• 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

灯盏花素与CHNO联合作用危及胶质瘤存活：部分与PSEN1/PI3K-AKT信号轴的抑制有关。

Combined Scutellarin and CHNO Imperils the Survival of Glioma: Partly Associated With the Repression of PSEN1/PI3K-AKT Signaling Axis.

作者信息

He Xiu-Ying, Xu Yang, Xia Qing-Jie, Zhao Xiao-Ming, Li Shan, He Xiao-Qiong, Wang Ru-Rong, Wang Ting-Hua

机构信息

Institute of Neurological Disease, Department of Anesthesiology, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, China.

Institute of Neuroscience, Laboratory Zoology Department, Kunming Medical University, Kunming, China.

出版信息

Front Oncol. 2021 Sep 9;11:663262. doi: 10.3389/fonc.2021.663262. eCollection 2021.

DOI:10.3389/fonc.2021.663262
PMID:34568005
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8460401/
Abstract

Glioma, the most common intracranial tumor, harbors great harm. Since the treatment for it has reached the bottleneck stage, the development of new drugs becomes a trend. Therefore, we focus on the effect of scutellarin (SCU) and its combination with CHNO (abbreviated as ) on glioma and its possible mechanism in this study. Firstly, SCU and CHNO both suppressed the proliferation of U251 and LN229 cells in a dose-dependent manner, and CHNO augmented the inhibition effect of SCU on U251 and LN229 cells . Moreover, there was an interactive effect between them. Secondly, SCU and CHNO decreased U251 cells in G2 phase and LN229 cells in G2 and S phases but increased U251 cells in S phase, respectively. Meanwhile, the combination could further reduce U251 cells in G2 phase and LN229 cells in G2 and S phases. Thirdly, SCU and CHNO both induced the apoptosis of U251 and LN229. The combination further increased the apoptosis rate of both cells compared with the two drugs alone. Furthermore, SCU and CHNO both inhibited the lateral and vertical migration of both cells, which was further repressed by the combination. More importantly, the effect of SCU and the combination was better than positive control-temozolomide, and the toxicity was low. Additionally, SCU and CHNO could suppress the growth of glioma , and the effect of the combination was better. Finally, SCU and the combination upregulated the presenilin 1 (PSEN1) level but inactivated the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT) signaling and . Accordingly, we concluded that scutellarin and its combination with CHNO suppressed the proliferation/growth and migration and induced the apoptosis of glioma, in which the mechanism might be associated with the repression of PSEN1/PI3K-AKT signaling axis.

摘要

胶质瘤是最常见的颅内肿瘤，危害极大。由于其治疗已进入瓶颈阶段，开发新药成为一种趋势。因此，在本研究中，我们聚焦于灯盏花素（SCU）及其与CHNO（简称 ）联合使用对胶质瘤的影响及其可能机制。首先，SCU和CHNO均以剂量依赖的方式抑制U251和LN229细胞的增殖，且CHNO增强了SCU对U251和LN229细胞的抑制作用。此外，它们之间存在交互作用。其次，SCU使U251细胞的G2期减少，CHNO使LN229细胞的G2期和S期减少，但分别使U251细胞的S期增加。同时，联合使用可进一步减少U251细胞的G2期以及LN229细胞的G2期和S期。第三，SCU和CHNO均诱导U251和LN229细胞凋亡。与单独使用两种药物相比，联合使用进一步提高了两种细胞的凋亡率。此外，SCU和CHNO均抑制两种细胞的横向和纵向迁移，联合使用进一步增强了这种抑制作用。更重要的是，SCU及其联合使用的效果优于阳性对照替莫唑胺，且毒性较低。此外，SCU和CHNO可抑制胶质瘤生长，联合使用效果更佳。最后，SCU及其联合使用上调了早老素1（PSEN1）水平，但使磷脂酰肌醇3激酶（PI3K）-蛋白激酶B（AKT）信号通路失活 。因此，我们得出结论，灯盏花素及其与CHNO联合使用可抑制胶质瘤的增殖/生长和迁移并诱导其凋亡，其机制可能与抑制PSEN1/PI3K-AKT信号轴有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/052a4c2b8107/fonc-11-663262-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/c8a1968cfb30/fonc-11-663262-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/60d2022f1b9a/fonc-11-663262-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/404e270f1b5f/fonc-11-663262-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/dcb2fea79887/fonc-11-663262-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/c498632b4cb8/fonc-11-663262-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/33da34e4e83b/fonc-11-663262-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/c805f1937b61/fonc-11-663262-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/7200babf49ac/fonc-11-663262-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/ef2450a97ce8/fonc-11-663262-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/d61bf3855699/fonc-11-663262-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/052a4c2b8107/fonc-11-663262-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/c8a1968cfb30/fonc-11-663262-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/60d2022f1b9a/fonc-11-663262-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/404e270f1b5f/fonc-11-663262-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/dcb2fea79887/fonc-11-663262-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/c498632b4cb8/fonc-11-663262-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/33da34e4e83b/fonc-11-663262-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/c805f1937b61/fonc-11-663262-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/7200babf49ac/fonc-11-663262-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/ef2450a97ce8/fonc-11-663262-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/d61bf3855699/fonc-11-663262-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b6a/8460401/052a4c2b8107/fonc-11-663262-g011.jpg

