• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Small molecule GL-V9 protects against colitis-associated colorectal cancer by limiting NLRP3 inflammasome through autophagy.小分子GL-V9通过自噬限制NLRP3炎性小体,从而预防结肠炎相关的结直肠癌。
Oncoimmunology. 2017 Sep 21;7(1):e1375640. doi: 10.1080/2162402X.2017.1375640. eCollection 2017.
2
GL-V9, a new synthetic flavonoid derivative, ameliorates DSS-induced colitis against oxidative stress by up-regulating Trx-1 expression via activation of AMPK/FOXO3a pathway.新型合成类黄酮衍生物GL-V9通过激活AMPK/FOXO3a途径上调Trx-1表达,减轻DSS诱导的结肠炎氧化应激。
Oncotarget. 2015 Sep 22;6(28):26291-307. doi: 10.18632/oncotarget.4657.
3
3-(2-Oxo-2-phenylethylidene)-2,3,6,7-tetrahydro-1H-pyrazino[2,1-a]isoquinolin-4(11bH)-one (compound 1), a novel potent Nrf2/ARE inducer, protects against DSS-induced colitis via inhibiting NLRP3 inflammasome.3-(2-氧代-2-苯基亚乙基)-2,3,6,7-四氢-1H-吡嗪并[2,1-a]异喹啉-4(11bH)-酮(化合物1),一种新型强效Nrf2/ARE诱导剂,通过抑制NLRP3炎性小体来预防右旋糖酐硫酸钠(DSS)诱导的结肠炎。
Biochem Pharmacol. 2016 Feb 1;101:71-86. doi: 10.1016/j.bcp.2015.11.015. Epub 2015 Nov 14.
4
Evodiamine Attenuates Experimental Colitis Injury Via Activating Autophagy and Inhibiting NLRP3 Inflammasome Assembly.吴茱萸碱通过激活自噬和抑制NLRP3炎性小体组装减轻实验性结肠炎损伤。
Front Pharmacol. 2020 Nov 9;11:573870. doi: 10.3389/fphar.2020.573870. eCollection 2020.
5
Pretreatment with a Heat-Killed Probiotic Modulates the NLRP3 Inflammasome and Attenuates Colitis-Associated Colorectal Cancer in Mice.热灭活益生菌预处理可调节 NLRP3 炎性体并减轻小鼠结肠炎相关结直肠癌。
Nutrients. 2019 Feb 28;11(3):516. doi: 10.3390/nu11030516.
6
Huaier aqueous extract protects against dextran sulfate sodium-induced experimental colitis in mice by inhibiting NLRP3 inflammasome activation.槐耳水提取物通过抑制NLRP3炎性小体激活对葡聚糖硫酸钠诱导的小鼠实验性结肠炎具有保护作用。
Oncotarget. 2017 May 16;8(20):32937-32945. doi: 10.18632/oncotarget.16513.
7
Curcumin alleviates DSS-induced colitis via inhibiting NLRP3 inflammsome activation and IL-1β production.姜黄素通过抑制 NLRP3 炎性小体激活和 IL-1β 产生缓解 DSS 诱导的结肠炎。
Mol Immunol. 2018 Dec;104:11-19. doi: 10.1016/j.molimm.2018.09.004. Epub 2018 Nov 3.
8
Hydrogen sulfide protects against DSS-induced colitis by inhibiting NLRP3 inflammasome.硫化氢通过抑制 NLRP3 炎性小体来防止 DSS 诱导的结肠炎。
Free Radic Biol Med. 2019 Jun;137:99-109. doi: 10.1016/j.freeradbiomed.2019.04.025. Epub 2019 Apr 23.
9
Wogonoside protects against dextran sulfate sodium-induced experimental colitis in mice by inhibiting NF-κB and NLRP3 inflammasome activation.汉防己甲素通过抑制 NF-κB 和 NLRP3 炎性小体激活来防治葡聚糖硫酸钠诱导的小鼠实验性结肠炎。
Biochem Pharmacol. 2015 Mar 15;94(2):142-54. doi: 10.1016/j.bcp.2015.02.002. Epub 2015 Feb 10.
10
Ginsenoside Rd ameliorates colitis by inducing p62-driven mitophagy-mediated NLRP3 inflammasome inactivation in mice.人参皂苷 Rd 通过诱导 p62 驱动的线粒体自噬介导的 NLRP3 炎症小体失活来改善结肠炎。
Biochem Pharmacol. 2018 Sep;155:366-379. doi: 10.1016/j.bcp.2018.07.010. Epub 2018 Jul 25.

