Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Tendinopathy is an aging-related disease, often caused by micro-scarring and degeneration due to overuse or trauma. Ascorbic acid (vitamin C) supplementation is reported to be a useful treatment for tendinopathy recovery. We compared the inhibitory effects of various ascorbic acid doses on tendon cell damage. HO was added to human-derived tendon cells in vitro (Group HO, control), followed by incubation with 150 µM or 30 mM of ascorbic acid (Group C, Group HC). The oxidative injury degree was evaluated by determining reactive oxygen species levels. The cytoskeletal structure was examined via fluorescence immunostaining of actin filaments. Quantitative polymerase chain reaction (qPCR) was performed to analyze the expressions of mitochondria transcription factor A, adenosine triphosphate 5A, type I collagen, and p16. Cell death was reduced, and oxidative stress was inhibited in C and HC groups. The cytoskeleton was maintained in the HC group but not in the C group. qPCR analysis revealed that p16 expression was inhibited in both the C and HC groups compared to the HO group; other markers had increased expression. The progression of cell death and cytoskeletal disruption was inhibited by the administration of high-dose vitamin C. Hence, high-dose vitamin C is a potential treatment for tendon cell degeneration.
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Source |
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http://dx.doi.org/10.3390/ijms252413358 | DOI Listing |
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