相似文献

1
Combined Scutellarin and CHNO Imperils the Survival of Glioma: Partly Associated With the Repression of PSEN1/PI3K-AKT Signaling Axis.灯盏花素与CHNO联合作用危及胶质瘤存活：部分与PSEN1/PI3K-AKT信号轴的抑制有关。
Front Oncol. 2021 Sep 9;11:663262. doi: 10.3389/fonc.2021.663262. eCollection 2021.
2
CHNO and Its Combination with Scutellarin Suppress the Proliferation and Induce the Apoptosis of Human Glioma Cells via Upregulation of Fas-Associated Factor 1 Expression.CHNO及其与灯盏花素联合通过上调Fas相关因子1表达抑制人胶质瘤细胞增殖并诱导其凋亡。
Biomed Res Int. 2019 Feb 20;2019:6821219. doi: 10.1155/2019/6821219. eCollection 2019.
3
Corrigendum: Combined Scutellarin and CHNO Imperils the Survival of Glioma: Partly Associated With the Repression of PSEN1/PI3K-AKT Signaling Axis.勘误：灯盏花素与CHNO联合使用危及胶质瘤的存活：部分与PSEN1/PI3K-AKT信号轴的抑制有关。
Front Oncol. 2022 Mar 7;12:872110. doi: 10.3389/fonc.2022.872110. eCollection 2022.
4
Microrchidia family CW‑type zinc finger 2 promotes the proliferation, invasion, migration and epithelial‑mesenchymal transition of glioma by regulating PTEN/PI3K/AKT signaling via binding to N‑myc downstream regulated gene 1 promoter.微线体家族 CW 型锌指蛋白 2 通过结合 N‑myc 下游调节基因 1 启动子调控 PTEN/PI3K/AKT 信号通路，促进胶质瘤的增殖、侵袭、迁移和上皮间质转化。
Int J Mol Med. 2022 Feb;49(2). doi: 10.3892/ijmm.2021.5071. Epub 2021 Dec 16.
5
Combinatorial therapy with adenoviral-mediated PTEN and a PI3K inhibitor suppresses malignant glioma cell growth in vitro and in vivo by regulating the PI3K/AKT signaling pathway.腺病毒介导的PTEN与PI3K抑制剂联合治疗通过调节PI3K/AKT信号通路抑制恶性胶质瘤细胞在体外和体内的生长。
J Cancer Res Clin Oncol. 2017 Aug;143(8):1477-1487. doi: 10.1007/s00432-017-2415-5. Epub 2017 Apr 11.
6
Effects of platycodin D on proliferation, apoptosis and PI3K/Akt signal pathway of human glioma U251 cells.桔梗皂苷D对人胶质瘤U251细胞增殖、凋亡及PI3K/Akt信号通路的影响
Molecules. 2014 Dec 19;19(12):21411-23. doi: 10.3390/molecules191221411.
7
Bone marrow mesenchymal stem cells suppress growth and promote the apoptosis of glioma U251 cells through downregulation of the PI3K/AKT signaling pathway.骨髓间充质干细胞通过下调 PI3K/AKT 信号通路抑制胶质瘤 U251 细胞的生长并促进其凋亡。
Biomed Pharmacother. 2019 Apr;112:108625. doi: 10.1016/j.biopha.2019.108625. Epub 2019 Feb 20.
8
Regulation of cellular growth, apoptosis, and Akt activity in human U251 glioma cells by a combination of cisplatin with CRM197.顺铂联合 CRM197 对人 U251 神经胶质瘤细胞的细胞生长、凋亡和 Akt 活性的调控。
Anticancer Drugs. 2012 Jan;23(1):81-9. doi: 10.1097/CAD.0b013e32834b9b72.
9
Tenascin C Promotes Glioma Cell Malignant Behavior and Inhibits Chemosensitivity to Paclitaxel via Activation of the PI3K/AKT Signaling Pathway.Tenascin C 通过激活 PI3K/AKT 信号通路促进神经胶质瘤细胞的恶性行为并抑制紫杉醇的化疗敏感性。
J Mol Neurosci. 2021 Aug;71(8):1636-1647. doi: 10.1007/s12031-021-01832-8. Epub 2021 Apr 19.
10
Inhibition of Cell Proliferation and Metastasis by Scutellarein Regulating PI3K/Akt/NF-κB Signaling through PTEN Activation in Hepatocellular Carcinoma.野黄芩素通过激活 PTEN 抑制 PI3K/Akt/NF-κB 信号通路抑制肝癌细胞增殖和转移。
Int J Mol Sci. 2021 Aug 17;22(16):8841. doi: 10.3390/ijms22168841.

