title: [Unsaturated fatty acid of Actinidia chinesis Planch seed oil enhances the antioxidative stress ability of rats with pulmonary fibrosis through activating Keap 1/Nrf 2 signaling pathway].
abstract: OBJECTIVE
  To observe the effects of unsaturated fatty acid of Actinidia chinesis Planch(USFA-ACP) seed oil on bleomycin-induced pulmonary fibrosis in rats, and to explore whether the effect is mediated by Kelch-like ECH-associated protein 1 (Keap 1)/nuclear factor-erythroid 2-related factor 2 (Nrf 2)signaling pathway.
  
  
  METHODS
  Sixty SD rats were randomly divided into control group, model group, (60, 120, 180) mg/kg USFA-ACP seed oil treatment group and 5 mg/kg prednisone group. Each group included 10 animals. Rats in the control group were intratracheally administered with normal saline, and the rest of five groups were intratracheally administered with bleomycin A5 to establish pulmonary fibrosis models. From the second day, rats in the three USFA-ACP seed oil treatment groups were intragastrically treated with 60, 120 and 180 mg/kg USFA-ACP seed oil correspondingly. The prednisone group were intragastrically administrated with 5 mg/kg prednisone acetate. Control and model groups were treated with normal saline. All rats were sacrificed on day 28. Pulmonary tissues were then removed, and HE and Masson staining were performed. The contents of hydroxyproline (HYP), reactive oxygen species(ROS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione-peroxidase (GSH-Px) in pulmonary tissue homogenates were measured through the commercial kits. The protein expressions of Keap 1 and Nrf2 in pulmonary tissues were analyzed using Western blotting.
  
  
  RESULTS
  Compared with the model group, the alveolitis and pulmonary fibrosis extent in 60, 120, 180 mg/kg USFA-ACP seed oil treatment groups as well as the prednisone group were significantly alleviated, HYP, ROS and MDA contents in pulmonary tissues, Keap 1 protein expression in the cytoplasm decreased remarkably, while SOD, CAT and GSH-Px contents in pulmonary tissues, Nrf2 protein expression in the nucleus increased. Moreover, compared with 60 mg/kg USFA-ACP seed oil treatment group, the above indicators were significantly improved in 120 and 180 mg/kg USFA-ACP seed oil treatment group and prednisone group. However, there was no significant difference between 120 and 180 mg/kg USFA-ACP seed oil treatment groups and prednisone group.
  
  
  CONCLUSIONS
  USFA-ACP seed oil can inhibit pulmonary fibrosis in rats, and the mechanism may be associated with the activation of the Keap1/Nrf 2 signaling pathway to increase the production of antioxidases in the pulmonary tissues.
authors.affiliation: School of Clinical Medicine, Hunan University of Medicine, Huaihua 418000; Department of Respiration, First Affiliated Hospital, Hunan University of Medicine, Huaihua 418000, China.
authors.forename: Lijing
authors.initials: L
authors.lastname: Liu
authors.affiliation: School of Clinical Medicine, Hunan University of Medicine, Huaihua 418000, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Qian
authors.affiliation: Department of Respiration, First Affiliated Hospital, Hunan University of Medicine, Huaihua 418000, China.
authors.forename: Huiming
authors.initials: H
authors.lastname: Yin
authors.affiliation: Department of Respiration, Huaihua First Peopie's Hospital, Huaihua 418000, China. *Corresponding author, E-mail: hjb0919@aliyun.com.
authors.forename: Jianbin
authors.initials: J
authors.lastname: He
authors.affiliation: Department of Respiration, First Affiliated Hospital, University of South China, Hengyang 421001, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Zhang
authors.affiliation: Department of Respiration, First Affiliated Hospital, University of South China, Hengyang 421001, China.
authors.forename: Zaiyan
authors.initials: Z
authors.lastname: Wang
mesh_terms: D029042:Actinidia / Q000737:chemistry*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage*; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D000072019:Kelch-Like ECH-Associated Protein 1; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000378:metabolism*; D010936:Plant Extracts / Q000008:administration & dosage*; D011658:Pulmonary Fibrosis / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism
chemical_list: D000975:Antioxidants; D005231:Fatty Acids, Unsaturated; D047908:Intracellular Signaling Peptides and Proteins; C486610:KEAP1 protein, rat; D000072019:Kelch-Like ECH-Associated Protein 1; D051267:NF-E2-Related Factor 2; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase