Rapamycin protects neurons from brain contusion‑induced inflammatory reaction via modulation of microglial activation

Song,Qi; Xie,Dujiang; Pan,Shiyong; Xu,Weijun

doi:10.3892/mmr.2015.4407

Rapamycin protects neurons from brain contusion‑induced inflammatory reaction via modulation of microglial activation

Authors:
- Qi Song
- Dujiang Xie
- Shiyong Pan
- Weijun Xu
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Affiliations: Department of Healthcare, Nanjing General Hospital of Nanjing Command, Nanjing, Jiangsu 210002, P.R. China, Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China
Published online on: October 1, 2015 https://doi.org/10.3892/mmr.2015.4407
Pages: 7203-7210
Copyright: © Song et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The inflammatory reaction is important in secondary injury following traumatic brain injury (TBI). Rapamycin has been demonstrated as a neuroprotective agent in a mouse model of TBI, however, there is a lack of data regarding the effects of rapamycin on the inflammatory reaction following TBI. Therefore, the present study was designed to assess the effects of treatment with rapamycin on inflammatory reactions and examine the possible involvement of microglial activation following TBI. Male imprinting control region mice were randomly divided into four groups: Sham group (n=23), TBI group (n=23), TBI + dimethyl sulfoxide (DMSO) group (n=31) and TBI + rapamycin group (n=31). Rapamycin was dissolved in DMSO (50 mg/ml) and injected 30 min after TBI (2 mg/Kg; intraperitoneally). A weight‑drop model of TBI was induced, and the brain tissues were harvested 24 h after TBI. The findings indicated that the administration of rapamycin following TBI was associated with decreased levels of activated microglia and neuron degeneration at the peri‑injury site, reduced levels of proinflammatory cytokines and increased neurobehavioral function, possibly mediated by inactivation of the mammalian target of rapamycin pathway. The results of the present study offer novel insight into the mechanisms responsible for the anti‑neuroinflammatory effects of rapamycin, possibly involving the modulation of microglial activation.

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