Abstract:Brain inflammation is involved in many brain disorders, such as brain ischemic injury, Alzheimer diseases, and Parkinson disease. Physical exercise has been recommended for the prevention and treatment of many brain inflammatory diseases. In the present study, the effects of exercise on motor function in relation with apoptotic neuronal cell death following neuroinflammation were investigated. Moreover, we compared the effect of forced exercise with voluntary exercise on neuroinflammation-induced motor malfunc… Show more
“…In the ischemic attack, increased expression of Bcl-2 inhibited apoptosis, while over-expression of Bax promoted apoptosis (Choi et al, 2017;Park et al, 2016). Increase of Bax to Bcl-2 ratio represents apoptotic cell death (Song et al, 2018). In the present study, caspase-3 expression in the hippocampal CA1 region was enhanced by the induction of cerebral ischemia insult.…”
Section: Discussionsupporting
confidence: 51%
“…Caspase-3 immunohistochemistry was performed according to a previously described method (Park et al, 2019;Song et al, 2018). The sections were incubated overnight with mouse anti-caspase-3 antibody (1:500; Santa Cruz Biotechnology, Santa Cruz, CA, USA) and then they were incubated for another 1 hr with the biotinylated mouse secondary antibody.…”
Section: Caspase-3 Immunohistochemistrymentioning
confidence: 99%
“…Western blot analysis was performed, as the previously described method (Kim et al, 2019;Park et al, 2019;Song et al, 2018). Brain tissues were lysed in an ice-cold whole cell lysate buffer.…”
Neuronal cell death in the hippocampus by cerebral ischemia causes disability of memory function. Cerebral ischemia also alters the expressions of brain-derived neurotrophic factor (BDNF), cyclic adenosine monophosphate-responsive element binding protein (CREB), extracellular signal-regulated protein kinase (ERK), and phosphatidylinositol 3-kinase/protein kinase B (Akt). In the present study, we investigated the effect of treadmill exercise on cerebral ischemia in relation with ERK-Akt-CREB-BDNF signaling pathway in the hippocampus using gerbils. Induction of cerebral ischemia deteriorated short-term memory with suppression of phosphorylation of ERK-Akt-CREB-BDNF pathway in the hippocampus of gerbils. Enhancement of apoptosis in the hippo-campus was accompanied in the ischemia gerbils. Treadmill exercise improved short-term memory through enhancing phosphorylation of ERK-Akt-CREB-BDNF pathway with suppressing apoptosis in the hippocampus of the ischemia gerbils. The present results suggest that improvement of memory function after cerebral ischemia by treadmill exercise may be involved in the ERK-Akt-CREB-BDNF signaling pathway, resulting in inhibition of apoptosis in the hippocampus.
“…In the ischemic attack, increased expression of Bcl-2 inhibited apoptosis, while over-expression of Bax promoted apoptosis (Choi et al, 2017;Park et al, 2016). Increase of Bax to Bcl-2 ratio represents apoptotic cell death (Song et al, 2018). In the present study, caspase-3 expression in the hippocampal CA1 region was enhanced by the induction of cerebral ischemia insult.…”
Section: Discussionsupporting
confidence: 51%
“…Caspase-3 immunohistochemistry was performed according to a previously described method (Park et al, 2019;Song et al, 2018). The sections were incubated overnight with mouse anti-caspase-3 antibody (1:500; Santa Cruz Biotechnology, Santa Cruz, CA, USA) and then they were incubated for another 1 hr with the biotinylated mouse secondary antibody.…”
Section: Caspase-3 Immunohistochemistrymentioning
confidence: 99%
“…Western blot analysis was performed, as the previously described method (Kim et al, 2019;Park et al, 2019;Song et al, 2018). Brain tissues were lysed in an ice-cold whole cell lysate buffer.…”
Neuronal cell death in the hippocampus by cerebral ischemia causes disability of memory function. Cerebral ischemia also alters the expressions of brain-derived neurotrophic factor (BDNF), cyclic adenosine monophosphate-responsive element binding protein (CREB), extracellular signal-regulated protein kinase (ERK), and phosphatidylinositol 3-kinase/protein kinase B (Akt). In the present study, we investigated the effect of treadmill exercise on cerebral ischemia in relation with ERK-Akt-CREB-BDNF signaling pathway in the hippocampus using gerbils. Induction of cerebral ischemia deteriorated short-term memory with suppression of phosphorylation of ERK-Akt-CREB-BDNF pathway in the hippocampus of gerbils. Enhancement of apoptosis in the hippo-campus was accompanied in the ischemia gerbils. Treadmill exercise improved short-term memory through enhancing phosphorylation of ERK-Akt-CREB-BDNF pathway with suppressing apoptosis in the hippocampus of the ischemia gerbils. The present results suggest that improvement of memory function after cerebral ischemia by treadmill exercise may be involved in the ERK-Akt-CREB-BDNF signaling pathway, resulting in inhibition of apoptosis in the hippocampus.
“…As previously described method (Song et al, 2018), we performed TUNEL staining using a Cell Death Detection Kit (Roche, Mannheim, Germany). The sections were postfixed in ethanol-acetic acid (2:1), rinsed, incubated with proteinase K (100 mg/mL), and rinsed again.…”
Section: Tunel Stainingmentioning
confidence: 99%
“…Bcl-2 can inhibit apoptosis by preventing the release of cytochrome c from mitochondria. However, Bcl-2 and Bcl-xL form heterodimers with the major pro-apoptotic members Bax and lose their ability in their preventive function (Kuwana and Newmeyer, 2003;Song et al, 2018). Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) analysis detects DNA fragmentation, one of the hallmarks of apoptotic cell death (Song et al, 2018).…”
Effect of swimming exercise on serotonin (5-hydroxytryptamine, 5-HT) expression and apoptosis in social isolation rats during old age was investigated. Rats in the old social isolation groups were housed alone per cage for 4 weeks. Rats in the swimming exercise groups were allowed to swim for 30 min once daily for 4 weeks. Morris water maze task determined spatial working memory and elevated plus maze test determined anxiety. Immunohistochemistry for tryptophan hydroxylase (TPH) and 5-HT in the dorsal raphe and for doublecortin (DCX) in the hippocampal dentate gyrus was conducted. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining in the hippocampal dentate gyrus was performed. Western blot analysis for Bax, Bcl-2, and cytochrome c in the hippocampus was conducted. Social isolation in rats of old age reduced spatial working memory and increased anxiety level. Swimming exercise enhanced spatial working memory and suppressed anxiety level. Social isolation in rats of old age inhibited TPH and 5-HT expression in dorsal rape. Swimming exercise increased TPH and 5-HT expression. Social isolation in rats of old age inhibited DCX-positive cells in the hippocampal dente gyrus. Swimming exercise increased DCX-positive cells. Social isolation in rats of old age increased TUNEL-positive cells, Bax and cytochrome c expression, and decreased Bcl-2 expression, which promoted apoptosis. Swimming exercise suppressed TUNEL-positive cells, Bax and cytochrome c expression, and increased Bcl-2 expression, which inhibited apoptosis. Swimming exercise improved 5-HT expression and suppressed apoptosis to alleviate anxiety and memory impairment during old age.
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