PubMed · 9536152
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E O Gregg. 1998. Peanut allergy.. https://doi.org/10.1177/014107689809100132
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The pathophysiological responses to immune stress (IS) include activation of several processes which are dependent on cytosolic Ca2+ elevation. Magnesium frequently acts as a natural Ca2+ antagonist. In this study we have observed that Mg2+ can protect guinea-pigs against IS. Antigen-sensitized guinea-pigs, which had been fed a magnesium-deficient diet, were given a single dose (15 mg) of MgCl2 intraperitoneally 1 h before antigen challenge. The development of anaphylactic shock (AS) was observed during the next 2 h, and the hearts were subsequently examined histologically for signs of cardiac myolysis (CM). Magnesium (i) reduced the incidence of CM from 40% to 10% (p < 0.05); (ii) reduced the incidence of AS from 61% to 35% (p < 0.05); (iii) attenuated the severity of the AS; and (iv) lowered mortality from 39% in the control to 19% in the Mg(2+)-treated group (p = 0.1). Serum and tissue total [Mg2+] were not affected by the administration of MgCl2. Also, the serum and heart Mg2+ levels were the same whether or not the guinea-pigs developed AS or CM. In cell culture we demonstrated that by elevating the [Mg2+] in the medium bathing sensitized rat basophilic leukemia (RBL) cells, the increase in cytosolic [Ca2+] subsequent to antigen challenge was reduced from 174 +/- 23.28% (1 mM) to 82.74 +/- 13.22% (3 mM). We conclude that a single treatment with Mg2+ can considerably diminish damage induced by immune stress, probably by its altering the Ca2+: Mg2+ ratio. Since the physiological reaction to different types of stress is similar, Mg2+ could prove beneficial in preventing stress-induced shock in general. Studies examining the mechanisms by which Mg2+ exerts its effects thus provide a scientific basis for the current clinical use of Mg2+ in acute myocardial infarction (AMI) and asthma.
BACKGROUND: Tongkyutang (TKT) is an Oriental herbal prescription, which has been successfully applied for the treatment of allergic disorders, mainly allergic-rhinitis in clinical medicine. However, its effect in experimental models remains unknown. METHODS: In a mouse model, the role of TKT was examined in mast cell-dependent allergic reactions and secretion of inflammatory cytokines. RESULTS: TKT concentration-dependently inhibited the ear-swelling response induced by intradermal injection of compound 48/80. TKT inhibited the compound 48/80-induced degranulation from mast cells in ear tissue. TKT dose-dependently inhibited the histamine release from the rat peritoneal mast cells by compound 48/80. TKT also showed inhibition of anti-dinitrophenyl IgE antibody-induced passive cutaneous anaphylaxis reaction by oral administration. Furthermore, TKT inhibited both IL-1beta and TNF-alpha secretion induced by PMA and A23187, respectively. CONCLUSIONS: Our findings provide evidence that TKT inhibits the mast cell-dependent allergic reactions and inflammatory cytokines secretion.