The present study assessed the effects of poly-arginine R18 and its promotion of neurocyte cell growth via autophagy in traumatic brain injury (TBI), and aimed to determine the possible mechanism by which this occurs. Brain water content was measured to analyze the effects of poly-arginine R18 in TBI. MTT and lactate dehydrogenase activity assays were performed to measure N2A cell growth. Western blotting and immunofluorescence staining were also performed to determine the protein expression of Bcl-2 associated X, LC3, Beclin-1 and p62. The results demonstrated that poly-arginine R18 treatment reduced neurocyte apoptosis and promoted neurocyte cell growth via the activation of autophagy in a rat model of TBI. Furthermore, poly-arginine R18 treatment promoted neurocyte cell growth, reduced apoptosis, induced the protein expression of LC3 and Beclin-1, and suppressed p62 expression by promoting autophagy in vitro. In addition, the inhibition of autophagy attenuated the effects of poly-arginine R18 on cell growth in vitro. Collectively, the results demonstrate the effects of poly-arginine R18 on neurocyte cell growth via autophagy activation in a model of TBI, and poly-arginine R18 is therefore a potential therapeutic target in TBI.
Keywords: autophagy; poly-arginine R18; traumatic brain injury.