Evidence of persistent glial cell dysfunction in the anterior cingulate cortex of juvenile idiopathic arthritis children: a proton MRS study

Han, Hao; Xiao, Ji Hong; Weng, Yifei; Liang, Hongyan; Han, Chao; Yi, Cuili; Lin, Kezhao; Wu, Hua

doi:10.1186/s12969-022-00711-9

Cited by 3 publications

(2 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Figure 2B shows a representative spectral image of the hippocampal CA1 region of mice. NAA is a specific biochemical marker to assess neuronal viability/integrity, and Cho and MI levels indicate information about glial metabolism [ 19 ]. The NAA/Cr ratio of the CI group was significantly reduced ( P < 0.05), and the NAA/Cr ratio was increased by alisol A treatment ( P < 0.05) and decreased by the AKT inhibitor ( P < 0.05) ( Figure 2C ).…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Neurovascular protection of alisol A on cerebral ischemia mice through activating the AKT/GSK3β pathway

Li,

Zhang,

Zhou

et al. 2023

Aging

View full text Add to dashboard Cite

Alisol A, a triterpene isolated from Alisma Orientale, has been shown to exhibit anti-inflammatory effects and vascular protection. This study was designed to observe the effect of alisol A on cerebral ischemia (CI)-induced neurovascular dysfunction in the hippocampus and to further explore the potential mechanisms. The results showed that alisol A treatment improved the neurological deficits and cognitive impairment of CI mice. Alisol A reduced gliosis and improved neuronal/glial metabolism. Accordingly, alisol A inhibited inflammatory factors IL-6 and IL-1β induced by overactivation of astrocytes and microglia, thus protecting the neurovasculature. Furthermore, alisol A promoted the survival of neurons by decreasing the ratio of Bax/Bcl-2, and protected brain microvascular endothelial cells (BMECs) by upregulating the expression of ZO-1, Occludin and CD31. The phosphorylation of protein kinase B (AKT) and glycogen synthase kinase 3β (GSK3β) increased after treatment with alisol A. To explore the underlying mechanism, AKT was inhibited. As expected, the neurovascular protection of alisol A above was eliminated by AKT inhibition. The present study primarily suggested that alisol A could exert neurovascular protection in the hippocampus of CI mice by activating the AKT/GSK3β pathway and may potentially be used for the treatment of CI.

show abstract

Section: Resultsmentioning

confidence: 99%

“…Decreased NAA has been identified as a strong signal for neuronal loss [ 28 ]. The Cho concentration in glial cells is higher than that in neurons and may be used as a marker of gliosis [ 19 ]. MI is also a marker of glial proliferation [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Neurovascular protection of alisol A on cerebral ischemia mice through activating the AKT/GSK3β pathway

Li,

Zhang,

Zhou

et al. 2023

Aging

View full text Add to dashboard Cite

show abstract

Persistent neuroinflammation of the right insular cortex in children with juvenile idiopathic arthritis: a proton MRS study

et al. 2023

View full text Add to dashboard Cite

Blood brain barrier permeability and astrocyte-derived extracellular vesicles in children with juvenile idiopathic arthritis: a cross-sectional study

Berntson,

Elfving,

Samuelsson

et al. 2024

Pediatr Rheumatol

View full text Add to dashboard Cite

Background Juvenile idiopathic arthritis (JIA) is the most prevalent rheumatic disease in children, and the inflammatory process is widely studied, primarily characterized by its impact on joint health. Emerging evidence suggests that JIA may also affect the central nervous system (CNS). This study investigates the potential CNS involvement in JIA by analyzing the presence of astrocyte-derived extracellular vesicles (EVs) and the S100B protein in plasma, both of which are indicative of astrocyte activity and blood-brain barrier (BBB) integrity. Methods EDTA plasma from 90 children diagnosed with JIA and 10 healthy controls, matched by age and gender, was analyzed for extracellular vesicles by flow cytometric measurement. Astrocyte-derived EVs were identified using flow cytometry with markers for aquaporin 4 (AQP-4) and glial fibrillary acidic protein (GFAP). Levels of the S100B protein were measured using a commercial ELISA. Disease activity was assessed using the Juvenile Arthritis Disease Activity Score (JADAS27, 0–57), and pain levels were measured using a visual analogue scale (VAS, 0–10 cm). Results Our analyses revealed a significantly higher concentration of astrocyte-derived EVs in the plasma of children with JIA compared with healthy controls. Furthermore, children with JADAS27 scores of 1 or higher exhibited notably higher levels of these EVs. The S100B protein was detectable exclusively in the JIA group. Conclusion The elevated levels of astrocyte-derived EVs and the presence of S100B in children with JIA provide evidence of BBB disruption and CNS involvement, particularly in those with higher disease activity. These findings underscore the importance of considering CNS health in the comprehensive management of JIA. Further research is required to elucidate the mechanisms behind CNS engagement in JIA and to develop treatments that address both joint and CNS manifestations of the disease.

show abstract

Evidence of persistent glial cell dysfunction in the anterior cingulate cortex of juvenile idiopathic arthritis children: a proton MRS study

Cited by 3 publications

References 34 publications

Neurovascular protection of alisol A on cerebral ischemia mice through activating the AKT/GSK3β pathway

Neurovascular protection of alisol A on cerebral ischemia mice through activating the AKT/GSK3β pathway

Persistent neuroinflammation of the right insular cortex in children with juvenile idiopathic arthritis: a proton MRS study

Blood brain barrier permeability and astrocyte-derived extracellular vesicles in children with juvenile idiopathic arthritis: a cross-sectional study

Contact Info

Product

Resources

About