CURCUMA BOSWELLIA ZENZERO DALLE CAUSE AI SINTOMI DELL’ALLERGIA

L’allergia è una risposta esagerata di una parte del Sistema immunitario acquisito, il Sistema linfocitarioTH2, che reagisce in maniera esagerata ove avvenga il contatto con una sostanza a cui si è allergici (pollini, pelo del gatto ecc.)Il sistema TH2 appena entra in contatto con l’allergene produce una serie di anticorpi specifici (IGE) che scatenano una risposta infiammatoria di tipo umorale. Numerosi fattori contribuiscono a questa esagerata risposta, oltre ai fattori genetici e l’esposizione a sostanze allergicizzanti vi sono altri elementi che contribuiscono ad amplificarne la risposta ad esempio:

BATTERI GRAM NEGATIVI
I batteri, in particolare quelli del nostro intestino qualora sia in stato di disbiosi, possono predisporre a risposte pro infiammatorie che concorrono ad aumentare la risposta allergica. Il lipopolisaccaride (LPS) componente della membrana esterna dei batteri Gram negativi esercita un rilascio di TNF alfa e IL6, che scatena infiammazione. I batteri intestinali della famiglia bacteroides, appartenenti alla famiglia dei Bacteroidetes, sono gram negativi quindi potenzialmente proinfiammatori, così come i proteobatteri patogeni(E.Coli, klebsiella, shigella ) sono gram negativi, così come i fusobatteri ecc. . Sempre nel genere Bacteroidetes abbiamo i Prevotella , questo tipo tipo di batteri di provenienza orale se in eccesso possono anch’essi produrre infiammazione. L’altro grande ceppo che invece sono gram positivi, così come gli Actinobacteria di cui il più famoso è il Bifidobatterio (Longum , brevis, bifidum e animalis) spesso carenti. Ovviamente il microbiota è molto complesso e serve un delicato equilibrio tra le varie classi, in questo breve articolo volevo enfatizzare il ruolo fondamentale di una corretta eubiosi nel controllo dell’infiammazione, allergia compresa.
ESTROGENI E XENOESTROGENI
Gli estrogeni in eccesso (pillola, latticini, eccesso di rame, carenza di zinco, upregulation delle aromatasi ecc.) attivano il sistema TH2 collegato con le varie forme di allergia, così come gli xenoestrogeni di origine ambientale, pesticidi, bisfenolo A ecc.

Front Immunol. 2015 Nov 16;6:568. doi: 10.3389/fimmu.2015.00568. eCollection 2015.
Estrogen Signaling Modulates Allergic Inflammation and Contributes to Sex Differences in Asthma.
Keselman A1, Heller N1.
Author information
Abstract
Asthma is a chronic airway inflammatory disease that affects ~300 million people worldwide. It is characterized by airway constriction that leads to wheezing, coughing, and shortness of breath. The most common treatments are corticosteroids and β2-adrenergic receptor antagonists, which target inflammation and airway smooth muscle constriction, respectively. The incidence and severity of asthma is greater in women than in men, and women are more prone to develop corticosteroid-resistant or “hard-to-treat” asthma. PUBERTY, MENSTRUATION, PREGNANCY, MENOPAUSE, AND ORAL CONTRACEPTIVES ARE KNOWN TO CONTRIBUTE TO DISEASE OUTCOME IN WOMEN, SUGGESTING A ROLE FOR ESTROGEN AND OTHER HORMONES IMPACTING ALLERGIC INFLAMMATION. In typical Th2-type allergic asthma, interleukin (IL)-4 and IL-13 predominate, driving IgE production and recruitment of eosinophils into the lungs. Chronic Th2-inflammation in the lung results in structural changes and activation of multiple immune cell types, leading to a deterioration of lung function over time. Most immune cells express estrogen receptors (ERα, ERβ, or the membrane-bound G-protein-coupled ER) to varying degrees and can respond to the hormone. Together these receptors have demonstrated the capacity to regulate a spectrum of immune functions, including adhesion, migration, survival, wound healing, and antibody and cytokine production. THIS REVIEW WILL COVER THE CURRENT UNDERSTANDING OF ESTROGEN SIGNALING IN ALLERGIC INFLAMMATION AND DISCUSS HOW THIS SIGNALING MAY CONTRIBUTE TO SEX DIFFERENCES IN ASTHMA AND ALLERGY.

