Enriched environment may improve secondary brain injury after traumatic brain injury by regulating the TLR2/NF-κB signaling pathway

Traumatic brain injury (TBI) can cause damage to the blood-brain barrier, resulting in neuroinflammatory reactions and brain edema that seriously affect the recovery of neurological function. We hypothesize that an enriched environment (EE) regulates the TLR2/NF-κB signaling pathway and thereby modulates the integrity of the blood-brain barrier to achieve neuroprotective effects.

Inhibition of TLR2 with EE might constitute a successful approach in the management of TBI.

We established a TBI model using Sprague-Dawley rats and implemented EE intervention or TLR2 siRNA to reduce TLR2. Western-blot analysis, real-time PCR, immunofluorescence staining, ELISA, TUNEL and FJC staining, wet-dry methods, rotarod testing, and neurological scoring were then applied for analysis.

This study evaluated the expression of toll-like receptor (TLR)-2 after TBI in a rat model, with the aim of determining whether TLR2/NF-κB improves secondary brain injury by inhibiting the release of inflammatory factors and reducing brain edema.

Our results revealed that TLR2 was activated after TBI in rats and that EE or silencing of TLR2 with TLR2 siRNA reduced the level of inflammation, significantly alleviating brain edema, neuronal apoptosis, and degeneration. TBI exacerbated brain edema and nerve damage caused by TLR2/NF-κB signaling, and EE appeared to regulate neuroinflammation and brain edema by reducing TLR2. Conclusions: Inhibition of TLR2 with EE might constitute a successful approach in the management of TBI.