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5-羟色胺受体3拮抗剂通过IκBα/NF-κB信号通路抑制脂多糖诱导RAW264.7细胞炎症反应 被引量:1
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作者 邓邺云 任晓曦 +2 位作者 刘康瑞 陈茜 张建亮 《中国生物化学与分子生物学报》 CAS CSCD 北大核心 2023年第5期750-758,共9页
在败血症等炎症相关疾病中,巨噬细胞过度产生的炎症因子在疾病的发病机制中发挥关键作用。5-羟色胺受体3(5-hydroxytryptamine receptor 3,5-HT_(3)R)拮抗剂,近来被发现在免疫系统中具有抑制炎症的作用,但其具体机制尚不清楚。本文使用... 在败血症等炎症相关疾病中,巨噬细胞过度产生的炎症因子在疾病的发病机制中发挥关键作用。5-羟色胺受体3(5-hydroxytryptamine receptor 3,5-HT_(3)R)拮抗剂,近来被发现在免疫系统中具有抑制炎症的作用,但其具体机制尚不清楚。本文使用脂多糖(lipopolysaccharides,LPS)刺激小鼠巨噬细胞系RAW 264.7细胞,引发巨噬细胞炎症相关蛋白质的表达和炎症因子的释放。结果显示,在RAW 264.7细胞中,与无处理组相比,LPS以剂量和时间依赖的方式促进炎症相关蛋白质的表达和炎症因子的释放。进一步使用5-HT_(3)R拮抗剂格拉司琼(granisetron,GA)进行预处理,检测其抗炎作用。蛋白质免疫印迹和酶联免疫吸附测定的结果表明,与LPS处理组相比,随着GA浓度的升高,其抑制LPS诱导的RAW 264.7细胞炎症的效果越好(P<0.05)。同时,细胞活力和细胞毒性的结果也表明,所使用的GA对细胞不造成损伤。另外,通过免疫荧光实验和双荧光素酶检测表明,GA可以抑制LPS诱导的NF-κB的核移位和转录活性;进一步的蛋白质免疫印迹结果表明,GA可以通过抑制IκBα的磷酸化而抑制其降解,从而抑制NF-κB的功能。总之,本文的结果提示,GA可以通过抑制IκBα/NF-κB信号通路,抑制RAW 264.7巨噬细胞中炎症相关蛋白质的表达和炎症因子的释放。本研究结果为进一步探究5-HT_(3)R拮抗剂抗炎的分子机制,以及研发治疗败血症等炎症相关疾病的药物提供科学依据。 展开更多
关键词 败血症 抗炎 5-羟色胺受体3 格拉司琼 IκBα/NF-κB信号通路
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Role of 5-hydroxytryptamine type 3 receptors in the regulation of anxiety reactions 被引量:1
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作者 Yinan DU Zhiwei LI +3 位作者 Yukui ZHAO Jing HAN Weiping HU Zhiqiang LIU 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2024年第1期23-37,共15页
5-Hydroxytryptamine(5-HT)type 3 receptor(5-HT_(3)R)is the only type of ligand-gated ion channel in the 5-HT receptor family.Through the high permeability of Na+,K+,and Ca2+and activation of subsequent voltage-gated ca... 5-Hydroxytryptamine(5-HT)type 3 receptor(5-HT_(3)R)is the only type of ligand-gated ion channel in the 5-HT receptor family.Through the high permeability of Na+,K+,and Ca2+and activation of subsequent voltage-gated calcium channels(VGCCs),5-HT_(3)R induces a rapid increase of neuronal excitability or the release of neurotransmitters from axon terminals in the central nervous system(CNS).5-HT_(3)Rs are widely expressed in the medial prefrontal cortex(mPFC),amygdala(AMYG),hippocampus(HIP),periaqueductal gray(PAG),and other brain regions closely associated with anxiety reactions.They have a bidirectional regulatory effect on anxiety reactions by acting on different types of cells in different brain regions.5-HT_(3)Rs mediate the activation of the cholecystokinin(CCK)system in the AMYG,and theγ-aminobutyric acid(GABA)“disinhibition”mechanism in the prelimbic area of the mPFC promotes anxiety by the activation of GABAergic intermediate inhibitory neurons(IINs).In contrast,a 5-HT_(3)R-induced GABA“disinhibition”mechanism in the infralimbic area of the mPFC and the ventral HIP produces anxiolytic effects.5-HT_(2)R-mediated regulation of anxiety reactions are also activated by 5-HT_(3)R-activated 5-HT release in the HIP and PAG.This provides a theoretical basis for the treatment of anxiety disorders or the production of anxiolytic drugs by targeting 5-HT_(3)Rs.However,given the circuit specific modulation of 5-HT_(3)Rs on emotion,systemic use of 5-HT_(3)R agonism or antagonism alone seems unlikely to remedy anxiety,which deeply hinders the current clinical application of 5-HT_(3)R drugs.Therefore,the exploitation of circuit targeting methods or a combined drug strategy might be a useful developmental approach in the future. 展开更多
关键词 5-Hydroxytryptamine type 3 receptor(5-ht_(3)r) ANXIETY Medial prefrontal cortex AMYGDALA HIPPOCAMPUS Periaqueductal gray
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5-HT_(3) receptor antagonists protect against pressure overload-induced cardiac hypertrophy in murine 被引量:1
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作者 Rong Huo Chang Chen +3 位作者 Yan Chen Zhe Li Yunlong Hou Deli Dong 《Acta Pharmaceutica Sinica B》 SCIE CAS 2012年第1期16-22,共7页
