World Neurosurg. 2017 Jan 5. pii: S1878-8750(16)31433-4. doi: 10.1016/j.wneu.2016.12.118. [Epub ahead of print]

Hyperbaric oxygen effects on depression-like behavior and neuroinflammation in traumatic brain injury rats.

Lim SW1, Sung KC2, Shiue YL3, Wang CC4, Chio CC2, Kuo JR5.

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The aim of this study was to determine whether hyperbaric oxygen (HBO) therapy causes attenuation of traumatic brain injury (TBI)-induced depression-like behavior and its associated anti-neuroinflammatory effects after fluid percussion injury.


Anesthetized male Sprague-Dawley rats were divided into three groups: sham operation + NBA (normobaric air: 21% O2 at 1 absolute atmosphere [ATA]), TBI + NBA, and TBI + HBO (100% O2 at 2.0 ATA). HBO was applied immediately for 60 min/day after TBI for 3 days. Depression-like behavior was tested by a forced-swimming test, motor function by an inclined plane test, and infarction volume by TTC staining on days 4, 8 and 15. Neuronal apoptosis (TUNEL assay), microglial (marker OX42) activation, and TNF-α expression in microglia in the hippocampus CA3 were measured by immunofluorescence methods.


Compared to the TBI controls, without significant changes in triphenyltetrazolium chloride (TTC) staining or in the motor function test, TBI-induced depression-like behavior was significantly attenuated by HBO therapy by day 15 after TBI. Simultaneously, TBI-induced neuronal apoptosis, microglial (marker OX42) activation, and TNF-α expression in the microglia in the hippocampus CA3 were significantly reduced by HBO.


Our results suggest that HBO treatment may ameliorate TBI-induced depression-like behavior in rats by attenuating neuroinflammation, representing one possible mechanism by which depression-like behavior recovery might occur. We also recommend HBO as a potential treatment for TBI-induced depression-like behavior if early intervention is possible.