引用本文的文献

1
Autophagy in inflammatory bowel disease: immunization, etiology, and therapeutic potential.炎症性肠病中的自噬:免疫、病因及治疗潜力
Front Immunol. 2025 Aug 6;16:1543040. doi: 10.3389/fimmu.2025.1543040. eCollection 2025.
2
Flavonoid GL-V9 suppresses development of human hepatocellular cancer cells by inhibiting Wnt/β-Cantenin signaling pathway.类黄酮GL-V9通过抑制Wnt/β-连环蛋白信号通路抑制人肝癌细胞的发展。
Discov Oncol. 2025 Apr 4;16(1):462. doi: 10.1007/s12672-025-01845-4.
3
Inflammation in cancer: therapeutic opportunities from new insights.癌症中的炎症:新见解带来的治疗机遇
Mol Cancer. 2025 Feb 24;24(1):51. doi: 10.1186/s12943-025-02243-8.
4
Inflammasomes in Intestinal Disease: Mechanisms of Activation and Therapeutic Strategies.肠道疾病中的炎性小体:激活机制与治疗策略
Int J Mol Sci. 2024 Dec 4;25(23):13058. doi: 10.3390/ijms252313058.
5
GL-V9 Promotes Autophagy-Mediated YAP1 Degradation and Activates Mitochondrial Apoptosis in PDAC Cells.GL-V9促进胰腺导管腺癌(PDAC)细胞中自噬介导的YAP1降解并激活线粒体凋亡
Pharmaceuticals (Basel). 2024 Oct 10;17(10):1352. doi: 10.3390/ph17101352.
6
Nature of the Association between Rheumatoid Arthritis and Cervical Cancer and Its Potential Therapeutic Implications.类风湿关节炎与宫颈癌之间关联的本质及其潜在的治疗意义。
Nutrients. 2024 Aug 5;16(15):2569. doi: 10.3390/nu16152569.
7
alleviates chemotherapy-induced intestinal mucositis by enhancing intestinal mucus barrier.通过增强肠道黏液屏障减轻化疗引起的肠道黏膜炎。
Acta Pharm Sin B. 2024 Apr;14(4):1677-1692. doi: 10.1016/j.apsb.2023.12.015. Epub 2023 Dec 30.
8
GL-V9 inhibits the activation of AR-AKT-HK2 signaling networks and induces prostate cancer cell apoptosis through mitochondria-mediated mechanism.GL-V9抑制AR-AKT-HK2信号网络的激活,并通过线粒体介导的机制诱导前列腺癌细胞凋亡。
iScience. 2024 Feb 16;27(3):109246. doi: 10.1016/j.isci.2024.109246. eCollection 2024 Mar 15.
9
The Role of AMPK Signaling in Ulcerative Colitis.AMPK 信号通路在溃疡性结肠炎中的作用。
Drug Des Devel Ther. 2023 Dec 29;17:3855-3875. doi: 10.2147/DDDT.S442154. eCollection 2023.
10
Studies on the mechanism of local and extra-intestinal tissue manifestations in AOM-DSS-induced carcinogenesis in BALB/c mice: role of PARP-1, NLRP3, and autophagy.AOM-DSS诱导BALB/c小鼠致癌过程中局部和肠外组织表现机制的研究:PARP-1、NLRP3和自噬的作用
Naunyn Schmiedebergs Arch Pharmacol. 2024 Jun;397(6):4321-4337. doi: 10.1007/s00210-023-02878-8. Epub 2023 Dec 13.

