lignans and Anaphylaxis

Yangambin was initially selected from a number of lignans isolated from Brazilian plants for its ability to antagonize Platelet-Activating Factor (PAF, 1-O-hexadecyl-2-acetyl- sn-glyceryl-3-phosphorylcholine)-induced biological effects. Subsequently it was shown that, besides its antagonistic properties at PAF receptors, yangambin also prevents the cardiovascular collapse observed during anaphylactic and endotoxic/septic shocks, as well as the vascular and cardiac hyporesponsiveness to catecholamines in endotoxic shock. It is suggested that this naturally occurring compound could be of potential interest in the adjunctive management of the above mentioned pathologies. In the present article, we review the main studies investigating the pharmacological properties of yangambin related to the cardiovascular function.

Topics: Anaphylaxis; Animals; Blood Platelets; Cardiovascular Agents; Furans; Hemodynamics; In Vitro Techniques; Lignans; Plant Extracts; Platelet Activating Factor; Platelet Aggregation Inhibitors; Platelet Membrane Glycoproteins; Receptors, Cell Surface; Receptors, G-Protein-Coupled; Shock, Septic; Stereoisomerism

Topics: Anaphylaxis; Cardiovascular Diseases; Digestive System Diseases; Histamine H1 Antagonists; Histamine Release; Humans; Lignans; Lignin; Platelet Activating Factor; Terpenes

Mast cells (MCs) play critical roles in allergic reactions and modulating the activation of MCs could be an effective strategy to treat allergic diseases, which cause a rapidly increasing threat to the public health. Herein, we described that Magnolin, a major component from Flos magnoliae could inhibit IgE-dependent MCs activation. We found Magnolin inhibited IgE/Ag-induced calcium mobilization, degranulation, and cytokines release in LAD2 cells. Magnolin was also found to attenuate IgE/Ag-induced mice paw swelling in a dose-dependent manner. Further mechanistic studies suggested a possible anti-allergic and anti-inflammatory effects of Magnolin in IgE/Ag-induced anaphylactic reactions. Thereby, Magnolin could be a potential therapeutic agent for preventing mast cell-related immediate and delayed allergic diseases.

Topics: Anaphylaxis; Animals; Anti-Allergic Agents; Antigens; Calcium; Cell Line; Cell Survival; Cytokines; Edema; Histamine; Humans; Hypersensitivity; Immunoglobulin E; Lignans; Male; Mast Cells; Mice, Inbred BALB C; Mitogen-Activated Protein Kinases; Peptide Hydrolases

The Arctium lappa seeds (Arctii Fructus) and its major active compound, arctigenin (ARC), are known to have anticancer, antiobesity, antiosteoporosis, and anti-inflammatory activities. However, the effect of Arctii Fructus and ARC on mast cell-mediated allergic inflammation and its associated mechanism have not been elucidated. Therefore, we attempted to investigate the antiallergic activity of Arctii Fructus and ARC on mast cells and experimental mouse models. Arctii Fructus water extract (AFW) or ethanol extract (AFE) and ARC reduced the production of histamine and pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, IL-8, and TNF-α in mast cells. AFW, AFE, and ARC inhibited phosphorylation of MAPKs and NF-κB in activated mast cells. Moreover, IgE-mediated passive cutaneous anaphylaxis and compound 48/80-induced anaphylactic shock were suppressed by AFW, AFE, and ARC administration. These results suggest that Arctii Fructus and ARC are potential therapeutic agents against allergic inflammatory diseases.

Topics: Anaphylaxis; Animals; Anti-Allergic Agents; Arctium; Furans; Humans; Interleukin-6; Interleukin-8; Lignans; Male; Mast Cells; Mice; Mice, Inbred ICR; Plant Extracts; Tumor Necrosis Factor-alpha

Topics: Anaphylaxis; Anemarrhena; Animals; Anti-Allergic Agents; Cell Degranulation; Cell Line, Tumor; Disease Models, Animal; Dose-Response Relationship, Drug; Ethanol; Histamine; Leukemia, Basophilic, Acute; Lignans; Male; Mast Cells; Mice; Mice, Inbred C57BL; p-Methoxy-N-methylphenethylamine; Phytotherapy; Plant Extracts; Plants, Medicinal; Rats; Rhizome; Solvents

Topics: 4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyrazol-3-amine; Anaphylaxis; Animals; Anti-Inflammatory Agents, Non-Steroidal; Benzofurans; Blood Pressure; Diphenhydramine; Guinea Pigs; In Vitro Techniques; Lignans; Lung; Male; Platelet Activating Factor; Platelet Count; Pyrazoles

The role of platelet activating factor (PAF) and its inhibition by specific receptor antagonists was studied in hypersensitivity reactions in guinea pig lung parenchymal strips and in guinea pigs in vivo. Immunological challenge of isolated lung parenchymal strips with ovalbumin resulted in a contractile response of 184 +/- 16 mg (n = 38). Pretreatment of the strips with a combination of the antihistamine diphenhydramine, the dual lipoxygenase and cyclooxygenase product synthesis inhibitor BW-755C, and the PAF receptor antagonist kadsurenone totally inhibited the increase in tension. The bronchoconstrictor effects induced by immunological challenge were also totally inhibited when the leukotriene receptor antagonist FPL-55,712 was used to replace BW-755C or another PAF receptor antagonist, alprazolam was used to replace kadsurenone. Ovalbumin challenge in sensitized guinea pigs in vivo resulted in airway constriction, circulatory failure and an abrupt fall in continuously measured platelet count by 75 +/- 12%, followed by death of all animals within 5-8 min. Pretreatment with diphenhydramine, BW-755C and kadsurenone (or alprazolam) improved survival to 64% (i.e., 7 of 11 animals) compared to a survival rate of 0% (i.e., 0 of 8 vehicle treated controls). Despite the improved survival, the severe thrombocytopenia was unaltered with the combined therapy. PAF, histamine and peptide leukotrienes appear to act in concert in mediating the anaphylaxis-induced airway constriction and circulatory failure in guinea pigs, but are not apparently responsible for the accompanying thrombocytopenia.

Topics: Alprazolam; Anaphylaxis; Animals; Benzodiazepines; Benzofurans; Benzopyrans; Diphenhydramine; Guinea Pigs; Histamine; Lignans; Male; Muscle Contraction; Platelet Activating Factor; Platelet Membrane Glycoproteins; Receptors, Cell Surface; Receptors, G-Protein-Coupled; SRS-A