脂質(zhì)調(diào)節(jié)劑Resolvins是新近發(fā)現(xiàn)的一系列由奧米伽-3脂肪酸釋放的天然小分子,，對(duì)一系列急性慢性疾病具有治療潛力，特別是在消除感染和恢復(fù)免疫穩(wěn)態(tài)方面,。
如今,，研究人員在4月在線出版的《自然—醫(yī)學(xué)》期刊上報(bào)告，Resolvins有可能是一種治療炎癥疼痛的新型鎮(zhèn)痛藥,，可以緩解炎癥帶的疼痛，并作用于脊柱以預(yù)防慢性疼痛,。
關(guān)節(jié)炎和術(shù)后痛等是一種因組織損傷所引發(fā)的炎癥疼痛,，組織損傷所釋放的物質(zhì)會(huì)增強(qiáng)炎癥并在脊柱中發(fā)生作用導(dǎo)致慢性疼痛。
Ru-RongJi和同事發(fā)現(xiàn),，由某種奧米伽-3脂肪酸所產(chǎn)生的兩種脂質(zhì)調(diào)節(jié)劑RvE1和RvD1能緩解小鼠的疼痛癥狀,。他們指出，在緩解疼痛方面,，RvE1是它的父輩化合物力量的1萬(wàn)倍,，而且，一種人工合成的化合物Chemerin所需要結(jié)合的受體與RvE1和RvD1一樣,，這種人工化合物也能明顯降低疼痛癥狀,。除了抗炎癥效用之外，他們還發(fā)現(xiàn)RvE1可作用于脊柱以預(yù)防因神經(jīng)元活動(dòng)所導(dǎo)致的永久性慢性疼痛,。而且,，這種止痛作用并不會(huì)影響正常的疼痛反應(yīng)。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature Medicine Published online: 11 April 2010 | doi:10.1038/nm.2123
Resolvins RvE1 and RvD1 attenuate inflammatory pain via central and peripheral actions
Zhen-Zhong Xu1,3, Ling Zhang1,3, Tong Liu1, Jong Yeon Park1, Temugin Berta1, Rong Yang2, Charles N Serhan2,3 & Ru-Rong Ji1,3
AbstractInflammatory pain, such as arthritis pain, is a growing health problem1. Inflammatory pain is generally treated with opioids and cyclooxygenase (COX) inhibitors, but both are limited by side effects. Recently, resolvins, a unique family of lipid mediators, including RvE1 and RvD1 derived from omega-3 polyunsaturated fatty acid, have shown marked potency in treating disease conditions associated with inflammation2, 3. Here we report that peripheral (intraplantar) or spinal (intrathecal) administration of RvE1 or RvD1 in mice potently reduces inflammatory pain behaviors induced by intraplantar injection of formalin, carrageenan or complete Freund's adjuvant (CFA), without affecting basal pain perception. Intrathecal RvE1 injection also inhibits spontaneous pain and heat and mechanical hypersensitivity evoked by intrathecal capsaicin and tumor necrosis factor-α (TNF-α). RvE1 has anti-inflammatory activity by reducing neutrophil infiltration, paw edema and proinflammatory cytokine expression. RvE1 also abolishes transient receptor potential vanilloid subtype-1 (TRPV1)- and TNF-α–induced excitatory postsynaptic current increases and TNF-α–evoked N-methyl-D-aspartic acid (NMDA) receptor hyperactivity in spinal dorsal horn neurons via inhibition of the extracellular signal–regulated kinase (ERK) signaling pathway. Thus, we show a previously unknown role for resolvins in normalizing the spinal synaptic plasticity that has been implicated in generating pain hypersensitivity. Given the potency of resolvins and the well-known side effects of opioids and COX inhibitors, resolvins may represent new analgesics for treating inflammatory pain.
