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
Ethnopharmacological Relevance: Nao-Shuan-Tong (NST) in capsule form is a compound prescription formulated according to the meridian theory of traditional Chinese medicine (TCM) and is approved by the State Food and Drug Administration of China for the treatment of ischemic stroke.
Objectives: To test the neuroprotective effects of the Chinese medicine Nao-Shuang-Tong on cerebral ischemia in rats and to explore the underlying mechanisms.
Materials And Methods: 115 Male Sprague-Dawley rats were randomly divided into 5 groups: sham, ischemia-reperfusion (I/R), and I/R plus NST 0.25, NST 0.5 and NST 1 (n=23 in each group). Cerebral ischemia was induced by 1.5h of middle cerebral artery occlusion. Cerebral infarct area was measured by tetrazolium staining at 24h following reperfusion, and neurological functional deficits were assessed at 1, 3, 7 and 14 d after reperfusion. Neuronal apoptosis was studied by Nissl staining and DNA fragmentation assay at 1 and 3d after reperfusion. The activation of caspase-3, -8, -9 and Bax/Bcl-2 levels were analyzed by western blot 24h after reperfusion.
Results: NST (0.5 and 1g/kg) significantly reduced cerebral infarct area, attenuated neurological functional deficits, and reduced neuronal apoptosis in ischemic cortex and in the CA1 region of hippocampus. NST also suppressed overexpression of Bax and activated caspases-3, -8 and -9, and also inhibited the reduction of Bcl-2 expression and markedly depressed the Bax/Bcl-2 ratio.
Conclusions: These findings demonstrate that NST is neuroprotective against cerebral ischemia and is likely to act via inhibition of neuronal apoptosis associated with changes in levels of caspases-3 and -8, Bax and Bcl-2.
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http://dx.doi.org/10.1016/j.jep.2010.06.021 | DOI Listing |
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