oxadiazoles and Anaphylaxis
oxadiazoles has been researched along with Anaphylaxis* in 3 studies
Other Studies
3 other study(ies) available for oxadiazoles and Anaphylaxis
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Antiallergic activity profile in vitro RBL-2H3 and in vivo passive cutaneous anaphylaxis mouse model of new sila-substituted 1,3,4-oxadiazoles.
A new class of sila-substituted 1,3,4-oxadiazoles was synthesized and evaluated for antiallergic activity using RBL-2H3 as the in vitro model and the in vivo anaphylactic mouse model. We observed that compound 5c effectively suppressed DNP-HSA-induced mast cell degranulation, compared to carbon analogue 9, and also suppressed the expression of TNF-α mRNA and Akt phosphorylation in antigen-stimulated RBL-2H3 cells. We also studied the effect of 5c in an in vivo passive cutaneous anaphylaxis (PCA) mouse model. The suppression by 5c was more effective than that by diphenylhydramine (DPH), a typical anti-histamine drug. Topics: Anaphylaxis; Animals; Anti-Allergic Agents; beta-N-Acetylhexosaminidases; Cell Line; Gene Expression Regulation; Immunoglobulin E; Male; Mice; Organometallic Compounds; Oxadiazoles; Passive Cutaneous Anaphylaxis; Phosphorylation; Proto-Oncogene Proteins c-akt; Rats; RNA, Messenger; Silicon; Silver; Tumor Necrosis Factor-alpha | 2012 |
N(G)-nitro-L-arginine methyl ester, but not methylene blue, attenuates anaphylactic hypotension in anesthetized mice.
To clarify the role of NO in mouse anaphylactic hypotension, effects of a nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on antigen-induced hypotension and portal hypertension were determined in anesthetized BALB/c mice. Systemic arterial pressure (Psa), central venous pressure (Pcv), and portal venous pressure (Ppv) were directly and simultaneously measured. Mice were first sensitized with ovalbumin, and then the injection of antigen was used to decrease Psa and increase Ppv. Pretreatment with L-NAME (1 mg/kg) attenuated this antigen-induced systemic hypotension, but not the increase in Ppv. The effect of inhibitors of soluble guanylate cyclase on anaphylactic hypotension were studied with either methylene blue (3.0 mg/kg) or 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (10 mg/kg). Neither modulated any antigen-induced changes. Furthermore, methylene blue did not improve systemic hypotension induced by Compound 48/80 (4.5 mg/kg), a mast cell degranulator, which can produce non-immunological anaphylactoid reactions. These data show in anesthetized BALB/c mice that L-NAME attenuated anaphylactic hypotension without affecting portal hypertension. This beneficial effect of L-NAME appears not to depend on the soluble guanylate cyclase pathway. Topics: Anaphylaxis; Anesthesia; Animals; Blood Pressure; Enzyme Inhibitors; Guanylate Cyclase; Hypertension; Liver Circulation; Male; Methylene Blue; Mice; Mice, Inbred BALB C; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase Type III; Ovalbumin; Oxadiazoles; Quinoxalines | 2007 |
Anaphylactic shock depends on PI3K and eNOS-derived NO.
Anaphylactic shock is a sudden, life-threatening allergic reaction associated with severe hypotension. Platelet-activating factor (PAF) is implicated in the cardiovascular dysfunctions occurring in various shock syndromes, including anaphylaxis. Excessive production of the vasodilator NO causes inflammatory hypotension and shock, and it is generally accepted that transcriptionally regulated inducible iNOS is responsible for this. Nevertheless, the contribution of NO to PAF-induced shock or anaphylactic shock is still ambiguous. We studied PAF and anaphylactic shock in conscious mice. Surprisingly, hyperacute PAF shock depended entirely on NO, produced not by inducible iNOS, but by constitutive eNOS, rapidly activated via the PI3K pathway. Soluble guanylate cyclase (sGC) is generally regarded as the principal vasorelaxing mediator of NO. Nevertheless, although methylene blue partially prevented PAF shock, neither 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (ODQ) nor sGCalpha1 deficiency did. Also, in 2 different models of active systemic anaphylaxis, inhibition of NOS, PI3K, or Akt or eNOS deficiency provided complete protection. In contrast to the unsubstantiated paradigm that only excessive iNOS-derived NO underlies cardiovascular collapse in shock, our data strongly support the unexpected concept that eNOS-derived NO is the principal vasodilator in anaphylactic shock and define eNOS and/or PI3K or Akt as new potential targets for treating anaphylaxis. Topics: Anaphylaxis; Animals; Blood Pressure; Cardiovascular Diseases; Enzyme Inhibitors; Mice; Mice, Inbred C57BL; Mice, Knockout; Nitric Oxide; Nitric Oxide Synthase Type III; Oxadiazoles; Phosphatidylinositol 3-Kinases; Platelet Activating Factor; Quinoxalines; Serum Albumin, Bovine; Transcription, Genetic | 2006 |