<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li F</submitter><funding>Project of National Nature Science Foundation of China</funding><funding>Shanghai Pujiang Program</funding><funding>the Key International (Regional) Cooperative Project of National Natural Science Foundation of China</funding><pagination>230</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6249848</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>19(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Mitochondrial damage leading to oxidant stress may play an important role in the pathogenesis of airflow obstruction and emphysema. NLPR3 inflammasome can be activated by mitochondrial ROS (mtROS) and other stimuli. We examined the importance of mtROS and NLRP3 inflammasome and their interactions in multiple ozone-induced lung inflammation and emphysema.&lt;h4>Methods&lt;/h4>C57/BL6 mice were exposed to ozone (2.5 ppm, 3 h) or filtered air twice a week over 6 weeks. MitoTEMPO (20 mg/kg), an inhibitor of mtROS, and VX765 (100 mg/kg), an inhibitor of caspase-1 activity, were administered by intraperitoneal or intragastric injection respectively 1 h prior to each ozone exposure for 6 weeks.&lt;h4>Results&lt;/h4>Ozone-exposed mice had increased bronchoalveolar lavage (BAL) total cells a</pubmed_abstract><journal>Respiratory research</journal><pubmed_title>Roles of mitochondrial ROS and NLRP3 inflammasome in multiple ozone-induced lung inflammation and emphysema.</pubmed_title><pmcid>PMC6249848</pmcid><funding_grant_id>No.81470218</funding_grant_id><funding_grant_id>No.14PJD027</funding_grant_id><funding_grant_id>No.51420105010</funding_grant_id><pubmed_authors>Wang M</pubmed_authors><pubmed_authors>Zhang JJ</pubmed_authors><pubmed_authors>Adcock IM</pubmed_authors><pubmed_authors>Xu M</pubmed_authors><pubmed_authors>Li F</pubmed_authors><pubmed_authors>Zhang H</pubmed_authors><pubmed_authors>Chung KF</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Gong J</pubmed_authors><pubmed_authors>Zhou X</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Roles of mitochondrial ROS and NLRP3 inflammasome in multiple ozone-induced lung inflammation and emphysema.</name><description>&lt;h4>Background&lt;/h4>Mitochondrial damage leading to oxidant stress may play an important role in the pathogenesis of airflow obstruction and emphysema. NLPR3 inflammasome can be activated by mitochondrial ROS (mtROS) and other stimuli. We examined the importance of mtROS and NLRP3 inflammasome and their interactions in multiple ozone-induced lung inflammation and emphysema.&lt;h4>Methods&lt;/h4>C57/BL6 mice were exposed to ozone (2.5 ppm, 3 h) or filtered air twice a week over 6 weeks. MitoTEMPO (20 mg/kg), an inhibitor of mtROS, and VX765 (100 mg/kg), an inhibitor of caspase-1 activity, were administered by intraperitoneal or intragastric injection respectively 1 h prior to each ozone exposure for 6 weeks.&lt;h4>Results&lt;/h4>Ozone-exposed mice had increased bronchoalveolar lavage (BAL) total cells a</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Nov</publication><modification>2025-04-05T12:58:19.443Z</modification><creation>2019-03-27T00:09:01Z</creation></dates><accession>S-EPMC6249848</accession><cross_references><pubmed>30466433</pubmed><doi>10.1186/s12931-018-0931-8</doi></cross_references></HashMap>