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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Corni fructus is the fruit of Cornus officinalis Sieb. et Zucc, which is classified into the dogwood family of Cornaceae. Corni fructus has antineoplastic, antioxidative, and antidiabetic effects, but its anti-inflammatory and analgesic effects are unknown. Here, we investigated the anti-inflammatory and analgesic effects of an aqueous extract of corni fructus using murine RAW 264.7 macrophage cells. For this study, we used the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, western blot analysis, prostaglandin (PG) E(2) immunoassay, and nitric oxide (NO) detection. In addition, the analgesic effect of corni fructus was assessed by the acetic acid-induced writhing response in mice. The aqueous extract of corni fructus suppressed PGE(2) synthesis and NO production by inhibiting the lipopolysaccharide-induced expression of cyclooxygenase (COX)-2 and inducible NO synthase (iNOS) in murine RAW 264.7 macrophage cells. The extract also suppressed increases in nuclear factor-kappaB (NF-kappaB) levels in the nucleus. In vivo study showed that the extract suppressed the acetic acid-induced writhing response in mice. The aqueous extract of corni fructus exerts anti-inflammatory and analgesic effects by suppressing COX-2 and iNOS expression through the down-regulation of NF-kappaB binding activity.
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http://dx.doi.org/10.1089/jmf.2008.1011 | DOI Listing |