title: Inflammatory Macrophages Promotes Development of Diabetic Encephalopathy.
abstract: OBJECTIVE
  Diabetes and Alzheimer's disease are often associated with each other, whereas the relationship between two diseases is ill-defined. Although hyperglycemia during diabetes is a major cause of encephalopathy, diabetes may also cause chronic inflammatory complications including peripheral neuropathy. Hence the role and the characteristics of inflammatory macrophages in the development of diabetic encephalopathy need to be clarified.
  
  
  METHODS
  Diabetes were induced in mice by i.p. injection of streptozotocin (STZ). Two weeks after STZ injection and confirmation of development of diabetes, inflammatory macrophages were eliminated by i.p. injection of 20µg saporin-conjugated antibody against a macrophage surface marker CD11b (saporin-CD11b) twice per week, while a STZ-treated group received injection of rat IgG of same frequency as a control. The effects of macrophage depletion on brain degradation markers, brain malondialdehyde (MDA), catalase, superoxidase anion-positive cells and nitric oxide (NO) were measured.
  
  
  RESULTS
  Saporin-CD11b significantly reduced inflammatory macrophages in brain, without affecting mouse blood glucose, serum insulin, glucose responses and beta cell mass. However, reduced brain macrophages significantly inhibited the STZ-induced decreases in brain MDA, catalase and superoxidase anion-positive cells, and the STZ-induced decreases in brain NO.
  
  
  CONCLUSIONS
  Inflammatory macrophages may promote development of diabetic encephalopathy.
authors.affiliation: Department of Gerontology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China.
authors.forename: Beiyun
authors.initials: B
authors.lastname: Wang
authors.forename: Ya
authors.initials: Y
authors.lastname: Miao
authors.forename: Zhe
authors.initials: Z
authors.lastname: Zhao
authors.forename: Yuan
authors.initials: Y
authors.lastname: Zhong
mesh_terms: D000818:Animals; D000906:Antibodies / Q000494:pharmacology*; D001786:Blood Glucose / Q000378:metabolism; D001923:Brain Chemistry; D001927:Brain Diseases / Q000150:complications / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology; D039481:CD11b Antigen / Q000235:genetics / Q000276:immunology; D002374:Catalase / Q000235:genetics / Q000378:metabolism; D002452:Cell Count; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology; D015870:Gene Expression; D000922:Immunotoxins / Q000494:pharmacology*; D007328:Insulin / Q000097:blood; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D054789:Ribosome Inactivating Proteins, Type 1 / Q000494:pharmacology; D000076985:Saporins; D013311:Streptozocin; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism
chemical_list: D000906:Antibodies; D001786:Blood Glucose; D039481:CD11b Antigen; D000922:Immunotoxins; D007328:Insulin; D054789:Ribosome Inactivating Proteins, Type 1; D009569:Nitric Oxide; D008315:Malondialdehyde; D013311:Streptozocin; D002374:Catalase; D013482:Superoxide Dismutase; D000076985:Saporins