【摘 要】
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Chronic pain caused by peripheral inflammation has always been the difficulty for clinical treatment.Currently developed analgesic drugs from the endogenous analgesic substances,such as opioids and ca
【机 构】
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Department of Neurobiology,School of Basci Medicine,Tongji Medical College,Huahzong University of Sc
【出 处】
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第九届海内外华人神经科学家研讨会(The 9th Symposium for Chinese Neuroscientis
论文部分内容阅读
Chronic pain caused by peripheral inflammation has always been the difficulty for clinical treatment.Currently developed analgesic drugs from the endogenous analgesic substances,such as opioids and cannabinoids,have shown therapeutic effects,but long-term use of these drugs produced addiction and psychological side effects.Our recent study have demonstrated that Annexin 1(ANXA1),an anti-inflammatory mediator of glucocoticoid,exerts anti-nociceptive effect through formyl peptide receptor like 1(FPR2/ALX))at the dorsal root ganglia(DRGs)level in Complete Freunds adjuvant-induced rat model of chronic inflammatory pain.Based on the previous work,by applying calcium imaging,whole cell patch clamp,western blot and immunofluorescent staining techniques,we performed in vitro and in vivo experiments on the inflammatory pain model.We found that,after applying exogenous ANXA1 into the DRGs neurons,capsaicin induced TRPV1 current was dramatically reduced.This effect was proved to be mediated through activation of ANXA1-FPR2/ALX signal,that is,activation of phospholipase C,increase of intracellular calcium ion,upregulation of calmodulin and its interaction with TRPV1.Then,we performed similar studies on ANXA1 knock out(ANXA1-/-)mice and discovered that the ANXA1-FPR2/ALX signal was impaired and TRPV1 current was enhanced after ANXA1 gene deletion in inflammatory pain.We conclude that ANXA1-FPR2/ALX signal and its inhibition on TRPV1 is the molecular mechanism of ANXA1s role on anti-inflammatory pain.Our study elucidates the cellular and molecular mechanisms of ANXA1s anti-nociceptive effects and provides possible molecular target for developing new analgesic drugs.
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