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2019新型冠状病毒感染已严重威胁到人们的健康和生活,但目前尚无特效治疗药物对其进行有效的防控。大黄素作为蓼科植物大黄及虎杖的主要活性成分,具有广谱的抗病毒活性,对包括SARS冠状病毒(SARS-CoV)、流感病毒、HIV病毒、HBV病毒等的感染和复制具有抑制作用。因此,本文就抗SARS-CoV的中成药及中药复方、大黄素及复方制剂抗病毒的机制、含大黄及虎杖的复方制剂抗病毒的临床研究和大黄素用于治疗新型冠状病毒肺炎(COVID-19)的可能性进行综述,旨在探讨其治疗2019新型冠状病毒的临床可能性。 相似文献
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洛匹那韦/利托那韦抗新型冠状病毒治疗的可行性及临床评价 总被引:1,自引:0,他引:1
目的 评价洛匹那韦/利托那韦抗新型冠状病毒治疗的应用可行性、临床效果及安全性。方法 最近在中国暴发的新型冠状病毒肺炎(简称新冠肺炎)疫情,目前尚无针对性强的抗病毒药物,临床尝试"老药新用",以2003年严重急性呼吸综合征(SARS)和2012年中东呼吸综合征(MERS)疫情中使用的一线抗病毒药物洛匹那韦/利托那韦来抗新型冠状病毒治疗。分析该药的抗病毒药理作用、临床应用可行性,评价其临床应用效果和安全性。结果 洛匹那韦/利托那韦治疗冠状病毒感染性疾病有一定临床基础,可重建宿主的免疫功能,抗新型冠状病毒有一定疗效,但有较高的耐药屏障。结论 洛匹那韦/利托那韦用于抗新型冠状病毒治疗可行,临床疗效较好,但应用期间要加强药学监护,尤其是合并用药和特殊人群应用时,注重安全、合理用药。 相似文献
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目的 总结抗严重急性呼吸综合征冠状病毒2(SARS-CoV-2)小分子化合物的研究进展.方法 采用计算机检索SciFinder、PubMed、中国知网、万方、维普等数据库中相关文献,检索时限为2019年1月至2021年3月,中英文关键词为"COVID-19""SARS-CoV-2""small molecule""新型... 相似文献
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抗病毒颗粒是根据经典名方研制而成的,用于治疗上呼吸道感染及流行性感冒的独家中药复方制剂.本文综述了抗病毒颗粒在新发传染性疾病和新型冠状病毒肺炎(COVID-19)等疾病领域的临床应用潜在价值. 相似文献
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抗新型冠状病毒潜力药物——瑞德西韦 总被引:2,自引:2,他引:0
当前,新型冠状病毒(2019-n Co V)感染引发的肺炎疫情已经发展为严重的公共卫生安全问题。针对该病毒,目前临床上并没有针对性的抗病毒药物。瑞德西韦(remdesivir,GS-5734)是由美国吉利德科学公司(Gilead Science)研制的一种新型核苷酸类似物抗病毒药。由于瑞德西韦在抗同属冠状病毒的非典型性肺炎冠状病毒(SARS-Co V)和中东呼吸综合症冠状病毒(MERS-Co V)中表现出较好的作用,一项针对其抗2019-nCoV的临床试验已经在中国启动。本文就该药物的基本信息、作用机制、药动学、国内外研究现状等方面进行概述,以期为临床用药提供参考。 相似文献
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血管紧张素转换酶2(ACE2)是肾素-血管紧张素系统负向调节血压的关键因子,主要分布在心脏、肾脏和胃肠等部位。最新研究发现ACE2是新型冠状病毒(SARS-CoV-2)入侵的功能性受体。新型冠状病毒和SARS相关冠状病毒(SARS-CoV)都能利用宿主细胞表面ACE2作为受体,与病毒刺突糖蛋白(Spike)受体结合结构域(RBD)结合发生相互作用,介导病毒入侵宿主细胞。回顾性分析ACE2在抗SARS-CoV中的研究进展,结合目前对新型冠状病毒肺炎(COVID-19)疫情防治的认识及Spike-ACE2蛋白相互作用的最新研究成果,对ACE2抗新型冠状病毒的药理作用机制研究进行简要综述,以期为新冠肺炎抗病毒特效药的研发提供参考。 相似文献
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目的对虎杖解毒颗粒(无糖型)改制前后的药效、毒性展开研究,科学、客观地评价颗粒的安全性、有效性。方法通过最大给药量实验评价其急性毒性,并采用二甲苯致小鼠耳廓肿胀模型和干酵母致大鼠发热模型,分别观察颗粒改制前后的抗炎、解热作用。结果虎杖解毒颗粒(无糖型)、虎杖解毒颗粒对小鼠的最大给药量分别相当于成人日剂量的218倍和200倍,小鼠均未死亡,生存状况无异常;颗粒对二甲苯所致小鼠耳廓肿胀以及干酵母引起的大鼠发热均有一定抑制作用,强度与剂量相关。结论虎杖解毒颗粒(无糖型)改制前后毒性及药效无明显改变,制剂毒性低,具有一定抗炎、解热作用。 相似文献
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《International immunopharmacology》2014,22(2):354-360
Emodin, an anthraquinone derivative isolated from the rhizomes of Rheum palmatum, has been reported to have a protective effect against lipopolysaccharide (LPS)-induced mastitis. However, the underlying molecular mechanisms are not well understood. The aim of this study was to investigate the molecular mechanisms of emodin in modifying lipopolysaccharide (LPS)-induced signaling pathways in mouse mammary epithelial cells (MEC). The pro-inflammatory cytokines were determined by ELISA. Nuclear factor-κB (NF-κB), inhibitory kappa B (IκBα) protein, p38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and PPAR-γ were determined by Western blotting. The results showed that emodin suppressed tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), iNOS and COX-2 expression. We also found that emodin inhibited LPS-induced NF-κB activation, IκBα degradation, phosphorylation of ERK, JNK and P38. Furthermore, emodin could activate PPAR-γ and the anti-inflammatory effects of emodin can be reversed by GW9662, a specific antagonist for PPAR-γ. In conclusion, our results demonstrate that emodin activates PPAR-γ, thereby attenuating LPS-induced inflammatory response. 相似文献
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《International immunopharmacology》2009,9(3):319-323
