title: [NaHS inhibits A549 cell injury induced by lipopolysaccharide].
abstract: OBJECTIVE
  To observe the effect of NaHS on lipopolysaccharide (LPS)-induced injury of A549 lung cancer cells and explore the possible mechanisms.
  
  
  METHODS
  A549 cells were divided into 4 groups: control group, 10 μg/mL LPS treated group, 10 μmol/L NaHS treated group and the group treated with 10 μg/mL LPS plus 10 μmol/L NaHS. After treatment for 24 hours, C-reactive protein (CRP) content in culture solution was measured by ELISA, and the cell viability was detected by MTT assay and lactate dehydrogenase (LDH) assay. Transepithelial electrical resistance (TER) was evaluated by EVOM resistance meter, and the expression and distribution of zonula occludens-1 (ZO-1) protein was examined by immunofluorescence cytochemistry.
  
  
  RESULTS
  There were no significant differences in CRP content, TER, cell viability, the expression and distribution of ZO-1 between the control group and the NaHS group. Compared with the control group, CRP content distinctly increased, TER, cell viability and ZO-1 expression markedly decreased, and ZO-1 distribution was disrupted in the LPS group. Compared with the LPS group, CRP level was distinctly reduced, TER, cell viability and ZO-1 expression were raised, and the disrupted ZO-1 distribution was partly reversed in the LPS plus NaHS treated group.
  
  
  CONCLUSIONS
  NaHS can inhibit A549 cell injury induced by LPS via increasing cell viability, TER and the expression of ZO-1 as well as decreasing CRP level.
authors.affiliation: Department of Infectious Diseases, Hebei Provincial People's Hospital, Shijiazhuang 050051, China.
authors.forename: Zhancong
authors.initials: Z
authors.lastname: Niu
authors.affiliation: Public Medical Insurance Office, Hebei Provincial People's Hospital, Shijiazhuang 050051, China.
authors.forename: Shengjun
authors.initials: S
authors.lastname: Yang
authors.affiliation: Department of Infectious Diseases, Hebei Provincial People's Hospital, Shijiazhuang 050051, China. *Corresponding author, E-mail: DUANGUOC@126.com.
authors.forename: Guochen
authors.initials: G
authors.lastname: Duan
authors.affiliation: Department of Infectious Diseases, Hebei Provincial People's Hospital, Shijiazhuang 050051, China.
authors.forename: Junxiao
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin 300070, China.
authors.forename: Hongguang
authors.initials: H
authors.lastname: Chen
authors.affiliation: Department of Infectious Diseases, Hebei Provincial People's Hospital, Shijiazhuang 050051, China.
authors.forename: Yanxia
authors.initials: Y
authors.lastname: Wang
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D002460:Cell Line; D006801:Humans; D008070:Lipopolysaccharides / Q000009:adverse effects; D013440:Sulfides / Q000494:pharmacology*; D062826:Zonula Occludens-1 Protein / Q000235:genetics / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D013440:Sulfides; C569042:TJP1 protein, human; D062826:Zonula Occludens-1 Protein; D002097:C-Reactive Protein; C025451:sodium bisulfide