相关实验视频

Updated: Sep 14, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

通过EGFR/Nrf2抗氧化剂信号通路,在小鼠中诱导皮质素减弱环胺 (CTX) 的免疫抑制

Mengling Zhong¹, Mingmei Feng¹, Xinlin Chen¹

¹School of Pharmaceutical Sciences, Nanjing Tech University (NanjingTech), 30 South Puzhu Road, Nanjing 211816, People's Republic of China.

International immunopharmacology

|July 22, 2025

概括

科尔迪塞通过恢复免疫细胞功能和平衡代谢途径,有效地对抗免疫抑制. 这种天然化合物通过EGFR激活Nrf2通路,为免疫功能障碍提供潜在的治疗益处.

科学领域:

免疫学免疫学免疫学
药理学药理学是指药理学的学科.
代谢学代谢学代谢学

背景情况:

免疫抑制增加了对感染,瘤和炎症状况的易感性.
科迪塞宾具有抗炎,抗氧化和抗瘤的特性,但其免疫调节机制尚不清楚.
了解康迪塞宾的作用对于开发免疫抑制治疗非常重要.

研究的目的:

为了研究cordycepin的免疫调节作用.
在免疫抑制模型中阐明cordycepin作用的潜在机制.

主要方法:

环胺 (CTX) 诱导的免疫抑制小鼠模型.
评估免疫细胞的增殖,血细胞计数,免疫球蛋白水平和细胞因子的产生.
和血清的代谢分析.
针对EGFR的网络药理学分析.
对关键蛋白质 (EGFR,Nrf2,NQO1,HO-1) 的西部斑分析.

主要成果:

在CTX治疗的小鼠中,科迪塞宾恢复了体重,器官指数和脏完整性.
增强了T和B淋巴细胞的增殖,使血细胞数量正常化,免疫球蛋白水平增加.
调节的细胞因子 (增加IL-2,IFN-γ;减少IL-10) 和抗氧化状态 (减少MDA,增加GSH,SOD,CAT).
逆转了代谢干扰,特别是在酸盐代谢中,并通过EGFR信号激活了Nrf2通路.

结论:

科迪塞宾通过逆转代谢功能障碍来改善CTX诱导的免疫抑制.
通过EGFR调节激活Nrf2通路是一个关键机制.
科尔迪塞作为免疫抑制治疗剂具有前景.

关键词:

科尔迪斯的头脑.欧洲农业基金会 (EGFR) 是一个基金.免疫抑制是一种免疫抑制.代谢学代谢学代谢学网络药理学网络药理学 Nrf2 路径的路径

更多相关视频

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease

Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease

Published on: May 10, 2024

相关概念视频

Inhibition of Cdk Activity

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

Positive Regulator Molecules

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.