Possible roles of COX-1 in learning and memory impairment induced by traumatic brain injury in mice.
People who suffer from traumatic brain injury (TBI) often experience cognitive deficits in spatial reference and working memory. The possible roles of cyclooxygenase-1 (COX-1) in learning and memory impairment in mice with TBI are far from well known. Adult mice subjected to TBI were treated with the COX-1 selective inhibitor SC560. Performance in the open field and on the beam walk was then used to assess motor and behavioral function 1, 3, 7, 14, and 21 days following injury. Acquisition of spatial learning and memory retention was assessed using the Morris water maze on day 15 post-TBI. The expressions of COX-1, prostaglandin E2 (PGE2), interleukin (IL)-6, brain-derived neurotrophic factor (BDNF), platelet-derived growth factor BB (PDGF-BB), synapsin-I, and synaptophysin were detected in TBI mice. Administration of SC560 improved performance of beam walk tasks as well as spatial learning and memory after TBI. SC560 also reduced expressions of inflammatory markers IL-6 and PGE2, and reversed the expressions of COX-1, BDNF, PDGF-BB, synapsin-I, and synaptophysin in TBI mice. The present findings demonstrated that COX-1 might play an important role in cognitive deficits after TBI and that selective COX-1 inhibition should be further investigated as a potential therapeutic approach for TBI.
Neurology Department, Peace Hospital Attached to Changzhi Medical College, Changzhi, China.
J L
JL
Shang
Neurology Department, Changzhi City People's Hospital, Changzhi, China.
Q
Q
Cheng
Neurology Department, People's Hospital of Dali, Dali, China.
W F
WF
Yang
Neurology Department, Peace Hospital Attached to Changzhi Medical College, Changzhi, China.
M
M
Zhang
Neurology Department, Peace Hospital Attached to Changzhi Medical College, Changzhi, China.
Y
Y
Cui
Neurology Department, Peace Hospital Attached to Changzhi Medical College, Changzhi, China.
Y F
YF
Wang
D000818:Animals; D000077214:Becaplermin; D015153:Blotting, Western; D001930:Brain Injuries / Q000150:complications*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D002540:Cerebral Cortex / Q000293:injuries*; D002541:Cerebral Decortication; D051545:Cyclooxygenase 1 / Q000378:metabolism / Q000502:physiology*; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use*; D015232:Dinoprostone / Q000032:analysis / Q000378:metabolism; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D006624:Hippocampus / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood; D007858:Learning / Q000187:drug effects*; D018782:Maze Learning / Q000187:drug effects; D008569:Memory Disorders / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D008810:Mice, Inbred C57BL; D020574:Proto-Oncogene Proteins c-sis / Q000378:metabolism; D011720:Pyrazoles / Q000627:therapeutic use*; D020127:Recovery of Function / Q000187:drug effects; D016708:Synaptophysin / Q000032:analysis / Q000378:metabolism
D019208:Brain-Derived Neurotrophic Factor; D016861:Cyclooxygenase Inhibitors; D015850:Interleukin-6; D020574:Proto-Oncogene Proteins c-sis; D011720:Pyrazoles; C115461:SC 560; D016708:Synaptophysin; D000077214:Becaplermin; D051545:Cyclooxygenase 1; D015232:Dinoprostone