Neuroinflammation [Neurosurgery Wiki]

This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong.
====== Neuroinflammation ======

[[Mutation]]s in the [[Complement factor I]] (CFI) gene have previously been identified as causes of recurrent CNS inflammation

----

[[Cerebral autoregulation]] is the ability of the brain to maintain a constant [[blood flow]] despite changes in [[blood pressure]]. Dysfunction in cerebral [[autoregulation]] can occur in acute brain injury, such as [[traumatic brain injury]] or [[stroke]], and can lead to poor outcomes. [[Neuroinflammation]] has been suggested as a potential mechanism underlying cerebral autoregulation dysfunction in these conditions.

===== Neuroinflammatory biomarkers =====

[[Neuroinflammatory biomarkers]].


----


===== Etiology =====

[[Alcohol induced neuroinflammation]].

SARS-CoV-2-mediated neuroinflammation

===== Neuroinflammation treatment =====
[[Microglia]]-related [[neuroinflammation]] is associated with a variety of [[neurodegenerative disease]]s. [[Flavonoid]]s have demonstrated different pharmacological effects, such as antioxidation, [[neuroprotection]] and anti-inflammation However, the effect of flavonoid 6-methoxyflavone (6-MeOF) on microglia-mediated neuroinflammation remain unknown.

A study aimed to study the antineuroinflammatory effects of 6-MeOF in lipopolysaccharide- (LPS-) induced microglia in vitro and in vivo.

Pretreatment of BV2 microglia cells with 6-MeOF for 1 h then stimulated with LPS (100 ng/ml) for 24 h. The expression levels of pro-inflammatory factors, NO and reactive oxygen species (ROS) were performed by the enzyme-linked immunosorbent assay (ELISA), Griess assay and flow cytometry. Western blotting was used to assess MAPK, NF-κB signal transducer and antioxidant enzymes-related proteins. Analysis of ROS and microglial morphology was confirmed in the zebrafish and mice brain, respectively.

The results demonstrated that 6-MeOF dose-dependently prevent cell death and decreased the levels of pro-inflammatory mediators in LPS-stimulated BV2 microglia cells. Phosphorylated NF-κB/IκB and TLR4/MyD88/p38 MAPK/JNK proteins after exposure to 6-MeOF was suppressed in LPS-activated BV-2 microglial cells. 6-MeOF also presented antioxidant activity by reduction of NO, ROS, iNOS and COX-2 and the induction of the level of HO-1 and NQO1 expressions in LPS-activated BV2 microglial cells. Furthermore, we demonstrated that 6-MeOF inhibited LPS-induced NO generation in an experimental zebrafish model and prevent the LPS-induced microgliosis in the prefrontal cortex and substantia nigra of mice.

These results explored that 6-MeOF possesses potential as anti-inflammatory and anti-oxidant agents against microglia-associated neuroinflammatory disorders
((Chen WF, Shih YH, Liu HC, Cheng CI, Chang CI, Chen CY, Lin IP, Lin MY, Lee CH. 6-methoxyflavone suppresses neuroinflammation in lipopolysaccharide- stimulated microglia through the inhibition of TLR4/MyD88/p38 MAPK/NF-κB dependent pathways and the activation of HO-1/NQO-1 signaling. Phytomedicine. 2022 Mar 1;99:154025. doi: 10.1016/j.phymed.2022.154025. Epub ahead of print. PMID: 35272244.)).