title: [Parthenolide inhibits neuroinflammation and promotes neurogenesis in the ischemic striatum following transient middle cerebral artery occlusion in the adult rat brain].
abstract: OBJECTIVE
  The objective of this study was to test the hypothesis that parthenolide suppresses ischemia-induced neuroinflammation in the MCAO model of adult rat.
  
  
  METHODS
  MCAO rats were treated i.p. with parthenolide (500 microg/kg). Brain sections were analyzed for BrdU, BrdU-DCX, BrdU-Tuj-1, BrdU-MAP-2 and BrdU-GFAP staining. Total protein was extracted from ischemic striatum, and Western blot was used to determine TNF-alpha expression.
  
  
  RESULTS
  Cerebral ischemia increases expression of TNF-alpha in the ischemic striatum. Parthenolide suppressed the expression of TNF-alpha and enhances the proliferation of newborn cells in the ischemic striatum. The cell number of BrdU(+)-DCX(+), BrdU(+)-Tuj-1(+), and BrdU(+)-MAP-2(+) is increased in the ischemic striatum after parthenolide treatment at 3 d, 7 d or 28 d after MCAO. Furthermore, parthenolide depressed the cell number of BrdU(+)-GFAP(+) in the ischemic striatum at 3 d, 7 d and 28 d after MCAO.
  
  
  CONCLUSIONS
  Parthenolide inhibits neuroinflammation induced by cerebral ischemia and promotes neurogenesis in the ischemic striatum. Further study of the effects of parthenolide on inflammatory gene expression using model animal systems as described here are critical to elucidating their mechanisms of action.
authors.affiliation: Department of Human Anatomy, Southeast University, Nanjing 210009, China. zhinianlei@gmail.com
authors.forename: Zhi-nian
authors.initials: ZN
authors.lastname: Lei
authors.forename: Shui-lin
authors.initials: SL
authors.lastname: Zeng
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
authors.forename: Jian-bao
authors.initials: JB
authors.lastname: Zhu
authors.forename: Tao
authors.initials: T
authors.lastname: Li
mesh_terms: D000818:Animals; D001973:Bromodeoxyuridine / Q000378:metabolism; D000089662:Doublecortin Protein; D005786:Gene Expression Regulation / Q000187:drug effects; D020244:Infarction, Middle Cerebral Artery / Q000150:complications*; D007249:Inflammation / Q000150:complications / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D007511:Ischemia / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D017072:Neostriatum / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology*; D055495:Neurogenesis / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012717:Sesquiterpenes / Q000494:pharmacology* / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: C000714848:Dcx protein, rat; D000089662:Doublecortin Protein; D012717:Sesquiterpenes; D014409:Tumor Necrosis Factor-alpha; C002669:parthenolide; D001973:Bromodeoxyuridine