Abstract
This study was designed to investigate the neuroprotective effects of baicalein and the effect of the cortical 12/15-lipoxygenase (12/15-LOX) pathway on diabetic cognitive dysfunction. Our results showed that spatial learning and memory ability, as well as cortex neurons, were significantly impaired after the onset of diabetes. The fasting blood glucose and random blood glucose levels in the model group were significantly higher than those in the normal group. The levels of TG and TC in the plasma of the model group were significantly increased, but there was no significant difference in the LDL level. The insulin content in the plasma of diabetic rats was significantly lower than that of the normal group. The levels of inflammatory factors and 12(S)-HETE were significantly increased in diabetic rats, as were the protein expression levels of cPLA2, 12/15-LOX, p38MAPK, phospho-p38MAPK, caspase-3, caspase-9 and Aβ1–42; by contrast, protein expression of Bcl-2 was significantly decreased. Administration of baicalein was shown to improve the spatial learning and memory ability and significantly decrease the levels of inflammatory cytokines. However, baicalein did not significantly influence the levels of blood glucose, lipids or insulin in rats. Baicalein treatment significantly protected diabetes rats from neuron death; significantly attenuated the overexpression of cPLA2, 12/15-LOX, p38MAPK, phospho-p38MAPK, caspase-3, caspase-9 and Aβ1–42; and upregulated the expression of Bcl-2. These findings suggest that baicalein improves the cognitive function of diabetic rats by directly acting in the brain rather than by regulating the levels of blood glucose, lipids or insulin. In addition, baicalein can protect rat cortical neurons from damage caused by diabetes via inhibiting the 12/15-LOX pathway and relieving inflammation and apoptosis of the central nervous system.
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