<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang R</submitter><funding>Basic and Applied Research Foundation of Guangdong Province, China</funding><funding>Guangzhou Science and Technology Project</funding><funding>Science and Technology Basic and Applied Basic Research Project of Guangzhou</funding><funding>National Natural Science Foundation of China</funding><funding>National Natural Science Foundation of China</funding><pagination>40</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10910709</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>19(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Pyroptosis has been demonstrated being closely associated with the inflammatory progression in chronic rhinosinusitis (CRS). However, platycodon D (PLD) has emerged as a key anti-inflammatory mediator in the inflammatory progression of various respiratory diseases. This study aims at investigating whether PLD could reduce inflammatory progression of CRS by inhibiting pyroptosis.&lt;h4>Methods&lt;/h4>Nasal mucosal tissues from patients with CRS and the control group (simple nasal septal deviation) were analyzed for morphological difference using hematoxylin &amp; eosin staining and for the expression of pyroptosis-related makers by immunofluorescence (IF). Human nasal epithelial cells (HNEpCs) were cultured and co-stimulated with lipopolysaccharide (LPS)/adenosine triphosphate (ATP</pubmed_abstract><journal>Chinese medicine</journal><pubmed_title>Platycodon D protects human nasal epithelial cells from pyroptosis through the Nrf2/HO-1/ROS signaling cascade in chronic rhinosinusitis.</pubmed_title><pmcid>PMC10910709</pmcid><funding_grant_id>202201011211</funding_grant_id><funding_grant_id>82305325</funding_grant_id><funding_grant_id>81974581</funding_grant_id><funding_grant_id>2022-01-01-11-3016-0012</funding_grant_id><funding_grant_id>82274590</funding_grant_id><funding_grant_id>2021A1515110446</funding_grant_id><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Zhou M</pubmed_authors><pubmed_authors>Ruan Y</pubmed_authors><pubmed_authors>Zhu J</pubmed_authors><pubmed_authors>Wang R</pubmed_authors><pubmed_authors>He W</pubmed_authors><pubmed_authors>Lu Z</pubmed_authors><pubmed_authors>Fang C</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Yan Y</pubmed_authors><pubmed_authors>Xu W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Platycodon D protects human nasal epithelial cells from pyroptosis through the Nrf2/HO-1/ROS signaling cascade in chronic rhinosinusitis.</name><description>&lt;h4>Background&lt;/h4>Pyroptosis has been demonstrated being closely associated with the inflammatory progression in chronic rhinosinusitis (CRS). However, platycodon D (PLD) has emerged as a key anti-inflammatory mediator in the inflammatory progression of various respiratory diseases. This study aims at investigating whether PLD could reduce inflammatory progression of CRS by inhibiting pyroptosis.&lt;h4>Methods&lt;/h4>Nasal mucosal tissues from patients with CRS and the control group (simple nasal septal deviation) were analyzed for morphological difference using hematoxylin &amp; eosin staining and for the expression of pyroptosis-related makers by immunofluorescence (IF). Human nasal epithelial cells (HNEpCs) were cultured and co-stimulated with lipopolysaccharide (LPS)/adenosine triphosphate (ATP</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Mar</publication><modification>2025-04-05T11:39:09.521Z</modification><creation>2025-04-05T11:39:09.521Z</creation></dates><accession>S-EPMC10910709</accession><cross_references><pubmed>38433216</pubmed><doi>10.1186/s13020-024-00897-y</doi></cross_references></HashMap>