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[125I]CGP 42112 reveals a non-angiotensin II binding site in 1-methyl-4-phenylpyridine (MPP+)-induced brain injury.[125I]CGP 42112揭示了1-甲基-4-苯基吡啶(MPP+)诱导的脑损伤中的一种非血管紧张素II结合位点。
Cell Mol Neurobiol. 1994 Feb;14(1):99-104. doi: 10.1007/BF02088592.
2
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Quantitative autoradiography of angiotensin II AT2 receptors with [125I]CGP 42112.用[125I]CGP 42112对血管紧张素II AT2受体进行定量放射自显影。
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Angiotensin II receptor isoforms in the rat adrenal gland: studies with the selective subtype antagonists DuP 753 and CGP42112A.大鼠肾上腺中的血管紧张素II受体亚型:使用选择性亚型拮抗剂DuP 753和CGP42112A的研究
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Renal actions of the angiotensin AT2 receptor ligands CGP 42112 and PD 123319 after blockade of the renin-angiotensin system.肾素-血管紧张素系统阻断后血管紧张素AT2受体配体CGP 42112和PD 123319的肾脏作用
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Proximal tubule angiotensin AT2 receptors mediate an anti-inflammatory response via interleukin-10: role in renoprotection in obese rats.近端小管血管紧张素 AT2 受体通过白细胞介素-10 介导抗炎反应:在肥胖大鼠肾保护中的作用。
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Role of neuronal nitric oxide in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicity.神经元型一氧化氮在1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的多巴胺能神经毒性中的作用。
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Angiotensin II receptor subtypes: characterization, signalling mechanisms, and possible physiological implications.血管紧张素II受体亚型:特性、信号传导机制及可能的生理意义。
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Characterization of brain angiotensin II AT2 receptor subtype using [125I] CGP 42112A.
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Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis.人类因哌替啶类似物合成产物导致的慢性帕金森症。
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Pargyline prevents MPTP-induced parkinsonism in primates.帕吉林可预防灵长类动物中由1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱发的帕金森症。
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A primate model of parkinsonism: selective destruction of dopaminergic neurons in the pars compacta of the substantia nigra by N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.帕金森病的灵长类动物模型:N-甲基-4-苯基-1,2,3,6-四氢吡啶对黑质致密部多巴胺能神经元的选择性破坏。
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9
Peptides released by ameboid microglia regulate astroglial proliferation.阿米巴样小胶质细胞释放的肽调节星形胶质细胞增殖。
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10
Primate model of parkinsonism: selective lesion of nigrostriatal neurons by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine produces an extrapyramidal syndrome in rhesus monkeys.帕金森病灵长类动物模型:1-甲基-4-苯基-1,2,3,6-四氢吡啶对黑质纹状体神经元的选择性损伤在恒河猴中产生锥体外系综合征。
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[125I]CGP 42112揭示了1-甲基-4-苯基吡啶(MPP+)诱导的脑损伤中的一种非血管紧张素II结合位点。

[125I]CGP 42112 reveals a non-angiotensin II binding site in 1-methyl-4-phenylpyridine (MPP+)-induced brain injury.

作者信息

Viswanathan M, de Oliveira A M, Wu R M, Chiueh C C, Saavedra J M

机构信息

Section on Pharmacology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.

出版信息

Cell Mol Neurobiol. 1994 Feb;14(1):99-104. doi: 10.1007/BF02088592.

DOI:10.1007/BF02088592
PMID:7954664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11566791/
Abstract
  1. Intracerebral injection of the oxidative metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridine (MPP+), into the substantia nigra of adult rats resulted in a lesion at the injection site. 2. Using autoradiography, we localized specific [125I]CGP 42112 binding that was not recognized by angiotensin II or angiotensin II AT1 or AT2 receptor-selective ligands. 3. Our results suggest that [125I]CGP 42112 may be binding to activated microglia that appear at the lesion site.
摘要
  1. 向成年大鼠黑质内注射1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)的氧化代谢产物1-甲基-4-苯基吡啶(MPP+),在注射部位造成了损伤。2. 利用放射自显影技术,我们定位了特异性的[125I]CGP 42112结合,该结合不被血管紧张素II或血管紧张素II AT1或AT2受体选择性配体识别。3. 我们的结果表明,[125I]CGP 42112可能与出现在损伤部位的活化小胶质细胞结合。