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: 3122
Function: getPubMedXML
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
Purpose: Diabetes mellitus (DM) leads to disorders such as cardiac hypertrophy, cardiac myocyte apoptosis, and cardiac fibrosis. Previous studies have shown that Lactobacillus reuteri GMNL-263 decreases cardiomyopathy by reducing inflammation. In this study, we investigated the potential benefit of GMNL-263 supplementation in treating diabetes-induced cardiomyocytes in rats with DM.
Methods: Five-week-old male Wistar rats were randomly divided into three groups, control, DM, and rats with DM treated with different dosages of L. reuteri GMNL-263. After undergoing treatment for 4 weeks, all rats were euthanized for further analysis.
Results: We observed that cardiac function and structure of rats with DM was rescued by GMNL-263. Activation of toll-like receptor 4 (TLR4)-related inflammatory, hypertrophic, and fibrotic signaling pathways in the hearts of rats with DM was reduced by treatment with GMNL-263.
Conclusion: Our findings demonstrate that GMNL-263 inhibited diabetes-induced cardiomyocytes via the repression of the TLR4 pathway. Moreover, these findings suggest that treatment with high-dose GMNL-263 could be a precautionary therapy for reducing the diabetes-induced cardiomyopathy.
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Source |
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http://dx.doi.org/10.1007/s00394-020-02474-z | DOI Listing |
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