ABSTRACT
The concept of a 'gut-brain axis' was recently developed when the complex communications between the brain and the gut became evident. The interaction may affect emotions, motivation, mood, and higher cognitive functions as well as gut homeostasis. Human microbe symbiosis's merits are now acknowledged to transcend human mental health. Research has recently indicated that the gut-brain axis plays a vital role in brain health maintenance. The term 'gut-brain axis' can only partially capture the intricacy of these interactions. Dysbiosis of the gut commensals has been seen in patients with psychiatric diseases, such as depression. Major depressive disorder is caused by complicated interactions between the individual gene and the environment. In a forced swimming test, P. Zheng et al. discovered that germ-free mice with no gut microbiota had a shorter immobility duration than healthy mice. More radical effects were expressed on the use of probiotics rather than prebiotics and postbiotics in reducing the symptoms of depression in patients with major depressive disorder. One of prime importance can be given to exploring more microbiota to investigate the better therapeutic effects of probiotics, prebiotics, and postbiotics.
ABSTRACT
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ABSTRACT
Beraprost sodium is a new stable, orally active Prostaglandin I2 analogue. The aim of this study was to determine the effect of beraprost on cognitive dysfunction and locomotor impairment induced by bilateral common carotid artery occlusion in mice. We investigated the ameliorating effect of beraprost through PGI2 IP receptor by studying neurologic deficit assessment and T-maze testing in young and old male C57Bl/6 wild-type (WT) and IP receptor knockout (IP KO) mice following a 12 min bilateral common carotid artery occlusion (BCCAo) and 7 days of reperfusion. Beraprost reversed BCCAo induced cognitive impairment and neurological deficit in a dose dependent manner. Immunohistochemical studies showed attenuation of neuronal cell death, astrogliosis, microglial invasion, and myeloperoxidase (MPO) activity in both young and old WT mice after post treatment with beraprost. Moreover, after BCCAo, phosphorylated cAMP response element binding protein positive cell numbers were increased with beraprost treatment over vehicle treated controls. These results show that beraprost treatment attenuated cognitive dysfunction and neurological deficits induced by BCCAo, and suggest that this effect may be mediated by the neuroprotective effects of treatment.
ABSTRACT
Transient global cerebral ischemia causes delayed neuronal death in the hippocampal CA1 region. It also induces an up regulation of cyclooxygenase 2 (COX-2), which generates several metabolites of arachidonic acid, known as prostanoids, including Prostaglandin I2 (PGI2). The present study investigated whether the PGI2 IP receptor plays an important role in brain injury after global cerebral ischemia in aged mice. Adult young (2-3 months) and aged (12-15 months) male C57Bl/6 wild-type (WT) or IP receptor knockout (IP KO) mice underwent a 12 min bilateral common carotid artery occlusion (BCCAO) or a sham surgery. Behavior tests (neurologic deficit and T-maze) were performed 3 and 7 days after BCCAO. After seven days of reperfusion, the numbers of cells positive for markers of neurons, astrocytes, microglia, myeloperoxidase (MPO) and phosphorylated CREB (p-CREB) were evaluated immunohistochemically. Interestingly, in young and aged IP KO ischemic mice, there was a significant increase (p < 0.01) in cognitive deficit, hippocampal CA1 pyramidal neuron death, microglia and MPO activation, while p-CREB was reduced as compared to their corresponding WT controls. These data suggest that following ischemia, IP receptor deletion contributes to memory and cognitive deficits regulated by the CREB pathway and that treatment with IP receptor agonists could be a useful target to prevent harmful consequences.
