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    <identifier>10.57760/sciencedb.j00217.01530</identifier>
    <datestamp>2024-12-06T08:48:18Z</datestamp>
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<oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:date>2024-12-06</dc:date>
  <dc:title>Mechanism of miR-16-5p alleviates airway inflammation in asthma rats by targeting the TXNIP/NLRP3 signaling axis</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.j00217.01530</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>Objective To investigate the mechanism of miR-16-5p alleviates ovalbumin (OVA)-induced airway inflammation in asthmatic rats by targeting thioredoxin-interacting protein (TXNIP)/NOD-like receptor thermoprotein structural domain-related protein 3 (NLRP3) signaling axis.Methods Male Sprague-Dawley rats were randomly divided into the control, model, miR-16-5p mimic, NC mimic, miR-16-5p inhibitor, and NC inhibitor groups, with 6 rats in each group. A mixture of 10% OVA and 10% aluminum hydroxide was used for sensitization, and 4% OVA was given by nebulized inhalation to stimulate asthma. Dual luciferase reporter assay was performed to verify the target binding relationship; microscopic was used to observe inflammatory cell numbers in bronchoalveolar lavage fluid (BALF); ELISA was used to detect IL-1&amp;beta;, IL-6, TNF-&amp;alpha;, and MCP-1 levels; H&amp;amp;E staining was used to observe morphological changes of lung tissue; Masson staining was used to observe bronchial collagen deposition; Immunohistochemical staining was used to detect TXNIP and NLRP3 expression; Western blot was used to detect TXNIP, NLRP3, ASC, cleaved-caspase-1, and IL-1&amp;beta; proteins expression.Results Luciferase reporter assay showed that miR-16-5p could target and regulate TXNIP. Compared with the control group, the model group rats had damaged lung tissues, thickened airway walls, and massive collagen deposition; an increased number of inflammatory cells, significantly higher expression levels of IL-1&amp;beta;, IL-6, TNF-&amp;alpha; and MCP-1 (p &amp;lt; 0.05); TXNIP, NLRP3, ASC, cleaved-caspase-1, and IL-1&amp;beta; protein expression levels were significantly elevated in lung tissues (p &amp;lt; 0.05). Compared with the model group, lung histopathological damage was significantly improved in asthmatic rats after overexpression of miR-16-5b, and collagen deposition was reduced; the number of inflammatory cells was decreased; the levels of IL-1&amp;beta;, IL-6, TNF-&amp;alpha; and MCP-1 were significantly reduced (p &amp;lt; 0.05); the levels of TXNIP, NLRP3, cleaved-caspase-1, and IL-1&amp;beta; protein expression levels were significantly reduced (p &amp;lt; 0.05). MiR-16-5p inhibitor further aggravated the airway inflammatory response in asthmatic rats.Conclusion miR-16-5p can alleviate airway inflammation in asthmatic rats by targeting the TXNIP/NLRP3 signaling axis.</dc:description>
  <dc:subject>Asthma; Airway inflammation; miR-16-5p; TXNIP/NLRP3</dc:subject>
  <dc:creator>Weiwei.SHE</dc:creator>
  <dc:creator>Tianshou.SUN</dc:creator>
  <dc:creator>Chengfeng.LONG</dc:creator>
  <dc:creator>Meiyu.CHEN</dc:creator>
  <dc:creator>Xu.CHEN</dc:creator>
  <dc:creator>Qinxue.LIAO</dc:creator>
  <dc:creator>Mingdong.WANG</dc:creator>
  <dc:rights>PUBLIC</dc:rights>
  <dc:rights>https://creativecommons.org/licenses/by/4.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
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