Hyperbaric Oxygen Pretreatment Improves Cognition and Reduces Hippocampal Damage Via p38 Mitogen-Activated Protein Kinase in a Rat Model.
10.3349/ymj.2017.58.1.131
- Author:
Baisong ZHAO
1
;
Yongying PAN
;
Zixin WANG
;
Haiping XU
;
Xingrong SONG
Author Information
1. Department of Anesthesiology, Guangzhou Women and Children’s Medical Center, Guangzhou, China. songxingrong510623@163.com
- Publication Type:Original Article
- Keywords:
Hyperbaric oxygen;
astrocytes;
TNF-α;
cognitive dysfunction;
p38 MAPK
- MeSH:
Alzheimer Disease/*therapy;
Amyloid beta-Peptides/*administration & dosage;
Animals;
Apoptosis;
*Cognition/drug effects;
Disease Models, Animal;
Enzyme-Linked Immunosorbent Assay;
Hippocampus/*enzymology;
*Hyperbaric Oxygenation;
In Situ Nick-End Labeling;
Interleukin-10/biosynthesis;
Interleukin-1beta/biosynthesis;
Learning/drug effects;
Male;
Memory/drug effects;
Neurons;
Peptide Fragments/*administration & dosage;
Rats;
Rats, Sprague-Dawley;
Sodium Chloride/administration & dosage;
Tumor Necrosis Factor-alpha/biosynthesis;
p38 Mitogen-Activated Protein Kinases/*metabolism
- From:Yonsei Medical Journal
2017;58(1):131-138
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: To investigate the effects of hyperbaric oxygen (HBO) pretreatment on cognitive decline and neuronal damage in an Alzheimer’s disease (AD) rat model. MATERIALS AND METHODS: Rats were divided into three groups: normal saline (NS), AD, and HBO+AD. In the AD group, amyloid β peptide (Aβ)₁₋₄₀ was injected into the hippocampal CA1 region of the brain. NS rats received NS injection. In the HBO+AD group, rats received 5 days of daily HBO therapy following Aβ₁₋₄₀ injection. Learning and memory capabilities were examined using the Morris water maze task. Neuronal damage and astrocyte activation were evaluated by hematoxylin-eosin staining and immunohistochemistry, respectively. Dendritic spine density was determined by Golgi-Cox staining. Tumor necrosis factor-α, interleukin-1β, and interleukin-10 production was assessed by enzyme-linked immunosorbent assay. Neuron apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling. Protein expression was examined by western blotting. RESULTS: Learning and memory dysfunction was ameliorated in the HBO+AD group, as shown by significantly lower swimming distances and escape latency, compared to the AD group. Lower rates of neuronal damage, astrocyte activation, dendritic spine loss, and hippocampal neuron apoptosis were seen in the HBO+AD than in the AD group. A lower rate of hippocampal p38 mitogen-activated protein kinase (MAPK) phosphorylation was observed in the HBO+AD than in the AD group. CONCLUSION: HBO pretreatment improves cognition and reduces hippocampal damage via p38 MAPK in AD rats.
