The role and mechanism of dl-3-n-butylphthalide in inflammatory response after traumatic brain injury in mice

Abstract

Objective To investigate whether butylphthalide (NBP) can protect neurons by inhibiting microglial activation and inflammation after traumatic brain injury in mice. Methods One hundred and forty-four mice were randomly assigned to four experimental groups: sham, traumatic brain injury (TBI), TBI+ vehicle (V) and TBI+ NBP. Neurological score, Nissl staining were performed in each group of mice, immunofluorescence staining was used to localize the distribution of ionized calcium binding adapter molecule 1 (IBA-1) in the cerebral cortex of mice, and enzyme-linked immunosorbent assay (ELISA) was used to detect the contents of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the contusion and laceration brain tissue of mice. Statisticalanalysis of data using the statistical product and service solutions 22.0 software. Results NBP could improve the neurological function score, relieve neurodegeneration after brain injury in mice (t=6.320, 5.440, P<0.05). NBP can inhibit the expression of IBA-1 protein and the inflammatory factors TNF-α [(7.21±1.21) pg/mg] and IL-1β [(3.52±1.13) pg/mg] after brain injury in mice (t=3.370, 3.420, 3.350, 3.400, P<0.05). Conclusion NBP can inhibit the activation of microglia in mice after TBI, which is related to the decrease of the release of pro-inflammatory cytokines. Key words: Traumatic brain injury; Butylphthalide; Neuroprotection; Inflammatory factors