title: Cinnamaldehyde inhibits inflammation and brain damage in a mouse model of permanent cerebral ischaemia.
abstract: OBJECTIVE
  Recent findings suggest the importance of inflammation in the pathogenesis of cerebral ischaemia and its potential as a therapeutic target. Cinnamaldehyde is a diterpene with a wide range of anti-inflammatory effects thus may be advantageous in the treatment of cerebral ischaemia. The present study examined the potential therapeutic effects of cinnamaldehyde on cerebral ischaemia using a mouse model with permanent middle cerebral artery occlusion.
  
  
  METHODS
  Male CD-1 mice, which had the middle cerebral artery occluded, were treated (i.p.) with cinnamaldehyde. Neuroprotection by cinnamaldehyde was analysed by evaluating neurological deficit scores, brain oedema and infarct volume. Expressions of signal transduction molecules and inflammatory mediators were measured by Western blotting, qRT-PCR and immunohistochemical staining. Activation of NF-κB was assessed by Western blotting, immunohistochemistry and immunofluorescence.
  
  
  RESULTS
  Cinnamaldehyde reduced the neurological deficit scores, brain oedema and infarct volume. Cinnamaldehyde suppressed the activation of signal transduction molecules including toll-like receptor 4, tumour necrosis receptor-associated factor 6 and NF-κB, attenuated the increased levels of TNF-α, IL-1β, CCL2 and endothelial-leukocyte adhesion molecule-1 and ultimately reduced leukocyte infiltration into the ischaemic brain areas after cerebral ischaemia.
  
  
  CONCLUSIONS
  Cinnamaldehyde protects against cerebral ischaemia injury by inhibiting inflammation, partly mediated by reducing the expression of toll-like receptor 4, tumour necrosis receptor-associated factor 6 and the nuclear translocation of NF-κB. Our findings suggest that cinnamaldehyde may serve as a new candidate for further development as a treatment for stroke.
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.|Department of Neurology, Hebei General Hospital, Shijiazhuang, China.
authors.forename: Jingru
authors.initials: J
authors.lastname: Zhao
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.|Hebei Collaborative Innovation Center for Cardio-Cerebrovascular Disease, Shijiazhuang, China.|Hebei Key Laboratory of Vascular Homeostasis, Shijiazhuang, China.
authors.forename: Xiangjian
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Lipeng
authors.initials: L
authors.lastname: Dong
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Ya
authors.initials: Y
authors.lastname: Wen
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Xiufen
authors.initials: X
authors.lastname: Zheng
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Cong
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.|Hebei Collaborative Innovation Center for Cardio-Cerebrovascular Disease, Shijiazhuang, China.|Hebei Key Laboratory of Vascular Homeostasis, Shijiazhuang, China.
authors.forename: Rong
authors.initials: R
authors.lastname: Chen
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Ye
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Yaoru
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Tingting
authors.initials: T
authors.lastname: He
authors.affiliation: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, China.
authors.forename: Xingyuan
authors.initials: X
authors.lastname: Zhu
authors.affiliation: Department of Neurology, Hebei General Hospital, Shijiazhuang, China.
authors.forename: Litao
authors.initials: L
authors.lastname: Li
mesh_terms: D000171:Acrolein / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018932:Chemokine CCL2 / Q000235:genetics; D004195:Disease Models, Animal; D019040:E-Selectin / Q000235:genetics; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D053583:Interleukin-1beta / Q000235:genetics; D008297:Male; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D048029:TNF Receptor-Associated Factor 6 / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D014867:Water / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D019040:E-Selectin; D053583:Interleukin-1beta; D016328:NF-kappa B; D018696:Neuroprotective Agents; D012333:RNA, Messenger; D048029:TNF Receptor-Associated Factor 6; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D014867:Water; D000171:Acrolein; C012843:cinnamaldehyde