https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3936421/

Comment; Unfortunately, as well as curcumin works for inflammation & mast cell stabilization, there is no impetus for the pharmaceutical industry to develop it unless they can modify and thus patent what already works so well.  We need to change how this country deals with medications, disease and finance!

Other ISEAI commenters;

From: Sandeep Gupta, MD
Sent: Wednesday, February 21, 2018 3:23 AM

I also love boswellia, Neuroprotek, Thorne Quercenase and Ortho Natural DHist for lowering histamine and compounded ketotifen for mast cell stabilizer.

On Feb 20, 2018, at 8:56 PM, Mary Ackerley, MD wrote:
One of my favorite supplements for neuroinflammation.  I believe the Gulf war model of exposing rats to stress and toxic chemicals might be a model for exploring effects of mycotoxins on neuropsychiatric function in CIRS (when we get research funding going). My favorite curcumin supplements are Meriva (liposomal delivery, no black pepper), MitoForte (with huperzine, alpha lipoic, N Acetyl Carnitine, excellent for cognitive impairment) and CytoQuel (resveratrol seems to really help neuropathic pain).

Xian Li,1 Yue Lu,2 Ye Jin,1 Jong-Keun Son,1 Seung Ho Lee,1,* and Hyeun Wook Chang1,*

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Abstract

Curcumin is naturally occurring polyphenolic compound found in turmeric and has many pharmacological activities. The present study was undertaken to evaluate anti-allergic inflammatory activity of curcumin, and to investigate its inhibitory mechanisms in immunoglobulin E (IgE)/Ag-induced mouse bone marrow-derived mast cells (BMMCs) and in a mouse model of IgE/Ag-mediated passive systemic anaphylaxis (PSA). Curcumin inhibited cyclooxygenase-2 (COX-2) dependent prostaglandin D2 (PGD2) and 5-lipoxygenase (5-LO) dependent leukotriene C4 (LTC4) generation dose-dependently in BMMCs. To probe the mechanism involved, we assessed the effects of curcumin on the phosphorylation of Syk and its downstream signal molecules. Curcumin inhibited intracellular Ca2+ influx via phospholipase Cγ1 (PLCγ1) activation and the phosphorylation of mitogen-activated protein kinases (MAPKs) and the nuclear factor-κB (NF-κB) pathway. Furthermore, the oral administration of curcumin significantly attenuated IgE/Ag-induced PSA, as determined by serum LTC4, PGD2, and histamine levels. Taken together, this study shows that curcumin offers a basis for drug development for the treatment of allergic inflammatory diseases.

Curcumin is naturally occurring polyphenolic compound found in turmeric and has many pharmacological activities. The present study was undertaken to evaluate anti-allergic inflammatory activity of curcumin, and to investigate its inhibitory mechanisms in immunoglobulin E (IgE)/Ag-induced mouse bone marrow-derived mast cells (BMMCs) and in a mouse model of IgE/Ag-mediated passive systemic anaphylaxis (PSA). Curcumin inhibited cyclooxygenase-2 (COX-2) dependent prostaglandin D2 (PGD2) and 5-lipoxygenase (5-LO) dependent leukotriene C4 (LTC4) generation dose-dependently in BMMCs. To probe the mechanism involved, we assessed the effects of curcumin on the phosphorylation of Syk and its downstream signal molecules. Curcumin inhibited intracellular Ca2+ influx via phospholipase Cγ1 (PLCγ1) activation and the phosphorylation of mitogen-activated protein kinases (MAPKs) and the nuclear factor-κB (NF-κB) pathway. Furthermore, the oral administration of curcumin significantly attenuated IgE/Ag-induced PSA, as determined by serum LTC4, PGD2, and histamine levels. Taken together, this study shows that curcumin offers a basis for drug development for the treatment of allergic inflammatory diseases.

Keywords: Curcumin, Mast cell, Prostaglandin D2, Leukotriene C4, Mitogen activated protein kinase, Passive systemic anaphylaxis