TRP离子通道在瘙痒中的作用及机制研究进展
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摘要
瘙痒是由多种原因引起的令人不快的皮肤感觉,虽然瘙痒不会威胁到生命,但长期慢性瘙痒会严重影响患者的生活质量。瞬时感受器电位离子通道(transient receptor potential ion channels, TRP)参与从感觉到皮肤平衡的生理过程。大量研究已经证实,许多瘙痒介质诱发的痒与TRP离子通道的激活有关。该文首先就瘙痒与疼痛的区别进行阐述,并就TRP离子通道在多种瘙痒介质诱发瘙痒中的作用及机制进行详细阐述,为瘙痒治疗提供新的思路。
Pruritus is an unpleasant noxious sensation induced by a variety of causes. Although pruritus does not cause death directly, long-term chronic pruritus severely reduces the quality of life of patients. TRP(transient receptor potential ion channels) participate in the physiological process from the sensation to skin balance. A large number of studies have confirmed that many itch media are involved in signal transduction related to TRP ion channels. We review the difference between itch and pain, and the role and mechanism of TRP in itch, so as to provide new research targets for treatment of pruritus.
Pruritus is an unpleasant noxious sensation induced by a variety of causes. Although pruritus does not cause death directly, long-term chronic pruritus severely reduces the quality of life of patients. TRP(transient receptor potential ion channels) participate in the physiological process from the sensation to skin balance. A large number of studies have confirmed that many itch media are involved in signal transduction related to TRP ion channels. We review the difference between itch and pain, and the role and mechanism of TRP in itch, so as to provide new research targets for treatment of pruritus.
引文
[1] Ikoma A, Steinhoff M, Stander S, et al. The neurobiology of itch [J]. Nat Rev Neurosci, 2006,7(7): 535-47.
[2] Sun S, Dong X. Trp channels and itch [J]. Semin Immunopathol, 2016, 38(3): 293-307.
[3] 薛茹君, 张锡宝. 神经病理性瘙痒的研究进展 [J]. 中国医学文摘皮肤科学, 2015, 32(6): 586-92.[3] Xue R J, Zhang X B. The research progress of itch and neuropathic itch [J]. China Med Abstract Dermatol, 2015, 32(6): 586-92.
[4] Jeffry J, Kim S, Chen Z F. Itch signaling in the nervous system [J]. Physiology (Bethesda), 2011, 26(4): 286-92.
[5] Sun Y G, Zhao Z Q, Meng X L, et al. Cellular basis of itch sensation [J]. Science, 2009, 325(5947): 1531-4.
[6] Caterina M J, Pang Z. TRP channels in skin biology and pathophysiology [J]. Pharmaceuticals (Basel), 2016, 9(4): E77.
[7] 王胜兰, 戴毅, 刘晓丽, 等. TRP通道与偏头痛 [J]. 中国药理学通报, 2013, 29(10): 1352-4.[7] Wang S L, Dai Y, Liu X L, et al. TRP channels and migraine [J]. Chin Pharmacol Bull, 2013, 29(10): 1352-4.
[8] Shim W S, Tak M H, Lee M H, et al. TRPV1 mediates histamine-induced itching via the activation of phospholipase A2 and 12-lipoxygenase [J]. J Neurosci, 2007, 27(9): 2331-7.
[9] Zhu Y, Pan W H, Wang X R, et al. Tryptase and protease-activated receptor-2 stimulate scratching behavior in a murine model of ovalbumin-induced atopic-like dermatitis [J]. Int Immunopharmacol, 2015, 28(1): 507-12.
[10] Liu Q, Weng H J, Patel K N, et al. The distinct roles of two GPCRs, MrgprC11 and PAR2, in itch and hyperalgesia [J]. Sci Signal, 2011, 4(181): ra45.
[11] Cevikbas F, Wang X, Akiyama T, et al. A sensory neuron-expressed IL-31 receptor mediates T helper cell-dependent itch: Involvement of TRPV1 and TRPA1 [J]. J Allergy Clin Immunol, 2014, 133(2): 448-60.