Vitisin A, a resveratrol tetramer isolated from Vitis vinifera roots, exhibits antioxidative, anticancer, antiapoptotic, and anti-inflammatory effects. It also inhibits nitric oxide (NO) production. Here, we examined the mechanism by which vitisin A inhibits NO production in lipopolysaccharide (LPS)-induced RAW 264.7 macrophage cells. Vitisin A dose dependently inhibited LPS-induced NO production and inducible NO synthase (iNOS) expression. In contrast, the production of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) was not altered by vitisin A. To investigate the signaling pathway for NO inhibition by vitisin A, we examined nuclear factor-κB (NF-κB) activation in the mitogen-activated protein kinase (MAPK) pathway, an inflammation-induced signal pathway in RAW 264.7 cells. Vitisin A inhibited LPS-induced extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 phosphorylation and suppressed LPS-induced NF-κB activation in RAW 264.7 cells. This suggests that vitisin A decreased NO production via downregulation of ERK1/2 and p38 and the NF-κB signal pathway in RAW 264.7 cells. 相似文献
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Weon-Jong Yoon Soo-Jin Heo Sang-Chul Han Hye-Ja Lee Gyeoung-Jin Kang Eun-Jin Yang Sun-Soon Park Hee-Kyoung Kang Eun-Sook Yoo 《Food and chemical toxicology》2012
Bone diseases are characterized by the presence of pro-inflammatory cytokines that regulate bone turnover. The receptor activator of NF-κB ligand (RANKL) is a soluble osteoblast-derived protein that induces bone resorption through osteoclast differentiation and activation. Sargachromanol G (SG) was isolated from the brown algae Sargassum siliquastrum; SG has anti-osteoclastogenic activity, but its mechanism of action and its active components remain largely unknown. In the present study, we investigated the anti-osteoclastogenic effects of SG on the expression of interleukin-1β (IL-1β)-induced osteoclastogenic factors (PGE2, COX-2, IL-6, OPG, and RANKL) in the human osteoblast cell line MG-63. We also examined the role of the nuclear factor-κB (NF-κB) and the mitogen-activated protein kinase (MAPK) signaling pathways in IL-1β-stimulated MG-63 cells. SG dose-dependently inhibited the production of osteoclastogenic factors in MG-63 cells. SG also inhibited phosphorylation of MAPK (ERK1/2, p38, and JNK) and NF-κB (p65, p50, and IκB-α). These results suggest that the anti-osteoporotic effect of SG may be because of the modulation of osteoclastogenic factors via suppression of MAPK and NF-κB activation. 相似文献
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该实验拟通过扎冲十三味丸(Zhachong shisanwei pills, ZC-13)抗炎活性物质的筛选,明确其抗炎质量标志物并进一步探究其可能的作用机制。首先采用超高效液相色谱与串联四级杆飞行时间质谱仪联用技术(ultra performance liquid chromatography/quadrupole-time-of-flight-mass spectrum, UPLC/Q-TOF-MS)结合核因子-κB(nuclear factor kappa-B, NF-κB)双荧光报告基因系统及一氧化氮(NO)含量检测筛选扎冲十三味丸中的抗炎活性成分,明确其抗炎质量标志物,并通过网络药理学及生物信息学方法预测其质量标志物主要作用靶点和通路,验证木香烃内酯主要抗炎通路。结果从扎冲十三味丸中筛选到NF-κB抑制相关质量标志物4种:没食子酸、鞣花酸、芹糖甘草苷、甘草酸; NO释放抑制相关质量标志物4种:没食子酸、甘草素、木香烃内酯、去氢木香内酯。上述成分主要通过调控磷酸肌醇依赖性蛋白激酶1 (3-phosphoinositide-dependent protein kinase 1, ... 相似文献
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TAK1 is closely associated with the NF-κB and MAPK signaling pathways. In the present study, we aimed to explore the relationship between TAK1 and gout as well as the effects of resveratrol on TAK1 activity and MSU crystal-induced inflammation. The expression levels of total TAK1 and phosphorylated TAK1 in gout patients were detected by western blotting. The influence of resveratrol on TAK1 activity and MSU crystal-induced inflammation was investigated in THP-1 cell and murine models of gout. The results showed that TAK1 and p-TAK1 were highly expressed in gouty arthritis patients. MSU crystals accelerated the expression of TAK1 and p-TAK1 in human PBMCs. The anti-inflammatory effects of resveratrol on MSU crystal-induced inflammation in vitro and in vivo included the alleviation of pro-inflammatory cytokines, inflammatory cell recruitment and foot swelling. Resveratrol limited the activation of TAK1 and its downstream signaling pathway, including the degradation of IκBα, the activation of NF-κB P65 and the phosphorylation of P38 and JNK. In conclusion, resveratrol may have a potential therapeutic effect on gouty arthritis by inhibiting TAK1 activity. 相似文献