Treadmill exercise ameliorates memory impairment through ERK-Akt-CREB-BDNF signaling pathway in cerebral ischemia gerbils

Abstract

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.

Voluntary Wheel Running Improves Spatial Learning Memory by Suppressing Inflammation and Apoptosis via Inactivation of Nuclear Factor Kappa B in Brain Inflammation Rats

“…NF-κB serves as a basis for apoptosis cell death in neuroinflammation [9,10]. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining for finding of DNA fragmentation, caspase-3 expression acting as an executor of apoptosis, and imbalance of B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) versus Bcl-2 are biological markers representing apoptosis [6,11]. LPS-induced brain inflammation increased TUNEL-positive and caspase-3-positive cell number, improved Bax expression, and attenuated Bcl-2 expression, thereby enhancing the Bax versus Bcl-2 ratio in the motor cortex [6].…”

“…Exercise is known to reduce neurological impairment, promote learning ability and memory capability, and inhibit apoptotic neuronal cell death [11]. Voluntary exercise improves cognitive ability, promotes antiapoptotic action, and has neuroprotective effect [12].…”

Effect of Glycyrrhizic Acid on Scopolamine-Induced Cognitive Impairment in Mice

“…After electrophoresis, the protein was transferred onto a nitrocellulose blotting membrane. The membrane was blocked in 5% skim milk, and then incubated with primary antibodies (diluted 1:1,000): extracellular signal-regulated kinase (ERK), phospho-ERK, p38, phospho-p38, c-Jun NH2-terminal kinase (JNK), phosphor-JNK (Cell Signaling Technology, Beverly, MA, USA) [20,21]. After incubation with horseradish-peroxidase-conjugated secondary antibody (Cayman Chemical Co., Ann Arbor, MI, USA), protein bands were developed using an enhanced chemiluminescence kit, and then detected using…”

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“…Western blotting was performed according to the previously described method [18]. The bladder tissues were homogenized on chilled RIPA buffer (Cell Signaling Technology, Inc., Danvers, USA) with 1mM PMSF (Sigma Aldrich, ST Louis, MO, USA) and then centrifuged at 14,000 rpm for 30 minutes at 4°C.…”