Correlation study on pericyte depletion,eye-signs in blood stasis syndrome,and blood-brain barrier dys-function in neuropsychiatric systemic lupus erythematosus
10.3969/j.issn.1006-5725.2025.06.003
- VernacularTitle:周细胞脱失与神经精神性狼疮血瘀证目征和血脑屏障功能障碍的相关性
- Author:
Jianbin LI
1
;
Rui WU
1
Author Information
1. 南昌大学第一附属医院风湿免疫科(江西 南昌 330006)
- Publication Type:Journal Article
- Keywords:
pericytes;
neuropsychiatric systemic lupus erythematosus;
eye-signs in blood stasis syn-drome;
blood-brain barrier
- From:
The Journal of Practical Medicine
2025;41(6):790-799
- CountryChina
- Language:Chinese
-
Abstract:
Objective This study aims to investigate the pathological role and molecular mechanisms of pericyte depletion in neuropsychiatric lupus(NPSLE)and to assess the potential of the PDGFR-β signaling pathway as a novel therapeutic target for NPSLE.Methods NPSLE models were established using 8-week-old female MRL/lpr mice,from which those exhibiting abnormal behaviors were selected for further analysis.The PDGFR-β signaling pathway was modulated using an agonist to promote pericyte proliferation or an inhibitor to suppress pericyte apoptosis.The effects of these treatments on blood-brain barrier(BBB)integrity,eye-signs in blood stasis syndrome,neuronal integrity,and tight junction protein expression were evaluated.Evans blue staining,H&E staining,Nissl staining,and immunofluorescence staining were employed to assess the expression of tight junction proteins(Cadherin,ZO-1),endothelial cell markers(CD31),and pericyte markers(NG2).Results Mice in the NPSLE group exhibited significant anxiety,depression,and cognitive impairment.In the PDGFR-β inhibition group,eye-signs in blood stasis syndrome scores were significantly elevated(P<0.01),BBB permeability was markedly increased(P<0.001),neuronal numbers were significantly reduced,tight junction protein expression was diminished,and pericyte depletion was aggravated.Conversely,the PDGFR-β agonist group showed a significant reduction in eye-signs in blood stasis syndrome scores(P<0.01),improved pericyte survival,enhanced expression of tight junction proteins,reduced neuronal damage,and restoration of BBB function(P<0.001).Immunofluorescence staining further confirmed that PDGFR-β activation significantly protected pericytes.Conclusions Pericyte depletion is closely associated with increased BBB permeability and exacerba-tion of eye-signs in blood stasis syndrome.Modulation of the PDGFR-β signaling pathway may provide a promising therapeutic strategy for NPSLE.
