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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This study investigated the potential ameliorative effects of fermented red ginseng (FRG) extract on sarcopenia-related muscle atrophy in old mice and elucidated the underlying mechanisms. Mice, aged five and twenty months, were divided into seven groups: young and old controls, and old mice treated with extract (200 mg/kg/day), mixed ginsenosides (15 mg/kg/day), and FRG extract (50-200 mg/kg/day). Body weight and grip strength were assessed weekly. After six weeks of oral treatment, quadriceps, gastrocnemius, and soleus were photographed and weighed, and muscle fiber cross-sectional area was analyzed via hematoxylin-eosin staining. Additionally, the protein expression levels were measured using western blot analysis. FRG extract significantly improved muscle atrophy by activating the IGF-1/Akt/mTOR pathway, reducing degradation proteins FoxO3a, MuRF1, and Fbx32, and enhancing mitochondrial biogenesis-related proteins SIRT-1/PGC-1α. The findings suggest that FRG extract effectively mitigates age-related muscle atrophy through these molecular pathways, supporting its potential as a therapeutic agent for sarcopenia.
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Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11822148 | PMC |
http://dx.doi.org/10.1007/s10068-024-01702-0 | DOI Listing |