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In the behavior experiments, we found that intraplantar administration of GW7647 relieved the acidosis-evoked nociceptive responses in rats in a dose-dependent manner. The GW7647 exerted an analgesic effect on acidosis-evoked nociceptive responses through PPAR-±, since its effect was blocked by PPAR-± antagonist. Obviously, the behavioral data corroborated the electrophysiological data and vice versa. The combined data strongly demonstrated that PPAR-± activation indeed inhibited the activity of ASICs, not only at the cellular level but also at the behavioral level.
Pharmacological blockade reebok cross trainers of N-acylethanolamine acid amidase activity and preservation of endogenous PEA suppress visceral pain response elicited by intraperitoneal injections of acetic acid in mice through PPAR-± [ 38 ]. However, this visceral pain response is enhanced in female mice lacking PPAR-± [ 9 ].PPAR-±, belonging to a nuclear receptor super-family, can function directly as a transcription factor that control gene transcription. Genomic effects of PPAR-± have latencies of at least 30 minutes (and up to days) and are associated with changes in protein synthesis [ 12 ]. Moreover, PPAR-± can also act at non-transcriptional targets to produce more rapid effects.