PMID- 29939299
OWN - NLM
STAT- MEDLINE
DCOM- 20191003
LR  - 20191007
IS  - 1554-6578 (Electronic)
IS  - 0022-3069 (Linking)
VI  - 77
IP  - 8
DP  - 2018 Aug 1
TI  - Surgical Trauma Exacerbates Cognitive Deficits and Neuroinflammation in Aged 
      Rats: The Role of CX3CL1-CX3CR1 Signaling.
PG  - 736-746
LID - 10.1093/jnen/nly051 [doi]
AB  - Age is the most prominent risk factor for the development of postoperative 
      cognitive dysfunction. The present study investigated the role of CX3CL1-CX3CR1 
      signaling in age-related differences in surgery-induced cognitive deficits and 
      neuroinflammation. Adult and aged male Sprague-Dawley rats were subjected to 
      partial hepatectomy or partial hepatectomy with intracerebroventricular infusion 
      of CX3CL1. On postoperative days 3, 7, and 14, the rats were subjected to an open 
      field test and the Morris water maze test. Hippocampal interleukin-1beta, CX3CL1, 
      CX3CR1, brain derived neurotrophic factor (BDNF), ionized calcium-binding adapter 
      molecule 1 (Iba-1), and Arginase-1 (Arg1) levels were measured. Age exacerbated 
      cognitive impairment and increased neuroinflammation following surgery. 
      Surgery-induced decreases in CX3CL1 and CX3CR1 proteins were accompanied by 
      increased microglial activation, as indicated by increased Iba-1 expression. 
      Corresponding decline in Arg1 and BDNF levels were observed. Treatment with 
      CX3CL1 decreased proinflammatory cytokines expression, increased BDNF and Arg1 
      levels in the brain, and enhanced behavioral recovery. The surgery-induced 
      decreases in CX3CL1 and CX3CR1 expression exacerbated postoperative cognitive 
      deficits and exaggerated neuroinflammatory responses in this rodent model. 
      Treatment with CX3CL1 attenuated these effects, at least partly by inhibiting 
      microglial activation, decreasing the associated production of proinflammatory 
      cytokines, and enhancing BDNF expression.
FAU - Li, Zhe
AU  - Li Z
AD  - Department of Anesthesiology, The First Hospital of China Medical University, 
      Shenyang, Liaoning, China.
FAU - Cao, Xuezhao
AU  - Cao X
AD  - Department of Anesthesiology, The First Hospital of China Medical University, 
      Shenyang, Liaoning, China.
FAU - Ma, Hong
AU  - Ma H
AD  - Department of Anesthesiology, The First Hospital of China Medical University, 
      Shenyang, Liaoning, China.
FAU - Cui, Yong
AU  - Cui Y
AD  - Department of Anesthesiology, The First Hospital of China Medical University, 
      Shenyang, Liaoning, China.
FAU - Li, Xiaoqian
AU  - Li X
AD  - Department of Anesthesiology, The First Hospital of China Medical University, 
      Shenyang, Liaoning, China.
FAU - Wang, Na
AU  - Wang N
AD  - Department of Anesthesiology, The First Hospital of China Medical University, 
      Shenyang, Liaoning, China.
FAU - Zhou, Yongjian
AU  - Zhou Y
AD  - Department of Anesthesiology, The First Hospital of China Medical University, 
      Shenyang, Liaoning, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Neuropathol Exp Neurol
JT  - Journal of neuropathology and experimental neurology
JID - 2985192R
RN  - 0 (CX3C Chemokine Receptor 1)
RN  - 0 (CX3CR1 protein, rat)
RN  - 0 (Chemokine CX3CL1)
RN  - 0 (Cx3cl1 protein, rat)
SB  - IM
MH  - Aging/*metabolism/pathology
MH  - Animals
MH  - Brain/*metabolism/pathology
MH  - CX3C Chemokine Receptor 1/*physiology
MH  - Chemokine CX3CL1/*physiology
MH  - Cognitive Dysfunction/*metabolism/pathology
MH  - Hepatectomy/*adverse effects/trends
MH  - Liver/metabolism/surgery
MH  - Male
MH  - Maze Learning/physiology
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction/physiology
EDAT- 2018/06/26 06:00
MHDA- 2019/10/08 06:00
CRDT- 2018/06/26 06:00
PHST- 2018/06/26 06:00 [pubmed]
PHST- 2019/10/08 06:00 [medline]
PHST- 2018/06/26 06:00 [entrez]
AID - 5043161 [pii]
AID - 10.1093/jnen/nly051 [doi]
PST - ppublish
SO  - J Neuropathol Exp Neurol. 2018 Aug 1;77(8):736-746. doi: 10.1093/jnen/nly051.