title: [Effect of N(G)-nitro-L-arginine on inflammatory factor and neuronal apoptosis after focal cerebral ischemic injury in rats].
abstract: OBJECTIVE
  To evaluate the effect of NG-nitro-L-arginine (L-NA) on inflammatory factor and neuronal apoptosis after focal cerebral ischemic injury in rats and the possible mechanism of protective effect of L-NA against cerebral ischemic injury.
  
  
  METHODS
  Thirty male SD rats weighing 250-280 g were randomly divided into three groups (n=10): (1) Sham operated group (SH), (2) Ischemic group (IS), (3) L-NA group. In L-NA group L-NA 20 mg/kg was given intraperitoneally twice a day for 3 consecutive days. In IS group normal saline was given instead of L-NA. Focal cerebral ischemia was produced by middle cerebral artery occlusion (MCAO) for 12 h. A nylon thread with rounded tip which was inserted into left internal carotid artery cranially until resistance was felt. The distance from bifurcation of common carotid artery to the tip of the thread was about 18-19 mm. Focal cerebral ischemia was confirmed by left Horner's syndrome and right side hemiplegia. In SH group the carotid artery was exposed but no thread was inserted. The expression of TNF-alpha was determined by immunochemistry and the content of IL-1beta was measured by radio immunity. The Bcl-2 and Bax protein expression were detected by flow cytometry.
  
  
  RESULTS
  The expression of TNF-alpha and the content of IL-1 beta were markedly increased after MCAO. Significantly increased DNA fragmentation indication of apoptosis was detected after MCAO. The expression of TNF-alpha and the content of IL-1 beta was significantly lower in L-NA group than in IS group. The percentage of apoptosis cells and expression of Bax protein were markedly lower in L-NA group than in IS group but still significantly higher than in SH group. The expression of Bcl-2 protein was markedly higher in L-NA group than in IS group. There was no significant difference in the expression of Bcl-2 protein between IS and SH group.
  
  
  CONCLUSIONS
  L-NA could inhibit the increase in the expression of TNF-alpha and the content of IL-1beta, and protect neurons from apoptosis induced by focal cerebral ischemia through increasing the Bcl-2 protein expression and inhibiting the Bax protein expression.
authors.affiliation: Department of Pharmacology, Hebei Academy of Medical Sciences, Shijiazhuang 050021, China. jianxinzlang3@hotmail.com
authors.forename: Jian-xin
authors.initials: JX
authors.lastname: Zhang
authors.forename: Lan-fang
authors.initials: LF
authors.lastname: Li
authors.forename: Hui-xin
authors.initials: HX
authors.lastname: Zhang
authors.forename: Yong-hui
authors.initials: YH
authors.lastname: Li
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001930:Brain Injuries / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology*; D053583:Interleukin-1beta / Q000378:metabolism; D008297:Male; D019335:Nitroarginine / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D053583:Interleukin-1beta; D019253:Proto-Oncogene Proteins c-bcl-2; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein; D019335:Nitroarginine