本文引用的文献

1
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).自噬监测检测方法的使用与解读指南(第3版)
Autophagy. 2016;12(1):1-222. doi: 10.1080/15548627.2015.1100356.
2
GL-V9, a new synthetic flavonoid derivative, ameliorates DSS-induced colitis against oxidative stress by up-regulating Trx-1 expression via activation of AMPK/FOXO3a pathway.新型合成类黄酮衍生物GL-V9通过激活AMPK/FOXO3a途径上调Trx-1表达,减轻DSS诱导的结肠炎氧化应激。
Oncotarget. 2015 Sep 22;6(28):26291-307. doi: 10.18632/oncotarget.4657.
3
Wogonin prevents lipopolysaccharide-induced acute lung injury and inflammation in mice via peroxisome proliferator-activated receptor gamma-mediated attenuation of the nuclear factor-kappaB pathway.汉黄芩素通过过氧化物酶体增殖物激活受体γ介导的核因子-κB途径的减弱来预防脂多糖诱导的小鼠急性肺损伤和炎症。
Immunology. 2014 Oct;143(2):241-57. doi: 10.1111/imm.12305.
4
Inflammasome in intestinal inflammation and cancer.炎症小体与肠道炎症和癌症。
Mediators Inflamm. 2013;2013:654963. doi: 10.1155/2013/654963. Epub 2013 Mar 28.
5
CaMKIα regulates AMP kinase-dependent, TORC-1-independent autophagy during lipopolysaccharide-induced acute lung neutrophilic inflammation.钙调蛋白依赖性激酶 α 调控脂多糖诱导的急性肺中性粒细胞炎症中 AMP 激酶依赖性、TORC1 非依赖性自噬。
J Immunol. 2013 Apr 1;190(7):3620-8. doi: 10.4049/jimmunol.1102975. Epub 2013 Feb 27.
6
IL-1β mediates chronic intestinal inflammation by promoting the accumulation of IL-17A secreting innate lymphoid cells and CD4(+) Th17 cells.IL-1β 通过促进 IL-17A 分泌的固有淋巴细胞和 CD4(+) Th17 细胞的积累来介导慢性肠道炎症。
J Exp Med. 2012 Aug 27;209(9):1595-609. doi: 10.1084/jem.20111453. Epub 2012 Aug 13.
7
Treating inflammation by blocking interleukin-1 in a broad spectrum of diseases.在广泛的疾病中通过阻断白细胞介素-1来治疗炎症。
Nat Rev Drug Discov. 2012 Aug;11(8):633-52. doi: 10.1038/nrd3800.
8
Inflammaging: disturbed interplay between autophagy and inflammasomes.炎症衰老:自噬与炎性小体之间的相互作用紊乱
Aging (Albany NY). 2012 Mar;4(3):166-75. doi: 10.18632/aging.100444.
9
Activation of autophagy by inflammatory signals limits IL-1β production by targeting ubiquitinated inflammasomes for destruction.炎症信号激活自噬,通过靶向泛素化的炎性小体进行破坏,从而限制了 IL-1β 的产生。
Nat Immunol. 2012 Jan 29;13(3):255-63. doi: 10.1038/ni.2215.
10
Inflammasomes in intestinal inflammation and cancer.肠炎症和癌症中的炎性小体。
Gastroenterology. 2011 Dec;141(6):1986-99. doi: 10.1053/j.gastro.2011.10.002. Epub 2011 Oct 15.

小分子GL-V9通过自噬限制NLRP3炎性小体,从而预防结肠炎相关的结直肠癌。

Small molecule GL-V9 protects against colitis-associated colorectal cancer by limiting NLRP3 inflammasome through autophagy.

作者信息

Zhao Yue, Guo Qinglong, Zhao Kai, Zhou Yuxin, Li Wenjun, Pan Chuyue, Qiang Lei, Li Zhiyu, Lu Na

机构信息

State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, China.

Department of Medicine, Section of Dermatology, University of Chicago, Chicago, IL USA.

出版信息

Oncoimmunology. 2017 Sep 21;7(1):e1375640. doi: 10.1080/2162402X.2017.1375640. eCollection 2017.

DOI:10.1080/2162402X.2017.1375640
PMID:29296531
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5739552/
Abstract

Emerging evidence suggests that NLRP3 inflammasome provides a link between colitis-associated colorectal cancer and inflammatory bowel diseases. Autophagy is induced in macrophages by AMPK activation and regulates NLRP3 inflammasome to maintain intracellular homeostasis. Here we report that a small-molecule AMPK activator (GL-V9) exerts potent anti-inflammatory effects on macrophages and , which trigger autophagy to degraded NLRP3 inflammasome. Treatment with GL-V9 protected against colitis and tumorigenesis in colitis-associated colorectal cancer. This suggests that GL-V9 may be an interesting candidate for clinical evaluation in the treatment of colitis-associated colorectal cancer.

摘要

新出现的证据表明,NLRP3炎性小体在结肠炎相关的结直肠癌和炎症性肠病之间建立了联系。自噬由AMPK激活在巨噬细胞中诱导产生,并调节NLRP3炎性小体以维持细胞内稳态。在此,我们报告一种小分子AMPK激活剂(GL-V9)对巨噬细胞具有强大的抗炎作用,巨噬细胞触发自噬以降解NLRP3炎性小体。用GL-V9治疗可预防结肠炎相关结直肠癌中的结肠炎和肿瘤发生。这表明GL-V9可能是治疗结肠炎相关结直肠癌临床评估中一个有吸引力的候选药物。