Reprod Toxicol. 2016 Oct;65:224-229. doi: 10.1016/j.reprotox.2016.08.007. Epub 2016 Aug 16.
Exposure to bisphenol A and the development of asthma: A systematic review of cohort studies.
Xie MY1, Ni H2, Zhao DS1, Wen LY1, Li KS1, Yang HH1, Wang SS1, Zhang H1, Su H3.
Author information
Abstract
BACKGROUND:
There is conflicting evidence about the association between bisphenol A (BPA) exposure and childhood asthma risk. We aimed to review the epidemiological literature on the relationship between prenatal or postnatal exposure to BPA and the risk of childhood asthma/wheeze.

RESULTS:
Six studies fulfilled the eligibility criteria. Three studies found that prenatal BPA exposure is associated with an increased risk of childhood wheeze, while another study reported a reduced risk of wheeze. Regarding the postnatal BPA exposure, three studies demonstrated an increased risk of childhood asthma/wheeze.

CONCLUSIONS:
The mean prenatal BPA was associated with the risk of childhood wheeze/asthma. Besides, the influence of BPA exposure during the second trimester of pregnancy on the prevalence of childhood wheeze was marked.

Copyright © 2016 Elsevier Inc. All rights reserved.

IL RUOLO DEL FEGATO NELLA DETOSSIFICAZIONE DA XENOESTROGENI
In Medicina Cinese si è pensato al Fegato come organo responsabile dei fenomeni allergici, sensibile e iper reattivo in Primavera, con il Vento ecc. Da un punto di vista clinico ciò che lega il Fegato ai fenomeni infiammatori è sicuramente la sua capacità di eliminare o meno sostanze tossiche dall’organismo. Qualora non fosse in grado di eliminarle per carenza di elementi necessari allora l’entrata in circolo delle tossine (Xenostrogeni, Xenobiotici, metalli pesanti ecc.) scatenano una risposta infiammatoria che nei soggetti allergici è motivo di esacerbazione dei sintomi. Il fegato deve essere in grado di eliminare gli xenoestrogeni, i metalli pesanti (Nichel, Cadmio, Piombo ecc.)e tutte le tossine in grado di attivare una risposta proinfiammatoria, grazie a specifiche sostanze in grado di neutralizzarle , in particolar modo N acetil cisteina ( NAC) il grande precursore del Glutatione, Silimarina, Curcumina, S adenosil metionina (SAMe) ecc. tramite regolazione delle Fasi I e II di detossificazione.

I FATTORI INFIAMMATORI NEL SOGGETTO ALLERGICO
Una volta riequilibrato questi fattori allora si potrà fare una azione diretta con i fattori infiammatori responsabili della manifestazione allergica, in particolare Platelet Activating Factor (PAF) ritenuto mille volte più potente dell’istamina, l’Istamina e I leucotrieni tra i maggiori fattori tipici della risposta allergica, ecco di seguito alcune tra le piante più specifiche per diminuire la risposta infiammatoria.
CURCUMA, BOWELLIA , ZENZERO
J Cell Biochem. 2018 Nov;119(11):8713-8722. doi: 10.1002/jcb.27192. Epub 2018 Aug 11.
The regulatory role of curcumin on platelet functions.
Tabeshpour J1, Hashemzaei M2, Sahebkar A3,4,5.
Abstract
Curcumin, the main ingredient of Curcuma longa L., has been used as a spice and as a herbal medicine with different therapeutic characteristics for centuries in Asian countries. This phytochemical has been shown to possess beneficial antiplatelet activity that has introduced it as a promising candidate for the treatment of thromboembolism, atherothrombosis, and inflammatory diseases. Platelet dysfunction under different circumstances may lead to cardiovascular disease, and curcumin has been shown to have beneficial effects on platelet dysfunction in several studies. Therefore, this narrative review is aimed to summarize available evidence on the ANTIPLATELET ACTIVITY OF CURCUMIN and related molecular mechanisms for this activity.

© 2018 Wiley Periodicals, Inc.

Biochem Pharmacol. 1999 Oct 1;58(7):1167-72.
Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling.
Shah BH1, Nawaz Z, Pertani SA, Roomi A, Mahmood H, Saeed SA, Gilani AH.
Author information
Abstract
Curcumin, a dietary spice from turmeric, is known to be anti-inflammatory, anticarcinogenic, and antithrombotic. HERE, WE STUDIED THE MECHANISM OF THE ANTIPLATELET ACTION OF CURCUMIN. We show that curcumin inhibited platelet aggregation mediated by the platelet agonists epinephrine (200 microM), ADP (4 microM), platelet-activating factor (PAF; 800 nM), collagen (20 microg/mL), and arachidonic acid (AA: 0.75 mM). CURCUMIN PREFERENTIALLY INHIBITED PAF- AND AA-INDUCED AGGREGATION (IC50; 25-20 microM), whereas much higher concentrations of curcumin were required to inhibit aggregation induced by other platelet agonists.. Curcumin also inhibited the formation of thromboxane A2 (TXA2) by platelets (IC50; 70 microM). These results suggest that the curcumin-mediated preferential inhibition of PAF- and AA-induced platelet aggregation involves inhibitory effects on TXA2 synthesis and Ca2+ signaling, but without the involvement of PKC.

