Reactive oxygen species, inflammation, and apoptosis are major contributors to secondary injuries that follow traumatic brain injury (TBI) in diabetic patients. Hydrogen (H2) can selectively neutralize reactive oxygen species and downregulate inflammatory and apoptotic factors. Therefore, we investigated the effects of inhaled high and low concentrations of hydrogen on neurological function after TBI in diabetic rats and the potential mechanism. We found that the inhalation of high concentrations of H2 significantly improved outcomes following TBI in diabetic rats. The inhalation of 42% H2 for one hour per day for 48 h significantly reduced brain edema, decreased the extravasation of sodium fluorescein, and reduced oxidative stress markers (p < 0.05). In addition, the inhalation of a high concentration of H2 (42% for one hour per day for 7 days) improved neurological deficits (p < 0.05) and reduced the expression of apoptotic protein markers (p < 0.05). However, the inhalation of 3% H2 did not yield significant effects. These results showed that the inhalation of 42% H2 can alleviate nerve damage and improve neurological function after TBI in diabetic rats. Therefore, the inhalation of a high concentration of H2 may be associated with the treatment of traumatic brain injuries.