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Acta cir. bras; 37(6): e370605, 2022. graf, ilus

Artigo em Inglês | LILACS | ID: biblio-1402959

Resumo

Purpose: Traumatic brain injury (TBI) is a major cause of death and disability. Cerebrolysin (CBL) has been reported to be anti-inflammatory by reducing reactive oxygen species (ROS) production. However, the neuroprotection of CBL in TBI and the potential mechanism are unclear. We aimed to investigate the neuroprotection and mechanisms of CBL in TBI. Methods: The TBI model was established in strict accordance with the Feeney weight-drop model of focal injury. The neurological score, brain water content, neuroinflammatory cytokine levels, and neuronal damage were evaluated. The involvement of the early brain injury modulatory pathway was also investigated. Results: Following TBI, the results showed that CBL administration increased neurological scores and decreased brain edema by alleviating blood­brain barrier (BBB) permeability, upregulating tight junction protein (ZO­1) levels, and decreasing the levels of the inflammatory cytokines tumor necrosis factor­α (TNF­α), interleukin­1ß (IL­1ß), IL­6, and NF­κB. The TUNEL assay showed that CBL decreased hippocampal neuronal apoptosis after TBI and decreased the protein expression levels of caspase­3 and Bax, increasing the levels of Bcl­2. The levels of Toll­like receptor 2 (TLR2) and TLR4 were significantly decreased after CBL treatment. In TBI patients, CBL can also decrease TNF­α, IL­1ß, IL­6, and NF­κB levels. This result indicates that CBL­mediated inhibition of neuroinflammation and apoptosis ameliorated neuronal death after TBI. The neuroprotective capacity of CBL is partly dependent on the TLR signaling pathway. Conclusions: Taken together, the results of this study indicate that CBL can improve neurological outcomes and reduce neuronal death against neuroinflammation and apoptosis via the TLR signaling pathway in mice.

Biblioteca responsável: BR68.1