PMID- 35657279 OWN - NLM STAT- MEDLINE DCOM- 20221215 LR - 20221215 IS - 1532-2513 (Electronic) IS - 0892-3973 (Linking) VI - 44 IP - 6 DP - 2022 Dec TI - N-acetylcysteine decreases lung inflammation and fibrosis by modulating ROS and Nrf2 in mice model exposed to particulate matter. PG - 832-837 LID - 10.1080/08923973.2022.2086138 [doi] AB - Background and Objectives: Air pollutants can induce and incite airway diseases such as asthma. N-acetylcysteine (NAC) affects signaling pathways involved in apoptosis, angiogenesis, cell growth and arrest, redox-regulated gene expression, and the inflammatory response. However, it is not known how NAC change redox-regulated gene expression in asthma mouse model exposed to particulate matter (PM). To investigate the effects of NAC on asthma mice exposed to PM through Reactive oxygen species (ROS), nuclear factor erythroid 2-related factor 2 (Nrf2), and mucin 5 (Muc5).Methods: To investigate the effects of NAC (100 mg/kg) on redox-regulated gene expression and lung fibrosis in a mouse model of asthma exposed to PM. A mice model of asthma induced by ovalbumin (OVA) or OVA plus titanium dioxide (OVA + TiO(2)) was established using wild-type BALB/c female mice, and the levels of Nrf2 and mucin 5AC (Muc5ac) proteins following NAC treatment were examined by Western blotting and immunostaining. In addition, the protein levels of ROS were checked.Results: Airway hyperresponsiveness and inflammation, goblet cell hyperplasia, and lung fibrosis were higher in OVA, OVA + TiO(2) mice than in control mice. NAC diminished OVA + TiO(2)-induced airway hyperresponsiveness and inflammation, goblet cell hyperplasia, and lung fibrosis. Levels of ROS, Nrf2, and Muc5ac protein were higher in lung tissue from OVA + TiO(2) mice than that from control mice and were decreased by treatment with NAC.Conclusions: NAC reduce airway inflammation and responsiveness, goblet cell hyperplasia, and lung fibrosis by modulating ROS and Nrf2. FAU - Choi, Seon-Muk AU - Choi SM AD - Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea. FAU - Lee, Pureun-Haneul AU - Lee PH AD - Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea. FAU - An, Min-Hyeok AU - An MH AD - Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea. FAU - Yun-Gi, Lee AU - Yun-Gi L AD - Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea. FAU - Park, Shinhee AU - Park S AD - Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea. FAU - Baek, Ae Rin AU - Baek AR AD - Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea. FAU - Jang, An-Soo AU - Jang AS AD - Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea. LA - eng PT - Journal Article DEP - 20220711 PL - England TA - Immunopharmacol Immunotoxicol JT - Immunopharmacology and immunotoxicology JID - 8800150 RN - WYQ7N0BPYC (Acetylcysteine) RN - 0 (Particulate Matter) SB - IM MH - Female MH - Mice MH - Animals MH - Acetylcysteine/pharmacology MH - Particulate Matter/toxicity MH - *Pulmonary Fibrosis/chemically induced/drug therapy MH - Hyperplasia MH - *Pneumonia/chemically induced/drug therapy MH - *Respiratory Hypersensitivity OTO - NOTNLM OT - Asthma OT - N-acetylcysteine OT - Nrf2 OT - PM OT - ROS EDAT- 2022/06/04 06:00 MHDA- 2022/12/15 06:00 CRDT- 2022/06/03 09:52 PHST- 2022/06/04 06:00 [pubmed] PHST- 2022/12/15 06:00 [medline] PHST- 2022/06/03 09:52 [entrez] AID - 10.1080/08923973.2022.2086138 [doi] PST - ppublish SO - Immunopharmacol Immunotoxicol. 2022 Dec;44(6):832-837. doi: 10.1080/08923973.2022.2086138. Epub 2022 Jul 11.