07-HNSC Therapy Is More Neuroprotective Than Glibenclamide After Cardiac Arrest via Immunomodulation
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Resuscitation, Neuroscience, 2021
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The Society of Critical Care Medicine's Critical Care Congress features internationally renowned faculty and content sessions highlighting the most up-to-date, evidence-based developments in critical care medicine. This is a presentation from the 2021 Critical Care Congress held virtually from January 31-February 12, 2021.


Xiaofeng Jia

Introduction/Hypothesis: Cardiac arrest (CA) is a common but devastating disease, and neuroprotective therapy for brain injury after CA is a persistent difficulty in clinical practice. Neuroinflammation has been a focus for multiple potential therapies, including neural stem cell (NSCs) transplantation and glibenclamide (GBC) therapy. However, the underlying mechanism of immunoregulation remains unclear, and there is a lack of comparative evaluation between these two different interventions.

Methods: 24 Wistar rats were randomly assigned to three groups (Control, GBC, and hNSCs, N = 8/group). After 8 minutes of asphyxial CA, GBC was injected intraperitoneally or human (hNSCs) were administrated intranasally in the treatment groups. Neurological deficit scores (NDS) were performed at 24, 48, and 72h post return of spontaneous circulation (ROSC). Immunofluorescence was used to track the hNSCs, and the activation subtype and polarization phenotype of microglia were compared between

groups. The expression, quantification, and cellular specificity of the TLR4 ⁄ NLRP3 pathway-related proteins in the injured brain were compared between groups.

Results: The aggregate analysis of NDS shows a significant improvement in hNSCs or GBC group compared to the Control group (hNSCs VS. Control: P<0.01, GBC VS. Control: P<0.05), and NSCs treatment showed a superior neuroprotective effect compared to the GBC group (hNSCs VS. GBC: P<0.01). Analysis of microglia revealed that more inactive morphology (NSCs VS. GBC: 56.1% ± 4.4% VS. 35.6% ± 5.7%, P = 0.017) and more anti-inflammatory polarization phenotype hNSCs (CD206+ cells, hNSCs VS. GBC: 43.0% ± 7.1% VS. 38.9% ± 8.9%, P = 0.012) were found in the hNSCs treatment group. Quantitative analysis of immune-fluorescence and Western blot demonstrated the expression of the TLR4 / NLRP3 inflammatory pathway-related proteins (TLR4, NFκB, NLRP3, caspase-1, and IL-1β) were suppressed by both treatments.

Conclusions: NSC and GBC therapy regulated brain microglial activation and the neuroinflammatory response after CA through the TLR4/NLRP3 signaling pathway and ultimately improved neurological function. In addition, hNSCs showed a better therapeutic effect than GBC in the process of inflammation regulation. This work was partially supported by NIH R01NS110387 and R01HL118084 (both to X JIA).


Meta Tag
Content Type Presentation
Knowledge Area Resuscitation
Knowledge Area Neuroscience
Knowledge Level Advanced
Membership Level Select
Tag Asphyxia
Tag Cardiac Arrest
Year 2021
neurostem cell therapy
glabin-clamate (GBC)
neurological outcomes
TLR4, NLRP3 signaling pathway


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