Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3165
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
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Postoperative cognitive dysfunction (POCD) is common in older adult patients and affects their prognosis. Studies suggested that autophagy and oxidative stress are key factors in the pathogenesis of POCD. This study aimed to determine whether electroacupuncture (EA) pre-treatment improves POCD in aged rats and the underlying mechanisms. We established a model of POCD by using propofol anaesthesia and caesarean section in aged mice and assessed whether electroacupuncture at the Baihui and Neiguan points modulates autophagy and oxidative stress involved in the pathological process of POCD. The Morris water maze test assessed postoperative cognitive function. Oxidative stress was assessed using flow cytometry and enzyme-linked immunosorbent assay (ELISA) to determine the levels of superoxide dismutase (SOD), reactive oxygen species (ROS) and malondialdehyde (MDA). Transmission electron microscopy was used to observe the ultrastructure of the hippocampal cord neurons. In addition, protein blotting and quantitative real-time polymerase chain reaction (PCR) assays were performed to assess SIRT1, FOXO1, and autophagy markers at both the protein and mRNA levels. The results showed that anaesthesia/surgery significantly impaired cognitive performance, increased oxidative stress, decreased autophagy in the hippocampus, damaged hippocampal neurones and disrupted the mitochondrial structure in aged rats. EA pre-treatment improved cognitive function, restored neuronal and mitochondrial function, increased Beclin-1 and SIRT1 levels and attenuated oxidative damage and autophagy dysfunction in POCD rats. In conclusion, EA pre-treatment improved POCD in aged rats, and this mechanism may be related to the enhancement of autophagy and the inhibition of oxidative stress through SIRT1/FOXO1 signalling.
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Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11862894 | PMC |
http://dx.doi.org/10.1111/jcmm.70436 | DOI Listing |