Therapeutic effect of neural induced-stem cell-derived exosomes by regulating ERK/p38/NF-κB in traumatic brain injury.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Traumatic brain injury (TBI) can occur because of sudden external forces, such as falls or accidents, and it can cause immediate and long-term damage to the central nervous system. In this study, the therapeutic effects of neural-induced human adipose tissue-derived stem cell-derived exosomes (NI-Exo) on TBI were investigated. Exosomes were isolated and characterized through nanoparticle tracking analysis, cryo-transmission electron microscopy, and western blotting analysis. The therapeutic effects of NI-Exo were assessed in LPS-stimulated human microglial cells and TBI mice via behavioral tests (rotarod, elevated body swing, and cylinder tests), qPCR, western blotting analysis, and immunostaining. In the in vitro study, NI-Exo significantly downregulated pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) and upregulated anti-inflammatory cytokines (IL-4 and IL-10). In the in vivo study, NI-Exo (1 × 10⁴ or 1 × 10⁵ particles/mL) was administered intracerebroventricularly 1 h post-surgery to verify the effect on the in vivo model. In the TBI mouse model, NI-Exo improved asymmetric behaviors and reduced tissue disruption and cell loss. The protein levels of pro-apoptosis (p53, ROCK1, and Bax) decreased and those of anti-apoptosis (Mcl-1) increased in the NI-Exo group compared with those in the TBI group. Mechanistic investigations revealed that NI-Exo inhibited ERK and p38 phosph

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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