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EVALUATION OF MAST CELL STABILIZING EFFECT OF ERAIPPU NOI CHOORANAM (ENC) ON RAT MESENTRY
Abstract
Background: According to the Siddha research pharmacopoeia, Eraippu Noi Chooranam is a modied Siddha Poly Herbal formulation recommended for respiratory conditions. The suggested traditional claim was put into practise in order to assess its effectiveness in the treatment of bronchial asthma. Aim: The aim of this study is to evaluate the mast cell stabilizing effect of ENC on rat mesentry. Materials And Methods: Aqueous extract of ENC was tested in this study at various dose levels for its ability to stabilize mast cells in the rat mesentery. Result: The % protection offered by the standard drug ketotifen was found to be 70% and 32.5% , 50.5% with the trial drug ENC at the dosage of 270, 400 mg/kg respectively. Conclusion:The effectiveness of aqueous extract of ENC in the treatment of asthma may therefore be concluded.
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Background: Calendula officinalis Linn. (Asteraceae) is an aromatic herb growing in the forests of India, China, Central Europe, and some tropical areas. The study was designed to investigate the scientific basis for the traditional claim of C. Officinalis on asthma. In the present study, methanol extract of whole plants was evaluated for preliminary phytochemical screening and antiasthmatic activity on different animals. Subjects and Methods: The asthmatic activity was evaluated by histamine‑ or acetylcholine‑induced bronchospasm in guinea pigs, compound 48/80‑induced mast cell degranulation in wistar rats, histamine‑induced constriction on isolated guinea pig trachea, and ovalbumin‑induced sensitization in mice at different dose levels of C. Officinalis. The preconvulsion dyspnoea time at 0 th and 7 th days at the dose of 250 and 500 mg/kg in guinea pig, the percentage of granulated and degranulated mast cell of at the dose of 600, 800, 1000 μg/mL in rats, muscular contraction at the dose of 600, 800, and 1000 μg/mL on isolated guinea pig trachea and the inflammatory cell count, that is, eosinophils, neutrophills, lymphocytes, macrophages, interleukin (IL)‑4, IL‑5, and immunoglobulin‑E (IgE) from bronchoalveolar lavage fluid at the dose levels of 50, 100, and 250 mg/kg in mice were evaluated and compared with respective control groups. Results: Phytochemical studies revealed the presence of flavonoids, steroids, saponin, terpenoids, lignins, and phenolic compounds in the extract. In addition, the treatment of methanolic extract of C. officinalis (MECO) significantly (P < 0.001) decreased the bronchospasm induced by histamine or acetylcholine in guinea pigs, degranulation mast cell in rats, histamine‑induced constriction on isolated guinea pig trachea, and the level of inflammatory cells as compared with inducer groups. The antiasthmatic activity was potentiated in all the doses in dose‑dependent manner. Conclusion: The present study concludes that the antiasthmatic activity may be due to the presence of above phytoconstituents by antihistaminic, anticholinergic, antispasmodic, and mast cell stabilizing property.
Herbex-kid (HK), a polyherbal formulation was evaluated in various experimental allergic models of Type I hypersensitivity reactions. Compound 48/80 (C 48/80) has been shown to induce rat mesentery mast cell degranulation and HK (1.07, 10.75 and 107.5 mg ml(-1)) inhibited the mast cell degranulation in a dose dependent manner. HK (1.07, 10.75 and 107.5 mg kg(-1); p.o.) showed dose-dependent protection against C 48/80 induced systemic anaphylaxis in male Balb/C mice. In active anaphylaxis model, male Wistar rats orally administered with 10.75 and 107.5 mg kg(-1) of HK showed significant (P < 0.01) protection against mast cell degranulation, while in passive anaphylaxis model, only at 107.5 mg kg(-1) showed significant (P < 0.01) reduction in mast cell degranulation. HK at all dose levels was able to significantly decrease the time spent in nasal rubbing in Wistar rats sensitized to ovalbumin, while only at 107.5 mg kg(-1) it showed significant (P < 0.01) reduction in number of sneezes. In C 48/80-induced skin itch model, all dose levels of HK significantly (P < 0.001) decreased the time spent in itching and the number of itches. HK did not produce any significant inhibition in histamine induced contraction in guinea pig ileum. From the above findings we conclude that the HK possesses antiallergic activity mediated by reducing of the release mediators from mast cells and also by 5-HT antagonism without the involvement of histamine (H1) receptors.
The diverse effects of histamine are mediated by discrete histamine receptors. The principal repository of histamine in the body is the mast cell. However, the effects of histamine on mast cells, especially those of human origin, have not been fully elucidated. In this study, the expression of histamine receptors in human lung mast cells was evaluated. Moreover, the effects of histamine receptor engagement on both mediator release and chemotaxis were investigated. Mast cells were isolated and purified from human lung tissue. Histamine receptor expression was determined by RT-PCR and q-PCR. Both methods for the detection of histamine receptors were in accordance and human lung mast cells expressed mRNA for histamine H4 and histamine H1 receptors, variably expressed histamine H2 receptor but did not express histamine H3 receptor. The effects of selective histamine receptor agonists on the release of both pre-formed (histamine) and newly-synthesized (cysteinyl-leukotriene, prostaglandin D2) mediators were investigated. None of the agonists tested had any direct effects on mediator release. None of the agonists modulated release stimulated by anti-IgE. Further studies showed that histamine induced migration of mast cells. Chemotaxis appeared to be mediated by the histamine H4 receptor since JNJ28610244 (H4 agonist) was chemotactic for mast cells whereas 2-(2-pyridyl) ethylamine (H1 agonist) was not. Furthermore, the selective histamine H4 receptor antagonist, JNJ7777120, effectively reversed the chemotaxis of mast cells induced by JNJ28610244. Overall, these experiments identify the histamine H4 receptor as chemotactic for human lung mast cells. This mechanism might influence mast cell accumulation in the lung.
Allergic diseases have reached epidemic proportions worldwide. An understanding of the cellular and soluble mediators that are involved in allergic inflammatory responses not only helps in understanding the mechanisms of current treatments, but is also important for the identification of new targets that are amenable to both small-molecule and biological interventions. There is now considerable optimism with regards to tackling the allergy epidemic in light of improvements in systemic and mucosal allergen-specific immunotherapy, the identification of key cytokines and their receptors that drive T-helper-2-cell polarization, a clearer understanding of the pathways of leukocyte recruitment and the signalling pathways that are involved in cell activation and mediator secretion, and new approaches to vaccine development.
This study was conducted to identify and clarify the actions of pulmonary and systemic H1- and H2-receptors by utilizing specific histamine receptor antagonists. Histamine was infused in anesthetized dogs during control conditions, after H2-receptor blockade with metiamide, after H1-receptor blockade with chlorpheniramine, and after combined H1- and H2-receptor blockade. Histamine infusion, alone, induced marked systemic vasodilatation, pulmonary vasoconstriction, and transient increases in cardiac output and heart rate. H2-receptor blockade prevented the systemic vasocilatation and potentiated the pulmonary vasoconstriction induced by histamine. H1-receptor blockade augmented the systemic vasodilatation, prevented the pulmonary vasoconstriction, and increased the cardiac output and heart rate responses induced by histamine. Thus, H2-receptors appear to mediate the vasocilatation, tachycardia, and increased cardiac output induced by histamine, whereas H1-receptors appear to mediate the vasoconstrictor and the minimal cardiac depressent actions of histamine. Histamine stimulates only H1- and H2-receptors, since combined H1- and H2-receptor antagonism prevented almost all of the cardiovascular actions of histamine.
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- T Thirunarayanan
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