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
MicroRNA (miRNA) are emerging as critical regulators of neuropathic pain development. Neuroinflammation contributes to the development of neuropathic pain. miR‑142‑3p has been characterized as an inflammation‑related miRNA in various pathological processes. However, little is known about the role of miR‑142‑3p in neuroinflammation and neuropathic pain. The present study aimed to investigate the function of miR‑142‑3p in neuropathic pain by creating a murine model using spinal nerve ligation (SNL). A significant reduction in miR‑142‑3p expression was observed in the dorsal root ganglion of mice with SNL (P<0.05) compared with control mice. Overexpression of miR‑142‑3p significantly inhibited neuropathic pain and neuroinflammation in mice with SNL (P<0.05). High mobility group box 1 (HMGB1) was identified as a direct target gene of miR‑142‑3p by bioinformatic analysis and dual‑luciferase reporter assays. Overexpression of miR‑142‑3p significantly reduced the mRNA and protein expression levels of HMGB1 in vitro and in vivo (P<0.05). In addition, HMGB1 mRNA expression and miR‑142‑3p expression were inversely correlated in mice with SNL. Furthermore, overexpression of HMGB1 significantly reversed the inhibitory effect of miR‑142‑3p on neuroinflammation and neuropathic pain development (P<0.05). Overall, these results suggest that miR‑142‑3p functions as a negative regulator of neuropathic pain development through the downregulation of HMGB1, indicating that miR‑142‑3p may serve as a potential therapeutic target for neuropathic pain.
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Source |
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http://dx.doi.org/10.3892/ijmm.2017.3222 | DOI Listing |
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