title: Carbon monoxide alleviates lipopolysaccharide-induced oxidative stress injury through suppressing the expression of Fis1 in NR8383 cells.
abstract: Acute respiratory distress syndrome (ARDS) is one of the most devastating complications of sepsis lacking of effective therapy. Mitochondrial dynamics undergoing continuous fusion and fission play a crucial role in mitochondrial structure and function. Fis1, as a small protein located on the outer membrane of mitochondria, has been thought to be an important protein mediated mitochondrial fission. During ARDS, alveolar macrophages suffer from increased oxidative stress and apoptosis, and also accompanied by disrupted mitochondrial dynamics. In addition, as one of the products of heme degradation catalyzed by heme oxygenase, carbon monoxide (CO) possesses powerful protective properties in vivo or in vitro models, such as anti-inflammatory, antioxidant and anti-apoptosis function. However, there is little evidence that CO alleviates oxidative stress damage through altering mitochondrial fission in alveolar macrophages. In the present study, our results showed that CO increased cell vitality, improved mitochondrial SOD activity, reduced reactive oxygen species (ROS) production and inhibited cell apoptosis in NR8383 exposed to LPS. Meanwhile, CO decreased the expression of Fis1, increased mitochondrial membrane potential and sustained elongation of mitochondria in LPS-incubated NR8383. Overall, our study underscored a critical role of CO in suppressing the expression of Fis1 and alleviating LPS- induced oxidative stress damage in alveolar macrophages.
authors.affiliation: Department of Anesthesiology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Shi
authors.affiliation: Department of Anesthesiology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100, China. Electronic address: yujianbo11@126.com.
authors.forename: Jian-Bo
authors.initials: JB
authors.lastname: Yu
authors.affiliation: Department of Anesthesiology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
authors.affiliation: Department of Anesthesiology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Wang
authors.affiliation: Department of Anesthesiology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Anesthesiology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100, China.
authors.forename: Li-Rong
authors.initials: LR
authors.lastname: Gong
authors.affiliation: Department of Anesthesiology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100, China.
authors.forename: Shu-An
authors.initials: SA
authors.lastname: Dong
authors.affiliation: Department of Pharmacology, Institute of Acute Abdominal Diseases of Integrated Traditional Chinese and Western Medicine, Tianjin 300100, China.
authors.forename: Da-Quan
authors.initials: DQ
authors.lastname: Liu
mesh_terms: D000818:Animals; D002248:Carbon Monoxide / Q000494:pharmacology*; D002460:Cell Line; D015536:Down-Regulation / Q000187:drug effects* / Q000235:genetics; D008070:Lipopolysaccharides; D016676:Macrophages, Alveolar / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D024101:Mitochondrial Proteins / Q000235:genetics* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats
chemical_list: C503403:Fis1 protein, rat; D008070:Lipopolysaccharides; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; D002248:Carbon Monoxide
keywords: Carbon monoxide; Fis1; Mitochondria; Mitochondrial fission; Oxidative damage