RESUMO
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 diabetesassociated 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 mitogenactivated protein kinase (MAPK) cascades [extracellular signalregulated kinase (ERK), cJun Nterminal kinase (JNK) and p38], brainderived neurotrophic factor (BDNF) and apoptosisassociated proteins [caspase3, B-cell lymphoma 2 (Bcl2) and Bcl-2-associated X protein (Bax)] were detected by western blot analysis. Caspase3 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 Bcl2. Furthermore, diabetic rats showed increases in escape latency and mean path length in the water maze test, increases in the levels of hippocampal AChE, pJNK, pp38, caspase3 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.