{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T23:48:51Z","timestamp":1790725731083,"version":"4.1.0"},"reference-count":48,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2020,3,24]],"date-time":"2020-03-24T00:00:00Z","timestamp":1585008000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004480","name":"Natural Science Foundation of Shanxi Province","doi-asserted-by":"publisher","award":["2018\u2010319"],"award-info":[{"award-number":["2018\u2010319"]}],"id":[{"id":"10.13039\/501100004480","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81872589"],"award-info":[{"award-number":["81872589"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Applied Toxicology"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Atmospheric particulate matter with a diameter \u22642.5 \u03bcm (PM2.5) can induce inflammation of the respiratory system, which is the pathological basis of asthma or other respiratory diseases; however, the underlying regulation mechanism has not been clearly addressed. The aim of this study was to explore the potential role of the oxidative stress\u2010JAK\/STAT signaling pathway in the inflammation of human bronchial epithelial cells induced by PM2.5. The human bronchial epithelial cell line 16HBE cells were stimulated with PM2.5 at 50 and 100 \u03bcg\/mL doses for 12 or 24 hours. Intracellular reactive oxygen species (ROS) was detected using flow cytometry. Gene and protein expressions of JAK2, STAT3 and cyclooxygenase 2 (COX\u20102) were determined using reverse transcription\u2010polymerase chain reaction and western blotting, respectively. The ratio of intracellular glutathione\/glutathione disulfide (GSH\/GSSG) and the levels of interleukin (IL)\u20106 and IL\u20108 in cellular supernatant were analyzed using enzyme\u2010linked immunosorbent assay. The results indicated that PM2.5 treatment significantly increased gene expressions of JAK2\/STAT3 and protein levels of p\u2010JAK2\/p\u2010STAT3, accompanied by increased intracellular ROS levels, decreased GSH\/GSSG ratio at 50 and 100 \u03bcg\/mL of PM2.5, and significantly enhanced levels of IL\u20106, IL\u20108 and COX\u20102 at a dose of 100 \u03bcg\/mL. Pretreatment with\n                    <jats:italic>N<\/jats:italic>\n                    \u2010acetyl\u2010\n                    <jats:sc>l<\/jats:sc>\n                    \u2010cysteine (NAC) attenuated the oxidative stress induced by PM2.5; similarly, pretreatment with AG490 (an inhibitor of JAK) decreased the cytokine levels stimulated by PM2.5. Therefore, we concluded that PM2.5 exposure could activate oxidative stress\u2010JAK2\/STAT3 signaling pathway, elevate the levels of IL\u20106, IL\u20108 and COX\u20102 in 16HBE cells, which can be inhibited by the NAC or AG490.\n                  <\/jats:p>","DOI":"10.1002\/jat.3977","type":"journal-article","created":{"date-parts":[[2020,3,24]],"date-time":"2020-03-24T23:28:38Z","timestamp":1585092518000},"page":"1210-1218","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Interleukins 6\/8 and cyclooxygenase\u20102 release and expressions are regulated by oxidative stress\u2010JAK2\/STAT3 signaling pathway in human bronchial epithelial cells exposed to particulate matter \u22642.5 \u03bcm"],"prefix":"10.1002","volume":"40","author":[{"given":"Zhenzhen","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Environmental Health, School of Public Health Shanxi Medical University  Taiyuan Shanxi 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