title: [Inhibitory effects of curcumin on inflammatory cytokines in rats with paraquat poisoning].
abstract: OBJECTIVE
  To explore the mechanism of paraquat (PQ) poisoning and to observe the changes in inflammatory cytokines in PQ-exposed rats treated in different ways.
  
  
  METHODS
  Fifty 8-week-old clean male Wistar rats were randomly divided into high-dose curcumin plus conventional treatment group, low-dose curcumin plus conventional treatment group, high-dose curcumin group, PQ poisoning group, and blank control group. On days 1, 3, 5, 7, 14, and 21 after PQ exposure, serum levels of transforming growth factor-β₁(TGF-β₁) , tumor necrosis factor-α (TNF-α) , and interleukin-6 (IL-6) were measured. The pathological changes in lung tissue were evaluated by HE staining.
  
  
  RESULTS
  Compared with the blank control group, the high-dose curcumin plus conventional treatment group, low-dose curcumin plus conventional treatment group, high-dose curcumin group, and PQ poisoning group had significantly increased serum levels of TGF-β₁, TNF-α, and IL-6 (P<0.05) , and the three cytokines in each group reached peak levels on day 14 after exposure. Compared with the PQ poisoning group, the high-dose curcumin group had significantly reduced serum levels of TGF-β₁, TNF-α, and IL-6 (P<0.05). On day 21 after exposure, there were no significant differences in serum levels of TGF-β₁, TNF-α, and IL-6 between the high-dose curcumin plus conventional treatment group and the low-dose curcumin plus conventional treatment group (P>0.05). The HE staining revealed alveolar inflammatory changes on days 1~7 and massive pulmonary fibrosis on days 14~21 in the high-dose curcumin plus conventional treatment group, low-dose curcumin plus conventional treatment group, high-dose curcumin group, and PQ poisoning group, but the above changes were milder in the high-dose curcumin group than in the PQ poisoning group.
  
  
  CONCLUSIONS
  For rats with PQ poisoning, curcumin can significantly reduce inflammatory response and pathological changes in lung tissue and inhibit and delay the development and progression of body injury.
authors.affiliation: Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
authors.forename: Hongjun
authors.initials: H
authors.lastname: Li
authors.forename: Baonan
authors.initials: B
authors.lastname: Liu
authors.forename: Peng
authors.initials: P
authors.lastname: Li
authors.forename: Lingji
authors.initials: L
authors.lastname: Feng
authors.forename: Haihong
authors.initials: H
authors.lastname: Ma
authors.forename: Shimeng
authors.initials: S
authors.lastname: Xuan
authors.affiliation: E-mail: yz_cao@163.com.
authors.forename: Yongzhi
authors.initials: Y
authors.lastname: Cao
mesh_terms: D000818:Animals; D003474:Curcumin / Q000494:pharmacology*; D016207:Cytokines / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008168:Lung / Q000473:pathology*; D008297:Male; D010269:Paraquat / Q000506:poisoning*; D011658:Pulmonary Fibrosis / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D053773:Transforming Growth Factor beta1 / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D016207:Cytokines; D015850:Interleukin-6; C508962:Tgfb1 protein, rat; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D003474:Curcumin; D010269:Paraquat