Int J Mol Sci. 2014 Mar 4;15(3):3926-51. doi: 10.3390/ijms15033926.
Synthesis of analogues of gingerol and shogaol, the active pungent principles from the rhizomes of Zingiber officinale and evaluation of their anti-platelet aggregation effects.
Shih HC1, Chern CY2, Kuo PC3, Wu YC4, Chan YY5, Liao YR6, Teng CM7, Wu TS8.
Abstract
The present study was aimed at discovering novel biologically active compounds based on the skeletons of gingerol and shogaol, the pungent principles from the rhizomes of Zingiber officinale. Therefore, eight groups of analogues were synthesized and examined for their inhibitory activities of platelet aggregation induced by arachidonic acid, collagen, platelet activating factor, and thrombin. AMONG THE TESTED COMPOUNDS, [6]-PARADOL (5B) EXHIBITED THE MOST SIGNIFICANT ANTI-PLATELET AGGREGATION ACTIVITY. It was the most potent candidate, which could be used in further investigation to explore new drug leads.

AZIONE ANTISTAMINICA

BMC Complement Altern Med. 2018 Jul 16;18(1):217. doi: 10.1186/s12906-018-2223-8.
Curcumin derivative, 2,6-bis(2-fluorobenzylidene)cyclohexanone (MS65) inhibits interleukin-6 production through suppression of NF-κB and MAPK pathways in histamine-induced human keratinocytes cell (HaCaT).
Razali NA1, Nazarudin NA1, Lai KS2, Abas F3, Ahmad S4.
BACKGROUND:
Histamine is a well-known mediator involved in skin allergic responses through up-regulation of pro-inflammatory cytokines. Antihistamines remain the mainstay of allergy treatment, but they were found limited in efficacy and associated with several common side effects. Therefore, alternative therapeutic preferences are derived from natural products in an effort to provide safe yet reliable anti-inflammatory agents. Curcumin and their derivatives are among compounds of interest in natural product research due to numerous pharmacological benefits including anti-inflammatory activities. Here, we investigate the effects of chemically synthesized curcumin derivative, 2,6-bis(2-fluorobenzylidene)cyclohexanone (MS65), in reducing cytokine production in histamine-induced HaCaT cells.

RESULTS:
Histamine enhanced IL-6 production in HaCaT cells, with the highest production of IL-6 at 97.41 ± 2.33 pg/mL after 24 h of exposure. MS65 demonstrated a promising anti-inflammatory activity by inhibiting IL-6 production with half maximal inhibitory concentration (IC50) value of 4.91 ± 2.50 μM and median lethal concentration (LC50) value of 28.82 ± 7.56 μM. In gene expression level, we found that MS65 inhibits NF-κB and MAPK pathways through suppression of IKK/IκB/NFκB and c-Raf/MEK/ERK inflammatory cascades.

CONCLUSION:
TAKEN TOGETHER, OUR RESULTS SUGGEST THAT MS65 COULD BE USED AS A LEAD COMPOUND ON DEVELOPING NEW MEDICINAL AGENT FOR THE TREATMENT OF ALLERGIC SKIN DISEASES.

AZIONE ANTI LEUCOTRIENI
Phytomedicine. 2010 Sep;17(11):862-7. doi: Modulation of the immune system by Boswellia serrata extracts and boswellic acids.
Ammon HP1.

Thus, BAs inhibit activation of NFkappaB which is a product of neutrophile granulocytes. Consequently a down regulation of TNF-alpha and decrease of IL-1, IL-2, IL-4, IL-6 and IFN-gamma, which are proinflammatory cytokines by BEs and BAs has been reported. The inhibitory action of BAs on 5-LO leading to a decreased production of leukotrienes has received high attention by the scientific community since a variety of chronic inflammatory diseases is associatied with increased leukotriene activity.. From the pharmacological properties of BEs and BAs it is not surprising that positive effects of BEs in some chronic inflammatory diseases including rheumatoid arthritis, bronchial asthma, osteoarthritis, ulcerative colitis and Crohn’s disease have been reported

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