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Catechins and Caffeine in Tea: A Review of Health Risks and Benefits
Published in Barry D. Smith, Uma Gupta, B.S. Gupta, Caffeine and Activation Theory, 2006
Raymond Cooper, Talash A. Likimani, D. James Morŕe, Dorothy M. Morŕe
Cocoa contains methylxanthines, flavonoids, tyramine, phenylethylamine (PEA), magnesium, and possibly N-acylethanolamines. Cocoa has CNS stimulant, cardiac stimulant, coronary dilatory, and diuretic actions (Wolters Kluwer Co., 1999). Theobromine is the major methylxanthine found in cocoa and has only 10% of the cardiac activity of caffeine. In one study, consumption of 1.5 g/kg body weight of chocolate had no acute hemodynamic or physiologic effects on the hearts of healthy, young adults. Effects of cacao are similar to green tea for thermogenesis due to the presence of the methylxanthines.
Bone Regeneration Effect of Cassia occidentalis Linn. Extract and Its Isolated Compounds
Published in Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay, Phytochemistry of Plants of Genus Cassia, 2021
Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay
Luteolin has an immunomodulatory function that could beneficially impact RA. For example, luteolin (1 mg/kg) in combination with N-palmitoylethanolamide (PEA), an endogenous fatty acid amide belonging to the family of the N-acylethanolamines, significantly ameliorated the clinical signs of RA (erythema and oedema in hind paw) and pain and locomotor activity. Although PEA alone was effective in improving these parameters, the impact of the combination was better. Luteolin alone (1 mg/kg) had no effect. The combination therapy also inhibited neutrophil infiltration in the joint of RA mice as well as decreased the levels of inflammatory chemokines, macrophage inflammatory protein (MIP-1α) and MIP-2. Consequently, free radicals and oxidant molecules nitrotyrosine, a marker of nitrosative injury was increased in the joints of RA mice but significantly reduced in the RA mice treated with the combination of PEA and luteolin. The circulating levels of TNFα, IL-1β and IL-6 were also suppressed in the RA group receiving the combination treatment compared to the disease (RA) group. Moreover, thiobarbituric acid-reactant substance, an indicator of lipid peroxidation, was increased in the plasma of RA group, which was suppressed in the combination group. Thus, luteolin in combination with PEA improved experimental RA in mice by anti-inflammatory and analgesic mechanisms (Impellizzeri et al., 2013).
Pea
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
The topic of peroxisome proliferator-activated receptor (PPAR) ligands typically involves a discussion of the lipid-lowering effects of fibrates and the blood sugar-lowering effects of thiazolidinediones. However, more recent research has investigated the role of the endogenous PPAR-α ligand, palmitoylethanolamide (PEA) on inflammation, pain, neurodegenerative diseases, stroke, spinal cord injury, and neuropsychiatric disorders.1 Palmitoylethanolamide is a naturally occurring fatty acid belonging to the N-acylethanolamine (NAE) class of signaling molecules and can be isolated from egg yolks, peanut meal, and lecithin. It is rapidly metabolized in the human body via fatty acid amide hydrolase (FAAH) and N-acylethanolamine-hydrolyzing acid amidase (NAAA) to inactive metabolites palmitic acid and ethanolamide.2,3 Initial pharmacokinetic research by Lambert et al.2 assumed a ligand-binding relationship between PEA and the endogenous cannabinoid 2 (CB2) receptor. However, these initial claims proved to be incorrect and were explained as the entourage effect, where PEA competes with the endocannabinoid anandamide (AEA) for FAAH, resulting in higher concentrations of AEA.4 Although it does have a structural relationship to AEA and other endocannabinoids, PEA was found to have pharmacologic activity at PPAR-α, PPAR-γ, PPAR-δ, G protein-coupled receptor (GPR) 55, GPR119, transient receptor potential channel type (TRP) V1, ATP-sensitive potassium channels, and calcium-activated potassium channels. Additionally, PEA appears to inhibit ceramidases, and potassium channels Kv4.3 and Kv1.5, as well as interacting with NF-κB, cyclooxygenase (COX), TNFα, interleukin (IL)-4, IL-6, IL-8, nitric oxide (NO), and substance P mast cell activation. This variety of interactions has afforded PEA the title of being “promiscuous.”4,5
