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2015). These experiments, taken collectively, recommend that, Whilst a direct activation of GPR55 or PPAR‐α occurs, PEA can make its anti‐inflammatory motion from the intestine also by means of indirect activation of CB1 and CB2 receptors, most likely resulting from the flexibility of the compound to potentiate the motion of endocannabinoids a
PEA safeguards towards bacterial an infection by way of innate immune modulation involving MCs, macrophages and microglia. Prophylactic PEA at a dose of 0.one mg/kg overall body fat prolonged survival charge and minimized neuro-inflammation in an aged murine bacterial meningitis model, while in the absence of antibiotics [42].‐acylethanolamines (