title: [Effects of curcumin on pneumocyte apoptosis and CHOP in pulmonary ischemia/reperfusion injury of mice].
abstract: OBJECTIVE
  To investigate the effects of curcumin (CUR) on pneumocyte apoptosis and CCAAT/enhancer binding protein homologous protein (CHOP) in pulmonary ischemia/reperfusion injury (PIRI) in mice.
  
  
  METHODS
  Sixty C57BL/6J mice were randomly allocated into six groups (n = 10): Sham operation group (Sham group), ischemia/reperfusion group (I/R group), ischemia/reperfusion + dimethyl sulfoxide group (DMSO group), ischemia/reperfusion + curcumin pre-treated with respectively 100 mg/kg, 150 mg/kg and 200 mg/kg groups (CUR-100 group, CUR-150 group and CUR-200 group). Left lung tissue of each group was excised after reperfusion for 3 h. Wet lung weight to dry lung weight (W/D) and total lung water content (TLW) were tested. The morphological and ultrastructural changes of lung tissue were observed under light microscope and electron microscope, and index of quantitative evaluation for alveolar damage (IQA) was calculated. The expression levels of CHOP and glucose regulated protein 78 (GRP78) were detected by RT-PCR and Western Blot. Apoptosis index (AI) of lung tissue was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) method.
  
  
  RESULTS
  Compared with Sham group, the expression levels of CHOP, GRP78 mRNA and protein were all significantly increased (P < 0.05) in I/R group and DMSO group, W/D, TLW, IQA and AI were all notably higher (P < 0.01); morphological and ultrastructural injury in lung tissue were notably observed in I/R group. Compared with DMSO group, the expression levels of GRP78 mRNA and protein were increased higher (P < 0. 05) in CUR-100 group, CUR-150 group, and CUR-200 group, but the expression levels of CHOP mRNA and protein were decreased lower (P < 0.05), W/D, TLW, IQA and AI were also decreased (P < 0.05, P < 0.01); morphological and ultrastructural injury in lung tissue were gradually alleviated in CUR groups.
  
  
  CONCLUSIONS
  I/R induces excessive unfolded protein response (UPR) in lung tissue, in which CHOP participates in pneumocyte apoptosis, leading to lung injury; CUR has notable effects on lung protection against I/R injury, which may be related to inhibition of apoptosis mediated by CHOP in excessive UPR.
authors.affiliation: Department of Anesthesiology, First Affiliated Hospital, Wenzhou Medical College, Wenzhou 325035, China.
authors.forename: Jun-Hui
authors.initials: JH
authors.lastname: Zhou
authors.forename: Mao-Lin
authors.initials: ML
authors.lastname: Hao
authors.forename: Shan
authors.initials: S
authors.lastname: Zhao
authors.forename: Hai-E
authors.initials: HE
authors.lastname: Chen
authors.forename: Dan
authors.initials: D
authors.lastname: Chen
authors.forename: Lei
authors.initials: L
authors.lastname: Ying
authors.forename: Qin
authors.initials: Q
authors.lastname: Sun
authors.forename: Wan-Tie
authors.initials: WT
authors.lastname: Wang
mesh_terms: D056809:Alveolar Epithelial Cells / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis; D003474:Curcumin / Q000494:pharmacology*; D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D051742:Transcription Factor CHOP / Q000378:metabolism*
chemical_list: C497250:Ddit3 protein, mouse; D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins; C000717248:Hspa5 protein, mouse; D051742:Transcription Factor CHOP; D003474:Curcumin