At the heart of microbial conversations: endocannabinoids and the microbiome in cardiometabolic risk
Published in Gut Microbes, 2021
Ramsha Nabihah Khan, Kristal Maner-Smith, Joshua A. Owens, Maria Estefania Barbian, Rheinallt M. Jones, Crystal R. Naudin
In addition to the ‘true’ endocannabinoids AEA and 2-AG, which are formed on-demand (as opposed to being stored in vesicles), other members of the N-acylethanolamines which have structural similarities to the ‘true’ endocannabinoids can affect the endocannabinoid response, although they do not directly bind to the CB1 and CB2 receptors. These endocannabinoid analogues include N-oleoylethanolamine (OEA, 18:1-EA), N-stearoylethanolamine (SEA, 18:0-EA), and N-palmitoylethanolamine (PEA, 16:0-EA), and are synthesized from the hydrolysis N-acylphosphatidylethanolamines.29 Saturated and monounsaturated N-acylethanolamines, like OEA, SEA and PEA do not bind to cannabinoid receptors; however, they play a critical physiological role and are known to activate the peroxisome proliferator-activated receptor α (PPAR-α), as well as other nuclear and extracellular receptors. By activating these receptors, saturated and monounsaturated N-acylethanolamines mediate a variety of effects, including appetite suppression, adipogenesis and inhibiting inflammation,30 and have also been implicated in the regulation of cancer cell proliferation.31
Different roles for the acyl chain and the amine leaving group in the substrate selectivity of N-Acylethanolamine acid amidase
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Andrea Ghidini, Laura Scalvini, Francesca Palese, Alessio Lodola, Marco Mor, Daniele Piomelli
In the present study, we used a combination of enzyme kinetic and computational analyses to conduct a systematic investigation of the substrate selectivity of NAAA. The work of Ueda and collaborators has provided evidence for a marked selectivity of NAAA for PEA compared to other N-acylethanolamines. More specifically, the relative reactivities of the enzyme were found to be at 100% for PEA, 48% for N-myristoylethanolamine, approximately 20% for N-stearoylethanolamine and N-oleoylethanolamine, 13% for N-linoleoylethanolamine and only 8% for anandamide3. Building on this work1,3, we show here that the fatty acyl chain of the substrate, rather than its polar head, controls NAAA-mediated catalysis, such that even single-carbon deviations from the optimal 16-carbon saturated chain of PEA markedly decrease the catalytic efficiency. The results provide novel insight into NAAA’s catalytic mechanism and identify PEA as the primary substrate for this enzyme.
Cannabis for cancer – illusion or the tip of an iceberg: a review of the evidence for the use of Cannabis and synthetic cannabinoids in oncology
Published in Expert Opinion on Investigational Drugs, 2019
The EGFR family of extracellular protein ligands includes the receptor tyrosine kinases EGFR, human epidermal growth factor receptor 2 (HER2/Neu), Her 3, Her 4. EGFR is an important transmembrane protein, as mutations in its expression may result in cancer, and inhibition of its signaling pathways prevent tumor spread. Fatty acid amide hydrolase (FAAH), a serine hydrolase that metabolizes N-acylethanolamines like AEA, OEA, and PEA, is known to be overexpressed in certain cancer cells and its inhibition can enhance patient survival. Blockage of FAAH raises the level of AEA, inhibiting the EGFR signaling pathway and leading to cell arrest and apoptosis [61]. Both in vivo and in vitro, activation of CB2 receptors decreased migration and invasion of estrogen positive and negative breast cancer cells by suppressing EGFR and insulin-like growth factor tumorigenic pathways [62].