title: Using bosentan to treat paraquat poisoning-induced acute lung injury in rats.
abstract: BACKGROUND
  Paraquat poisoning is well known for causing multiple organ function failure (MODS) and high mortality. Acute lung injury and advanced pulmonary fibrosis are the most serious complications. Bosentan is a dual endothelin receptor antagonist. It plays an important role in treating PF. There is no related literature on the use of bosentan therapy for paraquat poisoning.
  
  
  OBJECTIVE
  To study the use of bosentan to treat acute lung injury and pulmonary fibrosis as induced by paraquat.
  
  
  METHODS
  A total of 120 adult Wister male rats were randomly assigned to three groups: the paraquat poisoning group (rats were intragastrically administered with paraquat at 50 mg/kg body weight once at the beginning); the bosentan therapy group (rats were administered bosentan at 100 mg/kg body weight by intragastric administration half an hour after paraquat was administered, then the same dose was administered once a day); and a control group (rats were administered intragastric physiological saline). On the 3rd, 7th, 14th, and 21st days following paraquat exposure, rats were sacrificed, and samples of lung tissue and venous blood were collected. The levels of transforming growth factor-β1 (TGF-β1), endothelin-1 (ET-1), and hydroxyproline (HYP) in the plasma and lung homogenate were determined. Optical and electronic microscopes were used to examine pathological changes.
  
  
  RESULTS
  The TGF-β1, ET-1, and HYP of the paraquat poisoning group were significantly higher than in the control group, and they were significantly lower in the 21st day therapy group than in the paraquat poisoning group on the same day. Under the optical and electronic microscopes, lung tissue damage was observed to be more severe but was then reduced after bosentan was administered.
  
  
  CONCLUSIONS
  Bosentan can reduce inflammation factor release. It has a therapeutic effect on acute lung injury as induced by paraquat.
authors.affiliation: Department of Poisoning and Occupational Disease, Qilu Hospital of Shandong University, Jinan, Shandong, China.
authors.forename: Zhongchen
authors.initials: Z
authors.lastname: Zhang
authors.forename: Xiangdong
authors.initials: X
authors.lastname: Jian
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Jieru
authors.initials: J
authors.lastname: Wang
authors.forename: Qian
authors.initials: Q
authors.lastname: Zhou
mesh_terms: D055371:Acute Lung Injury / Q000097:blood / Q000139:chemically induced* / Q000188:drug therapy* / Q000473:pathology; D056809:Alveolar Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D000818:Animals; D000077300:Bosentan; D004195:Disease Models, Animal; D019332:Endothelin-1 / Q000097:blood; D006909:Hydroxyproline / Q000378:metabolism; D008297:Male; D010269:Paraquat / Q000506:poisoning*; D051381:Rats; D017208:Rats, Wistar; D013449:Sulfonamides / Q000494:pharmacology / Q000627:therapeutic use*; D053773:Transforming Growth Factor beta1 / Q000097:blood
chemical_list: D019332:Endothelin-1; D013449:Sulfonamides; D053773:Transforming Growth Factor beta1; D010269:Paraquat; D000077300:Bosentan; D006909:Hydroxyproline