Dimethyl itaconate modulates neuroprotective effect on primary rat astrocytes under inflammatory condition by regulating the expression of neurotrophic factors and TrkA/B-P75 receptors
In conclusion, DMI may be able to support astrocyte survival and functions based on the restoration of neurotrophic factors and their receptors expression in LPS-stimulated astrocyte cells. This suggests that DMI could be a promising therapeutic option for neurodegenerative diseases characterized by inflammation-induced astrocyte dysfunction.
Authors
- Dian Dayer (ORCID: https://orcid.org/0000-0001-5893-6379)
- Mohammad Reza Tabandeh (ORCID: https://orcid.org/0000-0003-3258-8550)
- Malahat Rezaee (ORCID: https://orcid.org/0000-0003-0003-1993)
- Nina P. Azari
Institutions
- Islamic Azad University, Tehran (IR)
- Ahvaz Jundishapur University of Medical Sciences (IR)
- Shahid Chamran University of Ahvaz (IR)
- Islamic Azad University, Isfahan (IR)
- Islamic Azad University of Falavarjan (IR)
- Stem Cell Technology Research Center (IR)
Publication Details
- Journal
- Neurological Research
- Published
- 2024-11-03
- DOI
- https://doi.org/10.1080/01616412.2024.2423583
- Primary Topic
- Neuroinflammation and Neurodegeneration Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Islamic Azad University