PGE2 x IL-6 x TNF x COX-2 x IL-1β

Last update 08 May 2025

Basic Info

Related Targets

PGE2IL-6TNF[+2]

Drugs associated with PGE2 x IL-6 x TNF x COX-2 x IL-1β

GB2620210

Patent Mining

Target

COX-2 x IL-1β x IL-6 x PGE2 x TNF

Mechanism-

Active Org.

Spice Beverage Research Institute, Chinese Academy of Tropical Agricultural Sciences

Originator Org.

Spice Beverage Research Institute, Chinese Academy of Tropical Agricultural Sciences

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PGE2 x IL-6 x TNF x COX-2 x IL-1β

100 Translational Medicine associated with PGE2 x IL-6 x TNF x COX-2 x IL-1β

0 Patents (Medical) associated with PGE2 x IL-6 x TNF x COX-2 x IL-1β

597

Literatures (Medical) associated with PGE2 x IL-6 x TNF x COX-2 x IL-1β

01 Dec 2025·Immunologic Research

Lithospermic acid targeting heat shock protein 90 attenuates LPS-induced inflammatory response via NF-кB signalling pathway in BV2 microglial cells

Article

Author: Guo, Jie ; Li, Chen-Guang ; Wang, Yu-Long ; Chen, Ze-Hao ; Zhou, Ming-Chao ; Mai, Feng-Yi ; Liang, Jing-Rong ; Yang, Wen-Tao ; Luo, Jiao

Microglia function as a vital constituent in the maintenance of brain homeostasis. Aberrant microglial activation, however, may contribute to neurodegenerative diseases. Lithospermic acid (LA) is a plant-derived polycyclic phenolic carboxylic acid isolated from Salvia miltiorrhiza. The present study investigated the potential effects of lithospermic acid on LPS-induced neuroinflammation in BV2 microglial cells and determined the mechanism of action of this compound. Cells were pre-treated with lithospermic acid for 1 h and incubated with LPS for 24 h. qPCR, immunofluorescence, and immunoblot assays were used to determine the expression of iNOS, COX2, NF-κB p65, and HSP90 expression. ELISA was employed to measure the production of pro-inflammatory cytokines. Lithospermic acid dramatically reduced LPS-stimulated cell migration and decreased NF-κB p65 nuclear translocation. Furthermore, lithospermic acid also markedly decreased the production of pro-inflammatory cytokines, including IL-6, IL-1β, and TNF-α in a dose-dependent manner. Additionally, lithospermic acid inhibited NO and PGE2 production in response to LPS, and it also inhibited the expression of iNOS and COX2 in a dose-dependent manner. Molecular docking and experimental verification have demonstrated that lithospermic acid inhibits the activity and expression of HSP90. Small interfering RNA knockdown of HSP90 expression, which abrogated LPS-induced inflammation. These findings suggest that the lithospermic acid targeting HSP90 attenuates LPS-induced inflammatory response via the NF-κB signalling pathway in BV2 microglial cells. Collectively, lithospermic acid may offer therapeutic benefits for neurodegenerative disorders associated with microglial activation and could serve as a potential inhibitor/agent for the treatment of neuroinflammation.

01 Jun 2025·Cytokine

The synergistic effects of prostaglandin and IL-1β on myometrial and cervical stromal cells at the onset of labor

Article

Author: Huang, Qian ; Liu, Huishu ; Li, Pin ; Sha, Xiaoyan ; Jiang, Yanmin ; Lin, Baohua ; Wang, Lele ; Zheng, Zheng ; Bao, Junjie

Inflammatory cytokines such as IL-1β and prostaglandins (PGs) are pivotal in the initiation of labor. Nevertheless, the synergistic interaction between PGs and IL-1β remains to be fully elucidated. Labor is defined as regular and gradually increasing uterine contractions accompanied by progressive dilation of the cervix, and descent of the fetal. This study employed Luminex to monitor alterations in inflammatory cytokine levels within myometrial tissue (n = 10) during labor compared to non-labor (n = 10) conditions. And the synergistic relationship between PGs and IL-1β by investigating the primary myometrium cells and cervical stromal cells culture. The results showed that the inflammatory cytokines of IL-1β, IL-6, IL-8 and TNF-α in the myometrium tissue were increased in labor group. In myometrium cells, PGF2α and IL-1β synergistically up-regulated COX-2 mRNA, upregulated the transcription of PRA and PRB, PGF2α alleviated that IL-1β up-regulated IL-8 mRNA. In cervical stromal cells, IL-1β up-regulated the COX-2 and PRB protein expression. PGE2 abated that IL-1β up-regulated IL-8 mRNA. PGE increased the expression of PRs, which is more pronounced with the prolonged duration. Ratio of PRA/PRB show an increased trend with IL-1β and PGE2 co-regulated. This study further clarified the synergistic regulatory mechanism of IL-1β and PGs, offering a theoretical foundation for the development of strategies aimed at labor induction and the prevention and treatment of preterm birth.

01 Jun 2025·Journal of Psychiatric Research

rTMS ameliorates CUMS-induced anxiety-depression-like behaviour and cognitive dysfunction in rats by modulating the COX-2/PGE2 signalling pathway

Article

Author: Gu, Shina ; Hao, Ran ; Liu, Huanhuan ; Lang, Jiqing ; Zhang, Fuping ; Pei, Yanjiao ; Song, Jinggui ; Chen, Yuxin ; Li, Jiao ; Zhang, Zhaohui ; Peng, Qi

BACKGROUNDrTMS is a safe and effective neuromodulation method for treating depression, but the specifics of its antidepressant effects and the underlying mechanisms remain uncertain.METHODSMale SD rats were randomly divided into four groups: control group, CUMS group, CUMS + rTMS (10 Hz) group, and CUMS + celecoxib (25 mg/kg, as a positive control) group. Depression-like behavior was assessed by weight change, SPT, and FST; anxiety by OFT and EPM; and cognitive function by the Y-maze. WB, IF, ELISA, and qPCR were used to observe changes in COX-2/PGE2 signaling pathway-related proteins, inflammatory factors, and the activation of astrocytes and microglia in the hippocampus of rats.RESULTSCompared to the control group, rats in the CUMS group exhibited significant anxiety-depression-like behavior and cognitive dysfunction. Compared to the CUMS group, rTMS and celecoxib interventions improved anxiety-depression-like behavior and cognitive dysfunction, reduced the expression of microglia and astrocytes, reversed the upregulation of pro-inflammatory factors (IL-1β, IL-6, TNF-α), and downregulated the expression of proteins related to the COX-2/PGE2 signaling pathway in CUMS-induced rats.CONCLUSIONSThe study demonstrated that rTMS could improve anxiety-depression-like behavior and cognitive dysfunction in rats by modulating the COX-2/PGE2 pathway.

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