[12] Liu T, Han Q, Chen G, et al. Toll-like receptor 4 contributes to chronic itch, alloknesis, and spinal astrocyte activation in male mice [J]. Pain, 2016, 157(4): 806-17.
[13] Liu T, Berta T, Xu Z Z, et al. TLR3 deficiency impairs spinal cord synaptic transmission, central sensitization, and pruritus in mice [J]. J Clin Invest, 2012, 122(6): 2195-207.
[14] Liu T, Xu Z Z, Park C K, et al. Toll-like receptor 7 mediates pruritus [J]. Nat Neurosci, 2010, 13(12): 1460-2.
[15] Esancy K, Condon L, Feng J, et al. A zebrafish and mouse model for selective pruritus via direct activation of TRPA1 [J]. Elife, 2018, 7. pii: e32036. doi: 10.7554/eLife.32036.
[16] Min H, Lee H, Lim H, et al. TLR4 enhances histamine-mediated pruritus by potentiating TRPV1 activity [J]. Mol Brain, 2014, 7: 59.
[17] Trevisan G, Materazzi S, Fusi C, et al. Novel therapeutic strategy to prevent chemotherapy-induced persistent sensory neuropathy by TRPA1 blockade [J]. Cancer Res, 2013, 73(10): 3120-31.
[18] Haddadi N S, Foroutan A, Ostadhadi S, et al. Peripheral NMDA receptor/NO system blockage inhibits itch responses induced by chloroquine in mice [J]. Acta Derm Venereol, 2017, 97(5): 571-7.
[19] Huang C C, Kim Y S, Olson W P, et al. A histamine-independent itch pathway is required for allergic ocular itch [J]. J Allergy Clin Immunol, 2016, 137(4): 1267-70.
[20] Kang J, Ding Y, Li B, et al. TRPA1 mediated aggravation of allergic contact dermatitis induced by DINP and regulated by NF-kappaB activation [J]. Sci Rep, 2017, 7: 43586.
[21] Kido-Nakahara M, Buddenkotte J, Kempkes C, et al. Neural peptidase endothelin-converting enzyme 1 regulates endothelin 1-induced pruritus [J]. J Clin Invest, 2014, 124(6): 2683-95.
[22] Liu T, Ji R R. Oxidative stress induces itch via activation of transient receptor potential subtype ankyrin 1 in mice [J]. Neurosci Bull, 2012, 28(2): 145-54.
[23] Garcia-Elias A, Mrkonjic S, Jung C, et al. The TRPV4 channel [J]. Handb Exp Pharmacol, 2014, 222: 293-319.
[24] Akiyama T, Ivanov M, Nagamine M, et al. Involvement of TRPV4 in serotonin-evoked scratching [J]. J Invest Dermatol, 2016, 136(1): 154-60.
[25] Luo J, Feng J, Yu G, et al. Transient receptor potential vanilloid 4-expressing macrophages and keratinocytes contribute differentially to allergic and nonallergic chronic itch [J]. J Allergy Clin Immunol, 2018, 141(2): 608-19.
[2] Sun S, Dong X. Trp channels and itch [J]. Semin Immunopathol, 2016, 38(3): 293-307.
[3] 薛茹君, 张锡宝. 神经病理性瘙痒的研究进展 [J]. 中国医学文摘皮肤科学, 2015, 32(6): 586-92.[3] Xue R J, Zhang X B. The research progress of itch and neuropathic itch [J]. China Med Abstract Dermatol, 2015, 32(6): 586-92.
[4] Jeffry J, Kim S, Chen Z F. Itch signaling in the nervous system [J]. Physiology (Bethesda), 2011, 26(4): 286-92.
[5] Sun Y G, Zhao Z Q, Meng X L, et al. Cellular basis of itch sensation [J]. Science, 2009, 325(5947): 1531-4.
[6] Caterina M J, Pang Z. TRP channels in skin biology and pathophysiology [J]. Pharmaceuticals (Basel), 2016, 9(4): E77.
[7] 王胜兰, 戴毅, 刘晓丽, 等. TRP通道与偏头痛 [J]. 中国药理学通报, 2013, 29(10): 1352-4.[7] Wang S L, Dai Y, Liu X L, et al. TRP channels and migraine [J]. Chin Pharmacol Bull, 2013, 29(10): 1352-4.
