Anthocyanins restore behavioral and biochemical changes caused by streptozotocin-induced sporadic dementia of Alzheimer's type

Aims The aim of this study was to analyze if the pre-administration of anthocyanin on memory and anxiety prevented the effects caused by intracerebroventricular streptozotocin (icv-STZ) administration-induced sporadic dementia of Alzheimer's type (SDAT) in rats. Moreover, we evaluated whether the levels of nitrite/nitrate (NOx), Na+,K+-ATPase, Ca2 +-ATPase and acethylcholinesterase (AChE) activities in the cerebral cortex (CC) and hippocampus (HC) are altered in this experimental SDAT. Main methods Male Wistar rats were divided in 4 different groups: control (CTRL), anthocyanin (ANT), streptozotocin (STZ) and streptozotocin + anthocyanin (STZ + ANT). After seven days of treatment with ANT (200 mg/kg; oral), the rats were icv-STZ injected (3 mg/kg), and four days later the behavior parameters were performed and the animals submitted to euthanasia. Key findings A memory deficit was found in the STZ group, but ANT treatment showed that it prevents this impairment of memory (P < 0.05). Our results showed a higher anxiety in the icv-STZ group, but treatment with ANT showed a per se effect and prevented the anxiogenic behavior induced by STZ. Our results reveal that the ANT treatment (100 μM) tested displaces the specific binding of [3H] flunitrazepam to the benzodiazepinic site of GABAA receptors. AChE, Ca+-ATPase activities and NOx levels were found to be increased in HC and CC in the STZ group, which was attenuated by ANT (P < 0.05). STZ decreased Na+,K+-ATPase activity and ANT was able to prevent these effects (P < 0.05). Significance In conclusion, these findings demonstrated that ANT is able to regulate ion pump activity and cholinergic neurotransmission, as well as being able to enhance memory and act as an anxiolytic compound in animals with SDAT