title: [Effects of berberine on serum levels of inflammatory factors and inflammatory signaling pathway in obese mice induced by high fat diet].
abstract: OBJECTIVE
  To investigate the effect of berberine on serum levels of TNF-alpha, IL-6 and adiponectin in obese mice induced by high fat diet and its potential molecular mechanisms.
  
  
  METHODS
  Normal male Kunming mice were randomly divided into two groups taking normal chow (NC, n = 10) and high fat diet (HF, n = 30), respectively. After 13 weeks, HF mice were continuously given high fat diet and divided into three groups, model group (BM), low-dosage of berberine group (BL) and high-dosage of berberine group (BH). Mice in BL and BH were administered berberine by gavage at the dosage of 50 mg x kg(-1) and 150 mg x kg(-1), respectively. Two weeks later, oral glucose tolerance test was performed. At the end of the experiment, the mice were killed and blood samples were collected. The epididymal fat tissue and liver were removed promptly and weighed. The serum cytokine was measured by ELISA. The levels of IkappaB kinase beta (IKK-beta) and IKK-beta (ser181) were detected by Western blotting.
  
  
  RESULTS
  Serum levels of TNF-alpha, IL-6 in mice of BM were significantly higher than those in NC (P < 0.05). After two-week treatment of berberine, serum levels of TNF-alpha, IL-6 in BL and BH were lower than those in BM (P < 0.05, respectively). However, there were no significant difference of adiponectin among four groups. The degrees of phosphorylation of IKK-beta (ser181) were decreased in liver and adipose tissue in BH in comparison to that in BM, although the expression of total IKK-beta did not change. Furthermore, the glucose tolerance was improved, while the body weight and epididymal fat were reduced in mice treated with berebrine. 9: Berberine is able to reduce inflammatory cytokines expression and inhibit activation of IKK-beta (ser181) in obese mice, which may partly explain the therapeutic effect of berberine on insulin resistance and abnormal glucose metabolism.
authors.affiliation: Clinical Medical Research Center, First College of Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing 210046, China. wbshang@njutcm.edu.cn
authors.forename: Wenbin
authors.initials: W
authors.lastname: Shang
authors.forename: Jia
authors.initials: J
authors.lastname: Liu
authors.forename: Xizhong
authors.initials: X
authors.lastname: Yu
authors.forename: Juan
authors.initials: J
authors.lastname: Zhao
mesh_terms: D000818:Animals; D001599:Berberine / Q000008:administration & dosage*; D004041:Dietary Fats / Q000008:administration & dosage / Q000009:adverse effects; D004195:Disease Models, Animal; D005951:Glucose Tolerance Test; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D008820:Mice, Obese; D009765:Obesity / Q000097:blood / Q000188:drug therapy* / Q000276:immunology* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D004041:Dietary Fats; D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D001599:Berberine