Repetitive Hyperbaric Oxygenation Attenuates Reactive Astrogliosis and Suppresses Expression of Inflammatory Mediators in the Rat Model of Brain Injury

Figure 1

Effect of repetitive HBOT on GFAP expression after CSI. CSI provoked upregulation of GFAP expression both at mRNA (a) and protein (b) levels in the injured cortex compared to intact control and sham-operated animals, while repetitive HBOT reduced levels of GFAP mRNA to those detected in control groups. (a) Bars represent mean ± SEM of GFAP mRNA (relative to GAPDH). (b) Immunoblot analysis showed that GFAP was present as a single band with a molecular mass of about 50 kDa. Bars represent mean ± SEM of GFAP protein content (relative to β-actin). Samples are from 4 animals per each group. Dot line represents mean of GFAP mRNA or protein level ± SEM (gray area) measured in control animals. Letters indicate significance levels () between lesioned (L) and intact control group, L versus sham control (S) group, and L compared to lesioned group subjected to the HBO protocol (LHBO). The groups not sharing a common letter are statistically different. Level of significance was analyzed using Student’s -test. (c) The luminosity of glial scar is obtained by measuring GFAP staining intensity around the lesion site and presented on histogram. ((d) and (e)) Throughout the cortex of intact rats a small number of fibrous GFAP⁺ astrocytes is seen. ((f) and (g)) At 10 days after injury a huge number of reactive astrocytes with pronounced hypertrophy of cell body and processes ((g) inset) form glial scar around the lesion site. ((h) and (i)) Ten successive HBOT significantly reduced glial scar formation, and the majority of astrocytes attained fibrous morphology ((i) inset). Rectangles indicate where the high magnification images are taken from. Scale bar = 50 μm.