生物活性 | |||
---|---|---|---|
描述 | Paroxetine, at concentrations of 1 μM and 10 μM, significantly inhibits T cell migration induced by CX3CL1 by blocking GRK2 activity. This inhibition also extends to GRK2-mediated activation of the ERK signaling pathway[1]. At a concentration of 10 μM, Paroxetine decreases the levels of pro-inflammatory cytokines in LPS-stimulated BV2 microglial cells. Furthermore, Paroxetine (0-5 μM) shows a dose-dependent reduction in the LPS-induced production of TNF-α and IL-1β in these cells. It also curbs the LPS-induced production of nitric oxide (NO) and the expression of inducible nitric oxide synthase (iNOS) in BV2 cells. At 5 μM, Paroxetine inhibits LPS-induced JNK activation and reduces baseline ERK1/2 activity, contributing to its ability to mitigate microglial-mediated neurotoxicity and suppress pro-inflammatory cytokines and NO production in primary microglial cells[4]. |
临床研究 | |||||
---|---|---|---|---|---|
NCT号 | 适应症或疾病 | 临床期 | 招募状态 | 预计完成时间 | 地点 |
NCT00031317 | Panic Disorder | Phase 4 | Completed | - | United States, Maryland ... 展开 >> National Institute of Mental Health (NIMH) Bethesda, Maryland, United States, 20892 收起 << |
NCT00445679 | - | Completed | - | - | |
NCT00403455 | PTSD | Phase 3 | Completed | - | United States, South Carolina ... 展开 >> Ralph H. Johnson VA Medical Center, Charleston, SC Charleston, South Carolina, United States, 29401-5799 收起 << |
实验方案 | |||
---|---|---|---|
1mg | 5mg | 10mg | |
1 mM 5 mM 10 mM |
1.33mL 0.27mL 0.13mL |
6.67mL 1.33mL 0.67mL |
13.34mL 2.67mL 1.33mL |
参考文献 |
---|