Ameliorative Effects of Antioxidants on the Hippocampal Accumulation of Pathologic Tau in a Rat Model of Blast-Induced Traumatic Brain Injury

Figure 7

Quantification of blast-induced oligomeric Tau accumulation in the hippocampus. Densities of T22-positive cells in the PoDG (a) and GrDG (b) of the hippocampus from normal controls (NC), blast-exposed rats (B), and blast-exposed rats treated with a combinatorial antioxidant regimen (B/T) were calculated and statistically analyzed. In the PoDG, significantly more T22-positive cells were observed seven days after blast exposure in untreated rats (7D-B) compared to normal controls (). Antioxidant treatment significantly reduced the number of T22-positive cells in the PoDG seven days after blast exposure (7D-B/T, ). There was a significant difference between NC and 7D-B/T groups (). In the GrDG, significantly more T22-positive cells were observed twenty-four hours to twenty-one days after blast exposure in untreated and treated rats compared to NCs although many more positive cells were observed at seven days in untreated rats ( or 0.001). Antioxidant treatment significantly reduced the number of T22-positive cells in the GrDG seven days after blast exposure (7D-B/T, ). The number of T22-positive cells in both the PoDG and GrDG exhibited a significant decline between the seven- and twenty-one-day time points in untreated, blast-exposed rats (7D-B versus 21D-B, ), a trend which was not observed in blast-exposed rats subsequently treated with the antioxidants HPN-07 and NAC (7D-B/T versus 21D-B/T, ), likely owing to the marked treatment effect observed at the seven-day evaluation interval. These results indicate treatment effects of antioxidants on oligomeric Tau accumulation in the hippocampus. , , and , compared to NC. . Error bars represent standard error of the means.

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