Pinocembrin alleviates cognition deficits by inhibiting inflammation in diabetic mice.

Diabetic encephalopathy (DE) is one of the most common diabetic complications in diabetes mellitus and is characterized by cognitive impairment and neuroinflammation. It has been reported that hyperglycemia can induce hippocampal and cortical neuronal damage, which can result in severe spatial learning and memory impairment. Pinocembrin (Pino) has been widely used in the therapy of cancer and other diseases due to its anti-inflammatory, anti-allergic, anti-oxidant, anti-carcinogenic, and anti-viral activities. However, the effects of Pino on DE-induced cognition deficits and its precise mechanisms remain largely unknown. Therefore, the aim of this study was to investigate the neuroprotective effects of Pino on cognition and its potential mechanisms in a DE mouse model induced by streptozotocin (STZ, 150mg/kg). Here, we demonstrated that Pino significantly improved the behavior and cognitive deficits of DE mice in open field tasks and the Morris water maze. Pino also markedly increased neuronal survival in the frontal cortex and hippocampal CA3 region. Furthermore, western blotting was performed to measure nuclear translocation of nuclear factor-kappaB (NF-κB) and the expression of tumor necrosis factor-α (TNF-α) in the frontal cortex and hippocampus. The results demonstrated that Pino could suppress the nuclear translocation of NF-κB and decrease TNF-α expression in the cerebral cortex and the hippocampus of DE mice. Taken together, the results suggest that Pino alleviates cognition deficits by protecting neurons from inflammation injury in diabetic mice.