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dc.contributor.authorThazin Shween_US
dc.contributor.authorCherry Bo-Htayen_US
dc.contributor.authorBenjamin Ongnoken_US
dc.contributor.authorTitikorn Chunchaien_US
dc.contributor.authorThidarat Jaiwongkamen_US
dc.contributor.authorSasiwan Kerdphooen_US
dc.contributor.authorSirinart Kumfuen_US
dc.contributor.authorWasana Pratchayasakulen_US
dc.contributor.authorThienchai Pattarasakulchaien_US
dc.contributor.authorNipon Chattipakornen_US
dc.contributor.authorSiriporn C. Chattipakornen_US
dc.date.accessioned2022-10-16T07:02:01Z-
dc.date.available2022-10-16T07:02:01Z-
dc.date.issued2021-04-01en_US
dc.identifier.issn18726216en_US
dc.identifier.issn00476374en_US
dc.identifier.other2-s2.0-85101924560en_US
dc.identifier.other10.1016/j.mad.2021.111465en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85101924560&origin=inwarden_US
dc.identifier.urihttp://cmuir.cmu.ac.th/jspui/handle/6653943832/75705-
dc.description.abstractThe population of obese-elderly has increased prominently around the world. Both aging and obesity are major factors of neurodegeneration. The present study hypothesizes that HBOT attenuates metabolic disturbance, cognitive decline, hippocampal pathologies in aging and aging-obese model. Sixty Wistar rats were separated into 2 groups to receive normal-diet (ND) or high-fat diet (HFD) for 22 weeks. At week 13, ND rats were divided into two subgroups to receive vehicle (0.9 % NSS, s.c) or D-gal (150 mg/kg/d, s.c) for total 10 weeks. HFD rats were injected only D-gal (150 mg/kg/d, s.c; HFDD) for total 10 weeks. At week 20, rats in each subgroup were given sham-treatment (1ATA, 80 L/min, 80 min/day), or HBOT (2ATA, pure O2, 250 L/min, 80 min/day) for 14 days. Novel object location test, metabolic parameters, and hippocampal pathologies were determined after HBOT. D-gal induced insulin resistance, increased oxidative stress, autophagy impairment, microglial hyperactivation, apoptosis, synaptic dysplasticity which resulted in cognitive impairment. D-gal-treated HFD-fed rats had the highest levels of oxidative stress, apoptosis, dendritic spine loss. HBOT attenuated insulin resistance, cognitive impairment, hippocampal aging and pathologies in both models. These findings suggest that HBOT restored insulin sensitivity, hippocampal functions, cognition in aging and aging-obese models.en_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleHyperbaric oxygen therapy restores cognitive function and hippocampal pathologies in both aging and aging-obese ratsen_US
dc.typeJournalen_US
article.title.sourcetitleMechanisms of Ageing and Developmenten_US
article.volume195en_US
article.stream.affiliationsChiang Mai Universityen_US
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