引用本文的文献

1
Scutellarin combined with lidocaine exerts antineoplastic effect in human glioma associated with repression of epidermal growth factor receptor signaling.灯盏花素联合利多卡因通过抑制表皮生长因子受体信号传导对人胶质瘤发挥抗肿瘤作用。
PLoS One. 2025 Jan 31;20(1):e0318031. doi: 10.1371/journal.pone.0318031. eCollection 2025.
2
Engineering dendritic cell biomimetic membrane as a delivery system for tumor targeted therapy.工程树突状细胞仿生膜作为肿瘤靶向治疗的递送系统。
J Nanobiotechnology. 2024 Oct 27;22(1):663. doi: 10.1186/s12951-024-02913-7.
3
PDGFBB facilitates tumorigenesis and malignancy of lung adenocarcinoma associated with PI3K-AKT/MAPK signaling.

本文引用的文献

1
CHNO and Its Combination with Scutellarin Suppress the Proliferation and Induce the Apoptosis of Human Glioma Cells via Upregulation of Fas-Associated Factor 1 Expression.CHNO及其与灯盏花素联合通过上调Fas相关因子1表达抑制人胶质瘤细胞增殖并诱导其凋亡。
Biomed Res Int. 2019 Feb 20;2019:6821219. doi: 10.1155/2019/6821219. eCollection 2019.
2
Protein Network Analysis of the Serum and Their Functional Implication in Patients Subjected to Traumatic Brain Injury.创伤性脑损伤患者血清的蛋白质网络分析及其功能意义
Front Neurosci. 2019 Jan 31;12:1049. doi: 10.3389/fnins.2018.01049. eCollection 2018.
3
Scutellarin synergistically enhances cisplatin effect against ovarian cancer cells through enhancing the ability of cisplatin binding to DNA.
血小板衍生生长因子 BB 促进与 PI3K-AKT/MAPK 信号通路相关的肺腺癌的发生和恶性转化。
Sci Rep. 2024 Feb 20;14(1):4191. doi: 10.1038/s41598-024-54801-7.
4
Usenamine A triggers NLRP3/caspase-1/GSDMD-mediated pyroptosis in lung adenocarcinoma by targeting the DDX3X/SQSTM1 axis.乌司他丁 A 通过靶向 DDX3X/SQSTM1 轴触发肺腺癌中 NLRP3/半胱天冬酶-1/GSDMD 介导的细胞焦亡。
Aging (Albany NY). 2024 Jan 23;16(2):1663-1684. doi: 10.18632/aging.205450.
5
In Vitro Anti-Proliferative and Apoptotic Effects of Hydroxytyrosyl Oleate on SH-SY5Y Human Neuroblastoma Cells.羟基酪醇油酸酯对 SH-SY5Y 人神经母细胞瘤细胞的体外抗增殖和凋亡作用。
Int J Mol Sci. 2022 Oct 15;23(20):12348. doi: 10.3390/ijms232012348.