[8] Shim W S, Tak M H, Lee M H, et al. TRPV1 mediates histamine-induced itching via the activation of phospholipase A2 and 12-lipoxygenase [J]. J Neurosci, 2007, 27(9): 2331-7.
[9] Zhu Y, Pan W H, Wang X R, et al. Tryptase and protease-activated receptor-2 stimulate scratching behavior in a murine model of ovalbumin-induced atopic-like dermatitis [J]. Int Immunopharmacol, 2015, 28(1): 507-12.
[10] Liu Q, Weng H J, Patel K N, et al. The distinct roles of two GPCRs, MrgprC11 and PAR2, in itch and hyperalgesia [J]. Sci Signal, 2011, 4(181): ra45.
[11] Cevikbas F, Wang X, Akiyama T, et al. A sensory neuron-expressed IL-31 receptor mediates T helper cell-dependent itch: Involvement of TRPV1 and TRPA1 [J]. J Allergy Clin Immunol, 2014, 133(2): 448-60.
[12] Liu T, Han Q, Chen G, et al. Toll-like receptor 4 contributes to chronic itch, alloknesis, and spinal astrocyte activation in male mice [J]. Pain, 2016, 157(4): 806-17.
[13] Liu T, Berta T, Xu Z Z, et al. TLR3 deficiency impairs spinal cord synaptic transmission, central sensitization, and pruritus in mice [J]. J Clin Invest, 2012, 122(6): 2195-207.
[14] Liu T, Xu Z Z, Park C K, et al. Toll-like receptor 7 mediates pruritus [J]. Nat Neurosci, 2010, 13(12): 1460-2.
[15] Esancy K, Condon L, Feng J, et al. A zebrafish and mouse model for selective pruritus via direct activation of TRPA1 [J]. Elife, 2018, 7. pii: e32036. doi: 10.7554/eLife.32036.
[16] Min H, Lee H, Lim H, et al. TLR4 enhances histamine-mediated pruritus by potentiating TRPV1 activity [J]. Mol Brain, 2014, 7: 59.
[17] Trevisan G, Materazzi S, Fusi C, et al. Novel therapeutic strategy to prevent chemotherapy-induced persistent sensory neuropathy by TRPA1 blockade [J]. Cancer Res, 2013, 73(10): 3120-31.
[18] Haddadi N S, Foroutan A, Ostadhadi S, et al. Peripheral NMDA receptor/NO system blockage inhibits itch responses induced by chloroquine in mice [J]. Acta Derm Venereol, 2017, 97(5): 571-7.
[19] Huang C C, Kim Y S, Olson W P, et al. A histamine-independent itch pathway is required for allergic ocular itch [J]. J Allergy Clin Immunol, 2016, 137(4): 1267-70.
[20] Kang J, Ding Y, Li B, et al. TRPA1 mediated aggravation of allergic contact dermatitis induced by DINP and regulated by NF-kappaB activation [J]. Sci Rep, 2017, 7: 43586.
[21] Kido-Nakahara M, Buddenkotte J, Kempkes C, et al. Neural peptidase endothelin-converting enzyme 1 regulates endothelin 1-induced pruritus [J]. J Clin Invest, 2014, 124(6): 2683-95.
[22] Liu T, Ji R R. Oxidative stress induces itch via activation of transient receptor potential subtype ankyrin 1 in mice [J]. Neurosci Bull, 2012, 28(2): 145-54.
[23] Garcia-Elias A, Mrkonjic S, Jung C, et al. The TRPV4 channel [J]. Handb Exp Pharmacol, 2014, 222: 293-319.
[24] Akiyama T, Ivanov M, Nagamine M, et al. Involvement of TRPV4 in serotonin-evoked scratching [J]. J Invest Dermatol, 2016, 136(1): 154-60.
[25] Luo J, Feng J, Yu G, et al. Transient receptor potential vanilloid 4-expressing macrophages and keratinocytes contribute differentially to allergic and nonallergic chronic itch [J]. J Allergy Clin Immunol, 2018, 141(2): 608-19.