BACKGROUND: The ketogenic diet (the KD) is an effective treatment for intractable epilepsy, especially in the paediatric population, and a growing number of studies have shown the neuroprotective role of the KD. However, few studies focused on the neuroprotective effects of the KD in traumatic brain injury (TBI). The present study aimed to investigate the effects of the KD on TBI. METHODS AND PROCEDURES: Male Sprague-Dawley rats (n = 60) were randomly divided into four groups according to the diet fed (the KD vs normal diet) and whether brain was injured or not. TBI was produced using Feeney weight drop model. Brain oedema was estimated by wet/dry weight ratio; Bax and Bcl-2 mRNA levels were determined by RealTime-PCR; Bax and Bcl-2 protein levels were detected by Western blot. Furthermore, cellular apoptosis in the penumbra area was examined using terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) method. MAIN OUTCOMES AND RESULTS: The results indicated that both Bax mRNA and protein levels were significantly elevated 72 hours after TBI and decreased by KD administration. Neither TBI nor the KD affected Bcl-2 mRNA and protein levels. KD administration also reduced brain oedema and cellular apoptosis. CONCLUSION: These results suggest that the KD might be a useful treatment for children suffering from the consequences of TBI.
BACKGROUND: The ketogenic diet (the KD) is an effective treatment for intractable epilepsy, especially in the paediatric population, and a growing number of studies have shown the neuroprotective role of the KD. However, few studies focused on the neuroprotective effects of the KD in traumatic brain injury (TBI). The present study aimed to investigate the effects of the KD on TBI. METHODS AND PROCEDURES: Male Sprague-Dawley rats (n = 60) were randomly divided into four groups according to the diet fed (the KD vs normal diet) and whether brain was injured or not. TBI was produced using Feeney weight drop model. Brain oedema was estimated by wet/dry weight ratio; Bax and Bcl-2 mRNA levels were determined by RealTime-PCR; Bax and Bcl-2 protein levels were detected by Western blot. Furthermore, cellular apoptosis in the penumbra area was examined using terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) method. MAIN OUTCOMES AND RESULTS: The results indicated that both Bax mRNA and protein levels were significantly elevated 72 hours after TBI and decreased by KD administration. Neither TBI nor the KD affected Bcl-2 mRNA and protein levels. KD administration also reduced brain oedema and cellular apoptosis. CONCLUSION: These results suggest that the KD might be a useful treatment for children suffering from the consequences of TBI.