Pinocembrin alleviates memory impairment in transient global cerebral ischemic rats

Abstract

The aim of the present study was to investigate the effect of pinocembrin on cognitive ability impairment in a rat model of transient global cerebral ischemia (TGCI). The TGCI model was established by inducing global cerebral ischemia for 20 min, followed by reperfusion for two weeks. The rats were divided into five experimental groups, including the sham group that were not subjected to ischemia, and four ischemic groups where the rats were exposed to TGCI. The sham and control TGCI groups were administered a vehicle intravenously immediately after reperfusion, while the other three groups were intravenously treated with 1, 5 and 10 mg/kg pinocembrin, respectively. In the present study, neurological scores were analyzed at 0 and 24 h after reperfusion, and the effect of pinocembrin on cognitive ability impairment in the TGCI rat model was investigated using a Morris water maze test. Neuronal loss was observed under an optical microscope with the assistance of Nissl staining. In addition, glial fibrillary acidic protein (GFAP)-positive cells were observed under an optical microscope by an immunohistochemistry assay. Pinocembrin treatment was found to alleviate the cognitive impairments, decrease the neurological scores, diminish neuronal loss in the hippocampus and reduce the number of GFAP-positive cells in the hippocampal CA1 region of the TGCI rats. Therefore, pinocembrin alleviated memory impairment in the TGCI rats.

Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat

“…Astrocyte morphology change significantly when they become reactive following I/ R. Enhancement proliferation of reactive astrocytes to the injury site are associated with a sustained and progressive increase in GFAP levels in that cells. There is a close association with the degree of brain injury and over-expression of pro-inflammatory cytokines in I/R [109]. Chronic inhibition of glutamate transporters has been shown to significantly increase excitotoxic neuronal damage at the post-ischemic time.…”

The Inhibitory Activity of Plants from Central Argentina on p-Hydroxyphenylpyruvate Dioxygenase. Isolation and Mechanism of Inhibition of a Flavanone from Flourensia oolepis

“…The presence of synergism between extract components was thus discarded, pointing to 1 as the only compound responsible for the inhibitory action of the plant. As far as we know, this is the first time that the anti-HPPD effect of 1 has been reported [14,[22][23][24][25].…”

Re-oxygenation after anoxia induces brain cell death and memory loss in the anoxia-tolerant crucian carp

“…Nonetheless, crucian carp did not exhibit impaired spatial learning ability when given multiple days to recover in normoxic water, indicating that they are able to repair any brain damage caused by anoxia/re-oxygenation, and that this state was therefore transient. While comparable experiments to our knowledge are lacking for both other fish and anoxia-tolerant freshwater turtles, it is well established that memory is impaired in mammals suffering from brain ischaemia and reperfusion (Shih et al, 2013;Meng et al, 2014;Schimidt et al, 2014). However, the ability of mammals to regenerate neurons is limited and cognitive impairment in neonatal rats exposed to ischaemia and reperfusion is carried over into adulthood (Arteni et al, 2003).…”