title: Fructo-oligosaccharide attenuates the production of pro-inflammatory cytokines and the activation of JNK/Jun pathway in the lungs of D-galactose-treated Balb/cJ mice.
abstract: OBJECTIVE
  This study determined the effects of long-term D-galactose (DG) injection on the lung pro-inflammatory and fibrotic status and whether fructo-oligosaccharide (FO) could attenuate such effects.
  
  
  METHODS
  Forty Balb/cJ mice (12 weeks of age) were divided into four groups: control (s.c. saline) (basal diet), DG (s.c. 1.2 g DG/kg body weight) (basal diet), DG + FO (FO diet, 2.5% w/w FO), and DG + E (vitamin E diet, α-tocopherol 0.2% w/w) serving as an antioxidant control group. These animals were killed after 49 day of treatments. Another group of naturally aging (NA) mice without any injection was killed at 64 weeks of age to be an aging control group.
  
  
  RESULTS
  D-galactose treatment, generally similar to NA, increased the lung pro-inflammatory status, as shown in the IL-6 and IL-1β levels and the expression of phospho-Jun and phospho-JNK, and the fibrotic status as shown in the hydroxyproline level compared to the vehicle. FO diminished the DG-induced increases in the lung IL-1β level and expressions of total Jun, phospho-JNK, and attenuated DG effects on lung IL-6 and hydroxyproline, while α-tocopherol exerted anti-inflammatory effects on all parameters determined. FO, as well as α-tocopherol, modulated the large bowel ecology by increasing the fecal bifidobacteria and cecal butyrate levels compared with DG.
  
  
  CONCLUSIONS
  D-galactose treatment mimicked the lung pro-inflammatory status as shown in the NA mice. FO attenuated the DG-induced lung pro-inflammatory status and down-regulated JNK/Jun pathway in the lung, which could be mediated by the prebiotic effects and metabolic products of FO in the large intestine.
authors.affiliation: School of Nutrition, Chung Shan Medical University, No. 110, Sec. 1 Jianguo N. Rd., Taichung, Taiwan, ROC.
authors.forename: Shu-Lan
authors.initials: SL
authors.lastname: Yeh
authors.forename: Tzu-Chin
authors.initials: TC
authors.lastname: Wu
authors.forename: Shu-Ting
authors.initials: ST
authors.lastname: Chan
authors.forename: Meng-Jun
authors.initials: MJ
authors.lastname: Hong
authors.forename: Hsiao-Ling
authors.initials: HL
authors.lastname: Chen
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage; D002432:Cecum / Q000737:chemistry; D016207:Cytokines / Q000032:analysis / Q000096:biosynthesis* / Q000097:blood; D005232:Fatty Acids, Volatile / Q000032:analysis; D005243:Feces / Q000382:microbiology; D005632:Fructose / Q000008:administration & dosage*; D005690:Galactose / Q000008:administration & dosage*; D007249:Inflammation / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000032:analysis; D008168:Lung / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D009844:Oligosaccharides / Q000008:administration & dosage*; D010766:Phosphorylation; D024502:alpha-Tocopherol / Q000008:administration & dosage; D048051:p38 Mitogen-Activated Protein Kinases / Q000032:analysis
chemical_list: D000975:Antioxidants; D016207:Cytokines; D005232:Fatty Acids, Volatile; D009844:Oligosaccharides; D005632:Fructose; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D024502:alpha-Tocopherol; D005690:Galactose