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通过Toll样受体4(TLR4)和瞬时受体电位香草酸亚型1(TRPV1)受体相互作用激活肠伤害性神经元的机制

Mechanism of Activation of Enteric Nociceptive Neurons via Interaction of TLR4 and TRPV1 Receptors.

作者信息

Filippova L V, Fedorova A V, Nozdrachev A D

机构信息

Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia.

出版信息

Dokl Biol Sci. 2018 Mar;479(1):44-46. doi: 10.1134/S0012496618020023. Epub 2018 May 22.

Abstract

Evidence obtained by immunohistochemical double labeling and confocal laser scanning microscopy suggests that capsaicin, a ligand of the TRPV1 nociceptive vanilloid receptor, increases the number of TLR4-positive neurons in the rat colon myenteric plexus. In colitis caused by trinitrobenzene sulfonate, an increase in TRPV1 expression was more significant in both plexuses. Specific inhibitor of the TLR4 (C34) pattern-recognition receptor reduces TRPV1 expression in enteric neurons of both intact rats and rats with induced acute colitis. Thus, stimulation of nociceptive neurons by means of direct activation of their receptors of innate immunity (TLR4) is one of the possible mechanisms underlying the visceral pain in bacterial invasion and inflammatory bowel diseases.

摘要

通过免疫组织化学双重标记和共聚焦激光扫描显微镜获得的证据表明,辣椒素(TRPV1伤害性香草酸受体的一种配体)可增加大鼠结肠肌间神经丛中TLR4阳性神经元的数量。在三硝基苯磺酸引起的结肠炎中,两个神经丛中TRPV1表达的增加更为显著。TLR4模式识别受体的特异性抑制剂(C34)可降低完整大鼠和诱导性急性结肠炎大鼠肠神经元中TRPV1的表达。因此,通过直接激活其天然免疫受体(TLR4)来刺激伤害性神经元是细菌入侵和炎症性肠病中内脏痛的可能机制之一。

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