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Baicalin is an important active component of the medicinal herb Scutellaria baicalensis Georgi and has shown a variety of pharmacological actions. The present study aimed to evaluate the neuroprotective effects of baicalin against diabetes‑associated cognitive deficits (DACD) in rats and to elucidate the potential molecular mechanisms of action. A rat model of diabetes mellitus was prepared by intraperitoneal injection of streptozotocin. After the successful establishment of the diabetic rat model, baicalin (50, 100 and 200 mg/kg) or vehicle was administrated for seven weeks. Learning and memory function were assessed using the Morris water maze test. At the end of the experiment, the activities of acetylcholinesterase (AChE) and choline acetylase (ChAT) were determined using commercial kits. Furthermore, the expression of proteins involved in mitogen‑activated protein kinase (MAPK) cascades [extracellular signal‑regulated kinase (ERK), c‑Jun N‑terminal kinase (JNK) and p38], brain‑derived neurotrophic factor (BDNF) and apoptosis‑associated proteins [caspase‑3, B-cell lymphoma 2 (Bcl‑2) and Bcl-2-associated X protein (Bax)] were detected by western blot analysis. Caspase‑3 activity was also analyzed using a commercial kit. The results demonstrated that diabetic rats exhibited decreases in body weight, decreases in the percentage of time spent in the target quadrant and the number of times of crossing the platform in the water maze test, as well as decreases in neuronal survival, ChAT, phosphorylated (p)ERK, BDNF and Bcl‑2. Furthermore, diabetic rats showed increases in escape latency and mean path length in the water maze test, increases in the levels of hippocampal AChE, p‑JNK, p‑p38, caspase‑3 and Bax as well as plasma glucose. However, in diabetic rats treated with baicalin, all of the abovementioned observations were obviously reversed. The findings suggested that baicalin exerts neuroprotective effects against DACD via modulation of MAPK cascades, BDNF and apoptosis.

molecular medicine reports

Baicalin alleviates diabetes-associated cognitive deficits via modulation of mitogen-activated protein kinase signaling, brain-derived neurotrophic factor and apoptosis