Activation of cardiac sympathetic afferent reflex results in the increase of sympathetic activity.Serotonin(5-HT)activates cardiac sympathetic afferent through stimulating 5-HT_(3) receptors,the aim of present study i... Activation of cardiac sympathetic afferent reflex results in the increase of sympathetic activity.Serotonin(5-HT)activates cardiac sympathetic afferent through stimulating 5-HT_(3) receptors,the aim of present study is to test whether 5-HT_(3) receptor antagonists protect against cardiac hypertrophy.Cardiac hypertrophy induced by TAC for 4 weeks in mice was significantly inhibited by administration of 5-HT_(3) receptor antagonists,ondansetron(2.5 mg/kg,ip.)or tropisetron(2.5 mg/kg,ip.).Histological analysis revealed that the increased cardiac fibrosis in hypertrophic heart was relieved by ondansetron or tropisetron treatment.Ondansetron or tropisetron reduced the elevated plasma level of noradrenalin in mice with cardiac hypertrophy.Ondansetron and tropisetron had no effect on cardiomyocte hypertrophy induced by phenylephrine treatment in vitro.Finally,we took tropisetron as the representative drug and examined the effects of tropisetron on the desensitization of cardiac b-adrenergic receptor in rat treated with abdominal aortic banding(AB).Results showed that tropisetron restored the desensitization of cardiac b-adrenergic receptor in AB-treated rats.In conclusion,5-HT_(3) receptor antagonists protected against cardiac hypertrophy and restored the desensitization of cardiac adrenergic responsiveness,the mechanism in which may be through reducing the sympathetic activity. 展开更多
关键词 Cardiac hypertrophy 5-ht_(3)receptor 5-ht_(3)receptor antagonists
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Synthesis and biological evaluation of ^(99m)Tc-HEDTA/HYNIC-MPP4 complex for 5-HT_(1A) receptor imaging 被引量:1
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作者 FAN WeiWei LIN Yan +5 位作者 ZHANG XianZhong PANG Yan MA Cong TANG ZhiGang ZHANG JunBo WANG XueBin 《Science China Chemistry》 SCIE EI CAS 2009年第5期590-598,共9页
5-HT_(1A)receptor is associated with a variety of pathophysiology of neuropsychiatric disorders.Accordingly,we have synthesized a new 5-HT_(1A) receptor ligand(HYNIC-MPP4)and labeled it with^(99m)Tc using N-(2-hydroxy... 5-HT_(1A)receptor is associated with a variety of pathophysiology of neuropsychiatric disorders.Accordingly,we have synthesized a new 5-HT_(1A) receptor ligand(HYNIC-MPP4)and labeled it with^(99m)Tc using N-(2-hydroxyethyl)ethylenediaminetriacetic acid(HEDTA)as coligand.^(99m)Tc-HEDTA/HYNIC-MPP4 was prepared under pH 6 at room temperature.Biodistribution of^(99m)Tc-HEDTA/HYNIC-MPP4 in normal mice showed that this complex had moderate brain uptake(0.60%ID·g^(-1)at 2 min p.i.)and good retention.The hippocampus had the highest radioactivity uptake at 2 min p.i.(1.84%ID·g^(-1)).The ratio of Hipp/CB was 3.1 at 2 min p.i.and increased to 4.4 at 60 min p.i.After blocking with 8-hydroxy-2-(dipropylamino)tetralin,the uptake of hippocampus was decreased significantly from 1.84%ID·g^(-1) to 0.53%ID·g^(-1) at 2 min p.i.,while the cerebellum had no significant decrease.This^(99m)Tc complex could be a potent agent for 5-HT_(1A) receptor imaging. 展开更多
关键词 5-ht_(1A)receptor ^(99m)Tc N-{4-[4-(2-methoxyphenyl)piperazin-1-yl]butyl}-3-(6-hydrazinyl)pyridyl carboxamide(HYNIC-MPP4) BIODISTrIBUTION
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T罗拉匹坦关键中间体的合成 被引量:1
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作者 叶海伟 王志坚 +3 位作者 高立军 周丽萍 陈云华 成碟 《西北大学学报(自然科学版)》 CAS CSCD 北大核心 2017年第1期56-62,共7页
合成一种罗拉匹坦关键中间体(S)-1-((R)-1-(3,5-二(三氟甲基)苯基)乙氧基)-3-氧-2-苯基丙烷-2-基)氨基甲酸苄酯(1)。以N-Cbz-L-苯甘氨酸(2)与苯甲醛二甲缩醛(3)为原料,在三氟化硼乙醚体系中经缩合反应制得(2R,4S)-2,4-二苯基噁唑烷酮-3... 合成一种罗拉匹坦关键中间体(S)-1-((R)-1-(3,5-二(三氟甲基)苯基)乙氧基)-3-氧-2-苯基丙烷-2-基)氨基甲酸苄酯(1)。以N-Cbz-L-苯甘氨酸(2)与苯甲醛二甲缩醛(3)为原料,在三氟化硼乙醚体系中经缩合反应制得(2R,4S)-2,4-二苯基噁唑烷酮-3-甲酸苄酯(4),收率为92%;4与(S)-1-(3,5-二(三氟甲基)苯基)乙醇(5)经溴甲基化产物6在低温下发生取代反应,得到中间体7,收率为72%;7经四氢铝锂还原与碳酸氢钠水解,制得罗拉匹坦关键中间体1,两步收率为75%,反应总收率为50%。中间体及产物的结构经核磁共振和质谱确证。该法反应时间短,条件温和,操作简便,具有工业化应用前景。 展开更多
关键词 NK-1受体拮抗剂 罗拉匹坦 (S)-1-((r)-1-(3 5-二(三氟甲基)苯基)乙氧基)-3-氧-2-苯基丙烷-2-基)氨基甲酸苄酯 合成
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