Investigation of the mechanism of TRP channel mediated by a lipid mediator, 2ccPA, via LPA receptor

已有研究表明，环磷脂酸(CPA)及其衍生物2ccPA对C-初级传入的伤害性传递、逆转炎症性和神经病理性疼痛有很强的抑制作用。本研究旨在阐明CPA和2ccPA镇痛作用的分子机制。我们发现2ccPA激活LPA5受体并不影响TRPV1的激活。因此，我们将研究2ccPA对另一条Trp通道激活的影响。

We have been indicated that cyclic phosphatidic acid, cPA, and its derivative, 2ccPA, are potent inhibitors of nociceptive transmission by C-primary afferents, and reverse inflammatory and neuropathic pain. In this research, we aimed to clarify the molecular mechanism of analgesic function of cPA and 2ccPA. We found that the activation of LPA5 receptor by 2ccPA does not affect the activation of TRPV1. Therefore, we are going to examine the effect of 2ccPA on the other TRP channel activation.