[The protective mechanism of fructose-1, 6-diphosphate on ischemic brain injury]

To explore the protective mechanism of fructose-1, 6-diphosphate (FDP) on ischemic brain injury.

A model of permanent focal cerebral ischemia was performed in rats by intraluminal filament occlusion of middle cerebral artery. TTC staining, immunohistochemistry, Western blotting, and TUNEL staining were used to evaluate the effect of FDP on infarct area, apurinic/apyrimidinic endonuclease (APE/Ref-1) expression, and apoptosis in ischemic brain tissue.

The infarct areas of FDP intervening group and ischemia for 24 h group were 31.0 +/- 2.9 mm(2) and 47.3 +/- 6.0 mm(2) respectively. The numbers of TUNEL positive cells in ischemic penumbra were 69.3 +/- 2.4/mm(2) and 42.8 +/- 1.7/mm(2) in FDP group and ischemia for 24 h group respectively. FDP upregulated the expression of APE/Ref-1 protein in ischemic penumbra. The numbers of APE/Ref-1 immuno-positive cells in the ischemia for 24 h group and FDP group were 47 +/- 3.4/mm(2) and 26.3 +/- 2.9/mm(2) respectively. The values of optical density by Western blotting in these two groups were 5.3 +/- 3.2 and 13.8 +/- 5.4 respectively. The differences between these two groups were statistically significant.

Through upregulating the expression of APE/Ref-1 protein, FDP improves the repair ability of brain tissue in the course of ischemic injury and mitigated the quantity of apoptosis in penumbra, thus preventing the extension of cerebral infarction.