野黄芩苷通过增强顺铂与 DNA 的结合能力，协同增强顺铂对卵巢癌细胞的作用。
Eur J Pharmacol. 2019 Feb 5;844:9-16. doi: 10.1016/j.ejphar.2018.11.040. Epub 2018 Nov 29.
4
Scutellarin Enhances Antitumor Effects and Attenuates the Toxicity of Bleomycin in H22 Ascites Tumor-Bearing Mice.灯盏花素增强H22腹水瘤荷瘤小鼠的抗肿瘤作用并减轻博来霉素的毒性。
Front Pharmacol. 2018 Jun 14;9:615. doi: 10.3389/fphar.2018.00615. eCollection 2018.
5
Scutellarin Increases Cisplatin-Induced Apoptosis and Autophagy to Overcome Cisplatin Resistance in Non-small Cell Lung Cancer via ERK/p53 and c-met/AKT Signaling Pathways.灯盏花素通过ERK/p53和c-met/AKT信号通路增强顺铂诱导的细胞凋亡和自噬，以克服非小细胞肺癌中的顺铂耐药性。
Front Pharmacol. 2018 Feb 13;9:92. doi: 10.3389/fphar.2018.00092. eCollection 2018.
6
Scutellarin suppresses human colorectal cancer metastasis and angiogenesis by targeting ephrinb2.灯盏花素通过靶向 EphrinB2 抑制人结直肠癌转移和血管生成。
Am J Transl Res. 2017 Nov 15;9(11):5094-5104. eCollection 2017.
7
Scutellarin inhibits Hela cell growth and glycolysis by inhibiting the activity of pyruvate kinase M2.灯盏花素通过抑制丙酮酸激酶M2的活性来抑制Hela细胞生长和糖酵解。
Bioorg Med Chem Lett. 2017 Dec 15;27(24):5404-5408. doi: 10.1016/j.bmcl.2017.11.011. Epub 2017 Nov 10.
8
Silencing Pre-B-cell leukemia homeobox 3 decreases the proliferation of human glioma cells in vitro and in vivo.沉默 Pre-B 细胞白血病同源盒 3 可减少人神经胶质瘤细胞的体外和体内增殖。
J Neurooncol. 2017 Dec;135(3):453-463. doi: 10.1007/s11060-017-2603-9. Epub 2017 Aug 30.
9
Cytotoxic and chemosensitization effects of Scutellarin from traditional Chinese herb Scutellaria altissima L. in human prostate cancer cells.中药高茎黄芩中黄芩苷对人前列腺癌细胞的细胞毒性和化学增敏作用。
Oncol Rep. 2017 Sep;38(3):1491-1499. doi: 10.3892/or.2017.5850. Epub 2017 Jul 24.
10
Temozolomide and sorafenib as programmed cell death inducers of human glioma cells.替莫唑胺和索拉非尼作为人类神经胶质瘤细胞程序性死亡的诱导剂。
Pharmacol Rep. 2017 Aug;69(4):779-787. doi: 10.1016/j.pharep.2017.03.008. Epub 2017 Mar 14.