Effect of endothelin receptor antagonist bosentan on chronic hypoxia-induced inflammation and chemoafferent neuron adaptation in rat carotid body.
Effect of endothelin receptor antagonist bosentan on chronic hypoxia-induced inflammation and chemoafferent neuron adaptation in rat carotid body.
复制标题
内皮素受体拮抗剂波生坦对大鼠颈动脉体慢性缺氧炎症和化学传入神经元适应的影响。
DOI：
10.1089/ham.2012.1011
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发表时间：
2012
影响因子：
2.1
通讯作者：
Fidone,Salvatore
中科院分区：
文献类型：
--
作者：
Liu,Xuemei;He,Liang;Dinger,Bruce;Stensaas,Larry;Fidone,Salvatore
刘雪梅、梁贺、布鲁斯·丁格、拉里·斯滕萨斯和塞尔瓦托·费多内。内皮素受体拮抗剂波生坦对慢性低氧诱导的大鼠颈动脉体炎症和化学传入神经元适应的影响.高Alt Med Biol.13：209-216,2012.-慢性低氧(CH)诱导大鼠颈动脉体炎症反应，其特征是免疫细胞入侵和促炎细胞因子的表达.在本研究中，我们研究了A型内皮素(ET-A)受体在CH诱导的炎症发展中的作用。在CH(380 Torr)作用7天后，双标记免疫荧光研究显示，O2敏感的I型细胞中ET-A受体和酪氨酸羟基酶(TH)水平升高。在CH后，ET-A受体也表达在CD45+免疫细胞上，CD45+免疫细胞分布在化学感觉细胞小叶周围的组织中。免疫荧光和定量聚合酶链式反应研究表明，ET-A/B受体拮抗剂波生坦(2 0 0 mg/kg/d)可阻断CH诱导的ED-1+巨噬细胞的侵袭和细胞因子的上调，包括白介素1β(IL 1β)、白介素6(IL 6)、肿瘤坏死因子α和单核细胞趋化蛋白1(MCP 1)。此外，波生坦可阻断CH诱导的岩神经节(PG)化学传入神经元酸敏离子通道(ASICs)表达的增加。我们的发现与CH诱导的炎症涉及I型细胞ET-1的上调和释放的假设是一致的。ET-1可能通过化学感觉I型细胞和免疫细胞上的ET-A受体，以自分泌/旁分泌机制促进炎症反应。
Liu, Xuemei, Liang He, Bruce Dinger, Larry Stensaas, and Salvatore Fidone. Effect of endothelin receptor antagonist bosentan on chronic hypoxia-induced inflammation and chemoafferent neuron adaptation in rat carotid body.High Alt Med Biol.13:209–216, 2012.— Chronic hypoxia (CH) induces an inflammatory response in rat carotid body that is characterized by immune cell invasion and the expression of pro-inflammatory cytokines. In the present study, we have investigated the role of type-A endothelin (ET-A) receptors in the development of CH-induced inflammation. After 7 days of CH (380 Torr), double-label immunofluorescence studies demonstrated elevated levels of ET-A receptor and tyrosine hydroxylase (TH) in O2-sensitive type I cells. Following CH, ET-A receptors were also expressed on resident and invasive CD45+ immune cells distributed in tissue surrounding chemosensory cell lobules. Immnofluorescence and quantitative PCR studies showed that concurrent treatment with the ET-A/B receptor antagonist, bosentan (200 mg/kg/day), blocked CH-induced ED-1+ macrophage invasion and the upregulation of cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor α (TNFα), and monocyte chemoattractant protein-1 (MCP-1). Moreover, bosentan treatment blocked the CH-induced increases in expression of acid-sensitive ion channels (ASICs) in chemoafferent neurons in the petrosal ganglion (PG). Our findings are consistent with the hypothesis that CH-induced inflammation involves the upregulation and release of ET-1 from type I cells. ET-1 may act in an autocrine/paracrine mechanism via ET-A receptors on chemosensory type I cells and immune cells to promote an inflammatory response.
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DOI：
10.1152/ajplung.1995.269.5.l690
发表时间：
1995-11-01
影响因子：
4.9
作者：
DICARLO, VS;CHEN, SJ;OPARIL, S
通讯作者：
OPARIL, S
颈动脉体化学感受机制
DOI：
--
发表时间：
1995
期刊：
影响因子：
--
作者：
Constancio González;B. Dinger;S. Fidone
通讯作者：
S. Fidone
影响因子：
3.3
作者：
Chen, SJ;Chen, YF;Oparil, S
通讯作者：
Oparil, S
影响因子：
4.8
作者：
Yamashita, K;Discher, DJ;Webster, KA
通讯作者：
Webster, KA
DOI：
10.1523/jneurosci.20-23-08637.2000
发表时间：
2000-12
期刊：
The Journal of Neuroscience
影响因子：
--
作者：
Svea Sallmann;E. Jüttler;Simone Prinz;N. Petersen;U. Knopf;T. Weiser;M. Schwaninger
通讯作者：
Svea Sallmann;E. Jüttler;Simone Prinz;N. Petersen;U. Knopf;T. Weiser;M. Schwaninger