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
Previous studies have indicated that the adenosine triphosphate‑sensitive homomeric P2X7 receptor (P2X7R) plays an important role and exhibits therapeutic potential in a number of brain disorders, including temporal lobe epilepsy (TLE). The aim of the present study was to assess the expression of P2X7R, glutamate (GLU) and glial fibrillary acidic protein (GFAP) in the temporal neocortex and hippocampus of rats with lithium‑pilocarpine‑induced epilepsy as well as in patients with intractable TLE. The results demonstrated that the levels of P2X7R, GLU and GFAP were significantly upregulated in rats with spontaneous recurrent seizures, whereas they were reduced in rats that were treated with brilliant blue G (BBG), a P2X7R antagonist. To the best of our knowledge, the present study is also the first to demonstrate that P2X7R expression was elevated in patients with intractable TLE. These findings suggest that P2X7R plays a key role in the development of TLE and that BBG treatment may be a promising therapeutic strategy for TLE.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6522874 | PMC |
http://dx.doi.org/10.3892/mmr.2019.10202 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!