title: [Effect of Guanmaitong Tablet on ERK and p38 Protein of TLR2 Pathway Expression in Cerebral Ischemia/Reperfusion Rats: an Experimental Study].
abstract: OBJECTIVE
  To explore the inflammatory cascade mechanism through Toll like receptor 2 (TLR2) pathway after cerebral ischemia/reperfusion, and to study molecular mechanisms of Guanmaitong (GMT) Tablet for protecting brain damage.
  
  
  METHODS
  We used bolt-line method to block/release the middle cerebral artery, causing cerebral ischemia/reperfusion (I/R) injury model. GMT Tablet was given by gastrogavage. Rats were then divided into the high dose GMT group (1200 mg/kg), the middle dose GMT group (600 mg/kg), the low dose GMT group (300 mg/kg), the positive control group (Tanakan, 20 mg/kg). Their right brain tissues were fixed in 10% neutral formalin. TLR2 expressions were detected by immunofluorescence staining. The total protein was extracted from right brain tissues by ultrasonica- tion. Expression levels of extracellular regulated protein kinases (ERK), phospho-extracellular regulated protein kinases (p-ERK), p38-mitogen activated protein kinases (p-ERK), phospho-p38-mitogen activated protein kinases [p-p38-MAPKs(p-p38)] were assessed by Western blot. Abdominal aortic blood was withdrawn. IL-6 and IL-1β levels were detected by ELISA in brain tissues and serum.
  
  
  RESULTS
  Compared with the sham-oepration group, expression levels of TLR2, ERK, p-ERK, p38, p-p38 protein were up-regulated (P < 0.05, P < 0.01), and contents of IL-6 and IL-1β in brain tissues and serum were increased in the model group (P < 0.01). Expression levels of TLR2, ERK, p-ERK, p38, p-p38 were down-regulated (P < 0.05, P < 0.01), and contents of IL-6 and IL-1β were reduced in brain tissues and serum in middle and high dose GMT groups (P < 0.05, P < 0.01).
  
  
  CONCLUSIONS
  TLR2 pathway was involved in cerebral I/R injury. GMT protected neurons by down-regulating protein expressions of TLR2, ERK, p-ERK, p38, p-p38 and contents of IL-1β and IL-6.
authors.forename: Cui-xiang
authors.initials: CX
authors.lastname: Zhang
authors.forename: Jian-xun
authors.initials: JX
authors.lastname: Liu
authors.forename: Dan
authors.initials: D
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Li
authors.forename: Jian-hua
authors.initials: JH
authors.lastname: Fu
authors.forename: Jin-cai
authors.initials: JC
authors.lastname: Hou
authors.forename: Xue-mei
authors.initials: XM
authors.lastname: Du
authors.forename: Fa-chang
authors.initials: FC
authors.lastname: Zhang
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002545:Brain Ischemia / Q000378:metabolism*; D002544:Cerebral Infarction; D015536:Down-Regulation; D004365:Drugs, Chinese Herbal / Q000627:therapeutic use*; D053583:Interleukin-1beta; D015850:Interleukin-6; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury; D013607:Tablets; D051195:Toll-Like Receptor 2 / Q000378:metabolism*; D015854:Up-Regulation; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D004365:Drugs, Chinese Herbal; D053583:Interleukin-1beta; D015850:Interleukin-6; D013607:Tablets; D051195:Toll-Like Receptor 2; D048051:p38 Mitogen-Activated Protein Kinases