The activation of CB1 and CB2 inhibits the development of intracellular cAMP, hence resulting in a tremendous reduction from the excitatory result within the neurons [88,89]. On top of that, the activation of CB2 can additional avoid the mast mobile degranulation and the release of professional-inflammatory mediators, building the reduction in pain
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Owning recognized the palmitoylation motif of APLNR, we made a brief substrate sequence to competitively inhibit the palmitoylation of endogenous APLNR. This competitive peptide, which targets the APLNR palmitoylation site in combination with morphine, can inhibit the development of NCP, such as pain incidence, microglial activation, and inflammato