIGRL, increased both myeloperoxidase (MPO) activity and damage scores indicating colonic inflammation, and enhanced colonic permeability to (51)Cr-EDTA from 2 to 4 h after its infusion. "
02/01/2012 - "Acute colonic inflammation induced in rats by the PAR2 agonist SLIGRL-NH₂ was inhibited by oral administration of GB88 (10 mg/kg) with markedly reduced edema, mucin depletion, PAR2 receptor internalization, and mastocytosis. "
10/01/2004 - "Intrathecal SFLLRN-NH(2) and SLIGRL both produced thermal hyperalgesia. "
08/01/2007 - "The effect of mast cell stabiliser (doxantrazole, 1 mg/kg intraperitoneally, 2 h before and 6 h after intracolonic infusion of SLIGRL) on SLIGRL-induced visceral hyperalgesia was also assessed. "
10/01/2006 - "Mechanical and thermal hyperalgesia induced by PAR2 agonists (SLIGRL-NH2 and trypsin) was measured in rats submitted to the paw pressure or plantar tests, and Egr-1 expression was determined by immunohistochemistry in rat spinal cord dorsal horn. "
08/01/2007 - "4 days of dexamethasone as well as doxantrazole diminished the SLIGRL-induced hyperalgesia for all volumes of distension. "
10/01/2004 - "SLIGRL-induced hyperalgesia was also blocked by the selective inhibitors SC 58,560 [5-(4-fluorophenyl)-1-[4-(methylsulfonyl)phenyl]-3-(trifluoromethyl)-1H-pyrazole; cyclooxygenase (COX) 1] and SC 58,125 [5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-(trifluoromethyl)-1H-pyrazole; COX 2]. "
|5.||Hypotension (Low Blood Pressure)
01/01/1998 - "SLIGRL induced a more prolonged hypotension with a slow return to baseline, whereas SFLLRN- and TFLLRNPNDK-induced hypotension was followed by a rapid return towards baseline and a sustained moderate hypotension. "
01/01/1998 - "SFLLRN and TFLLRNPNDK, but not SLIGRL, decreased HR. N omega-Nitro-L-arginine methyl ester HCl (L-NAME), an inhibitor of nitric oxide synthesis, attenuated the cumulative hypotensive response to SLIGRL but had no effect on the SFLLRN and TFLLRNPNDK hypotension. "
02/01/1999 - "In WT mice, SLIGRL, a PAR-2 selective activating peptide, caused hypotension without changing HR at 0.3 micromol/kg. SLIGRL did not induce hypertension following Nomega-nitrol-arginine-methyl ester-HCl (L-NAME). "
|2.||Immunoglobulin E (IgE)
|5.||NG-Nitroarginine Methyl Ester (L-NAME)
|6.||Nitric Oxide (Nitrogen Monoxide)
|7.||Histamine (Histamine Dihydrochloride)
|8.||thrombin receptor peptide (42-47)
|9.||Caspase 3 (Caspase-3)