Dataset Information

Effect of Treadmill Exercise and Trans-Cinnamaldehyde against d-Galactose- and Aluminum Chloride-Induced Cognitive Dysfunction in Mice.

ABSTRACT: Mild cognitive impairment (MCI) generally refers to impairment in cognition above that which accompanies the normal age-related cognitive decline and has attracted attention in recent years. Trans-cinnamaldehyde (TCA), which is isolated from cinnamon, has anti-inflammatory and antioxidant properties. Treadmill exercise also has diverse positive effects. The purpose of this study was to investigate the combination effects of TCA and treadmill exercise on learning and memory in a cognitive impairment mouse induced by a combination of d-galactose (d-gal) and aluminum chloride (AlCl3). We found that exercise and TCA attenuated cognitive impairment in mice with induced MCI. This effect was further increased by costimulation of exercise and TCA. To clarify the mechanisms of the positive effects of TCA and exercise, we analyzed the nuclear factor erythroid 2-related factor (Nrf2) and related signaling pathways. We found that TCA and exercise upregulated Nrf2, NAD(P)H dehydrogenase quinone 1 (NQO-1), heme oxygenase 1 (HO-1), and superoxide dismutase 1 (SOD-1); this suggests that TCA and exercise attenuate cognitive dysfunction by reducing oxidative stress. We also found that Nrf2-related signaling pathways, i.e., the AMP-activated protein kinase (AMPK)/Nrf2 and SIRT1/PGC-1a/Nrf2-ARE pathways, exerted antioxidant effects. Together, these results suggest that costimulation with TCA and exercise may be a therapeutic candidate for mild cognitive impairment.

SUBMITTER: Ryu JS

PROVIDER: S-EPMC7693345 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Effect of Treadmill Exercise and Trans-Cinnamaldehyde against d-Galactose- and Aluminum Chloride-Induced Cognitive Dysfunction in Mice.

Ryu Jong-Sik JS Kang Ho-Youl HY Lee Jong Kil JK

Brain sciences 20201029 11

Mild cognitive impairment (MCI) generally refers to impairment in cognition above that which accompanies the normal age-related cognitive decline and has attracted attention in recent years. Trans-cinnamaldehyde (TCA), which is isolated from cinnamon, has anti-inflammatory and antioxidant properties. Treadmill exercise also has diverse positive effects. The purpose of this study was to investigate the combination effects of TCA and treadmill exercise on learning and memory in a cognitive impairm ...[more]

PMID: 33138104

Similar Datasets

Project description:BackgroundAging is closely associated to several deleterious conditions and cognitive impairment. Administration of low-dose paracetamol (APAP) has previously been reported to improve cognitive performance in both human and animal studies. However, the altered cognitive effects of low-dose APAP treatment in the aging brain have not been elucidated.ObjectivesThe purpose of this study was to determine whether low-dose APAP treatment improves cognitive dysfunction in a d-galactose (d-gal)-induced aging model.Materials and methodsAPAP (15 and 50 mg/kg p.o.) and vitamin E (Vit E 100 mg/kg p.o.) were administered once daily to d-gal-injected mice (200 mg/kg s.c.) for 6 weeks. The elevated plus maze (EPM), open field, novel object recognition (NOR), and Morris water maze (MWM) tests, respectively, were used to measure altered neurobehavioral functions, including anxiety-like behavior and exploratory locomotor activity, as well as learning and memory performance. The gene transcription of brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB) signaling in brain tissues was evaluated by real-time polymerase chain reaction.ResultsCompared to the control, d-gal significantly decreased exploratory locomotor activity and NOR and MWM performance but did not significantly change the activity in the EPM test. However, APAP50 and Vit E significantly reversed the effects of d-gal injection on exploratory locomotor activity. In addition, low-dose APAP (15 and 50 mg/kg) and Vit E significantly improved the reduction in NOR and MWM performance induced by d-gal. Real-time polymerase chain reaction analysis revealed that the mRNA expression of BDNF, neurotrophic tyrosine receptor kinase (NTRK), which is the gene coding TrkB receptor, and cAMP response element-binding protein (CREB) was significantly decreased in the frontal cortex and hippocampus of the d-gal mice. However, APAP50 and Vit E significantly increased BDNF and NTRK mRNA expression in both the frontal cortex and the hippocampus. A lower dose of APAP (15 mg/kg) significantly elevated the mRNA expression of NTRK, but only in the hippocampus. Moreover, APAP50 significantly increased CREB mRNA expression in the frontal cortex and hippocampus.ConclusionLow-dose APAP treatment has a neuroprotective effect on cognitive dysfunction in the d-gal aging model, and the underlying molecular mechanisms depend on the activation of BDNF/TrkB signaling.

Project description:Alzheimer's disease (AD) is a devastating neurodegenerative disorder without a cure. Hence, developing an effective treatment or protective agent is crucial for public health. The present study aims to characterize orange peel extract (OPE) through in vitro and in silico studies. Furthermore, it examines the protective effect of OPE against experimentally-induced Alzheimer's disease in rats. The total phenolic and flavonoid content of OPE was 255.86 ± 1.77 and 52.06 ± 1.74 (mg/100 g), respectively. Gallic acid, the common polyphenol in OPE detected by HPLC was 3388.60 μg/100 g. OPE antioxidant IC50 was 67.90 ± 1.05, 60.48 ± 0.91, and 63.70 ± 0.30 by DPPH, ABTS and Hydroxyl radical scavenging activity methods, respectively. In vitro anti-acetylcholinesterase (AChE) IC50 was 0.87 ± 0.025 mg/mL for OPE and 2.45 ± 0.001 mg/mL for gallic acid. Molecular docking analysis for human AChE (4EY7) with donepezil, gallic acid, and acetylcholine showed binding energy ΔG values of -9.47, -3.72, and -5.69 Kcal/mol, respectively. Aluminum chloride injection (70 mg/Kg/day for 6 weeks) induced Alzheimer's-like disease in male rats. OPE (100 and 200 mg/kg/d) and gallic acid (50 mg/kg/d) were administered orally to experimental animals for 6 weeks in addition to aluminum chloride injection (as protective). OPE was found to protect against aluminum chloride-induced neuronal damage by decreasing both gene expression and activity of acetylcholinesterase (AChE) and a decrease in amyloid beta (Aβ42) protein level, thiobarbituric acid-reactive substances (TBARS), and nitric oxide (NO), and increased reduced glutathione (GSH) level and activity of the antioxidant enzymes in the brain tissues. Additionally, gene expressions for amyloid precursor protein (APP) and beta secretase enzyme (BACE1) were downregulated, whereas those for presinilin-2 (PSEN2) and beta cell lymphoma-2 (BCL2) were upregulated. Furthermore, the reverse of mitochondrial alternation and restored brain ultrastructure might underlie neuronal dysfunction in AD. In conclusion, our exploration of the neuroprotective effect of OPE in vivo reveals that OPE may be helpful in ameliorating brain oxidative stress, hence protecting from Alzheimer's disease progression.

Dataset Information

Effect of Treadmill Exercise and Trans-Cinnamaldehyde against d-Galactose- and Aluminum Chloride-Induced Cognitive Dysfunction in Mice.

Publications

Effect of Treadmill Exercise and Trans-Cinnamaldehyde against d-Galactose- and Aluminum Chloride-Induced Cognitive Dysfunction in Mice.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets