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

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<p>Dominant behavior over the intruder of rats (n = 10) reated intramuscularly with vehicle (olive oil, 0.2 ml), boldenone (BOL), or stanazolol (ST) once a week according to Protocol I (4 weeks, 5 mg/kg), Protocol II (8 weeks, 2.5 mg/kg), or Protocol III (12 weeks, 1.25 mg/kg). Dominant behavior time for Protocol I (A), II (B), and III (C) and dominant behavior events for Protocol I (D), II (E), and III (F). *Denotes significant difference from the vehicle group. # Denotes significant difference between BOL and ST groups.</p

Neuroprotective effect of anthocyanins on acetylcholinesterase activity and attenuation of scopolamine-induced amnesia in rats

Anthocyanins are a group of natural phenolic compounds responsible for the color to plants and fruits. These compounds might have beneficial effects on memory and have antioxidant properties. In the present study we have investigated the therapeutic efficacy of anthocyanins in an animal model of cognitive deficits, associated to Alzheimer's disease, induced by scopolamine. We evaluated whether anthocyanins protect the effects caused by SCO on nitrite/nitrate (NOx) levels and Na+,K+-ATPase and Ca2+-ATPase and acetylcholinesterase (AChE) activities in the cerebral cortex and hippocampus (of rats. We used 4 different groups of animals: control (CTRL), anthocyanins treated (ANT), scopolamine-challenged (SCO), and scopolamine + anthocyanins (SCO + ANT). After seven days of treatment with ANT (200 mg kg−1; oral), the animals were SCO injected (1 mg kg−1; IP) and were performed the behavior tests, and submitted to euthanasia. A memory deficit was found in SCO group, but ANT treatment prevented this impairment of memory (P < 0.05). The ANT treatment per se had an anxiolytic effect. AChE activity was increased in both in cortex and hippocampus of SCO group, this effect was significantly attenuated by ANT (P < 0.05). SCO decreased Na+,K+-ATPase and Ca2+-ATPase activities in hippocampus, and ANT was able to significantly (P < 0.05) prevent these effects. No significant alteration was found on NOx levels among the groups. In conclusion, the ANT is able to regulate cholinergic neurotransmission and restore the Na+,K+-ATPase and Ca2+-ATPase activities, and also prevented memory deficits caused by scopolamine administration

Neuroprotective effect of taurine against cell death, glial changes, and neuronal loss in the cerebellum of rats exposed to chronic-recurrent neuroinflammation induced by LPS

The present study investigated the neuroprotective effect of taurine against the deleterious effects of chronic-recurrent neuroinflammation induced by LPS in the cerebellum of rats. Adult male Wistar rats were treated with taurine for 28 days. Taurine was administered at a dose of 30 or 100 mg/kg, by gavage. On days 7, 14, 21, and 28, the animals received LPS (250 μg/kg) intraperitoneally. The vehicle used was saline. The animals were divided into six groups: vehicle, taurine 30 mg/kg, taurine 100 mg/kg, LPS, LPS plus taurine 30 mg/kg, and LPS plus taurine 100 mg/kg. On day 29, the animals were euthanized, and the cerebellum was removed and prepared for immunofluorescence analysis using antibodies of GFAP, NeuN, CD11b, and cleaved caspase-3. LPS group showed a reduction in the immunoreactivity of GFAP in the arbor vitae and medullary center and of NeuN in the granular layer of the cerebellar cortex. LPS increased the immunoreactivity of CD11b in the arbor vitae and in the medullary center. Taurine protected against these effects induced by LPS in immunoreactivity of GFAP, NeuN, and CD11b, with the 100 mg/kg dose being the most effective. LPS induced an increase in the number of positive cleaved caspase-3 cells in the Purkinje cell layers, granular layer, arbor vitae, and medullary center. Taurine showed its antiapoptotic activity by reducing the cleaved caspase-3 cells in relation to the LPS group. Here, a potential neuroprotective role of taurine can be seen since this amino acid was effective in protecting the cerebellum of rats against cell death and changes in glial and neuronal cells in the face of chronic-recurrent neuroinflammation

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