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
Objective: To investigate the protective effect of CVB-D on cardiac myocytes injury induced by high sympathesis activity and its relationship with oxidative stress.
Methods: Primary culture cardiac myocyte of new-born rat was injuried by NE and then incubated with VE and CVB-D (10 and 50 micromol/L). Indexes of cardiac myoctye injury were assayed by morphologic change, MTT, and LDH leakage ratio. The activity of SOD and the content of MDA were investigated to identify oxidation and antioxygen.
Results: CVB-D (10 and 50 micromol/L) significantly increased the cell survival rate,and reduced the LDH leakage rate. CVE-D (50 micromol/L) significantly increased the activity of SOD, and decreased content of MDA in injuried cell.
Conclusion: CVB-D has protective effect against myocardial injury induced by high sympathesis activity, the mechanism involves in ameliorating oxidative stress.
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