It is sensitive to fluctuations in glucose levels, some studies showed that glucose administration could improve hippocampal function and cognitive ability, but chronic hyperglycemia might increase the impact of dementia.
The hippocampus is an important part of the CNS, participates in the regulation of various nervous systems, and plays a fundamental role in memory and learning. Without control of glycemic imbalance in CNS, it is considered to be the initiating factor in the development of it. Introductionĭiabetic cognitive dysfunction (DCD), a diabetic central nervous system (CNS) complication, is characterized by cognitive deficits, neurochemical electrophysiological neurostructural abnormalities. These data indicated that HPTQ ameliorates the hippocampus apoptosis in diabetic cognitive dysfunction mice by activating CREB/BDNF/TrkB signaling pathway. In addition, HPTQ restored DCD-induced decline of p-CREB, BDNF, TrkB, and p-Akt in the hippocampus. The levels of Bax/Bcl-2 protein ratio and caspase-3 increased in the DCD model while the HPTQ inhibited it. Besides, the results of molecular docking showed that the main chemical components of HPTQ could be well combined with the targets of Bcl-2-associated X (Bax) and B-cell lymphoma2 (Bcl-2) and caspase-3. HPTQ improved the learning and memory ability, hippocampal neuron damage, and the level of BDNF in the hippocampus of the DCD model treated with HFD/STZ for 12 weeks. To investigate the neuroprotective mechanism of HPTQ in DCD, molecular docking was used to predict the possible target proteins of different active components in HPTQ and then the WB was used to verify the expression of key target proteins in the hippocampus of mice. To investigate the neuroprotective effect of HPTQ in DCD, the Morris water maze (MWM), novel object recognition (NOR) test was used to detect the learning and memory changes of mice hematoxylin-eosin (HE) staining was used to investigate the damage of hippocampal neurons the western blot (WB) was used to examine the level of brain-derived neurotrophic factor (BDNF) of hippocampus. The purpose of this study was to investigate the neuroprotective mechanism of HPTQ in DCD mice based on molecular docking. However, the underlying neuroprotective mechanism of HPTQ treated for diabetic cognitive dysfunction (DCD) remains unclear.
Huang-Pu-Tong-Qiao formula (HPTQ), a traditional Chinese medicine (TCM) formula used to improve cognitive impairment.
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