PMID- 31018150
OWN - NLM
STAT- MEDLINE
DCOM- 20200424
LR  - 20220208
IS  - 1872-9754 (Electronic)
IS  - 0197-0186 (Linking)
VI  - 128
DP  - 2019 Sep
TI  - Activation of liver x receptors prevents the spinal LTP induced by skin/muscle 
      retraction in the thigh via SIRT1/NF-Kappab pathway.
PG  - 106-114
LID - S0197-0186(19)30034-8 [pii]
LID - 10.1016/j.neuint.2019.04.002 [doi]
AB  - It has been reported that skin/muscle incision and retraction (SMIR) in the 
      thigh, produces mechanical allodynia in the hind paw, far from the site of 
      incision/retraction. The mechanical allodynia lasts about 22 days, indicating 
      chronic post-operative pain develops. The precise mechanisms, however, are 
      largely unclear. In the current study, we further found that SMIR surgery induced 
      LTP of c-fiber evoked field potentials that lasted at least 4 h. The mRNA and 
      protein level of tumor necrosis factor-alpha (TNFalpha) and acetylated nuclear 
      factor-kappaB p65 (ac-NF-kappaB p65) in the lumbar spinal dorsal horn was gradually 
      increased during LTP development, while pretreatment with either TNFalpha 
      neutralization antibody or NF-kappaB inhibitor PDTC completely prevented the 
      induction of LTP. Moreover, the expression of Silent information regulator 1 
      (SIRT1) in the lumbar spinal dorsal horn was decreased and activation of SIRT1 by 
      SRT1720 also prevented the induction of LTP. Importantly, the spinal expression 
      of Liver X receptors (LXRs) was increased, both at mRNA and protein level 
      following SMIR. Application of LXRs agonist T0901317 to the spinal dorsal horn 
      prevented LTP induction following SMIR. Mechanistically, T0901317 enhanced the 
      expression of SIRT1 and decreased the expression of ac-NF-kappaB p65 and TNFalpha. Spinal 
      application of SIRT1 antagonist EX-527, 30 min before T0901317 administration, 
      completely blocked the inhibiting effect of T0901317 on LTP, and on expression of 
      ac-NF-kappaB p65 and TNFalpha. These results indicated that activation of LXRs prevented 
      SMIR-induced LTP by inhibiting NF-kappaB/TNFalpha pathway via increasing SIRT1 
      expression.
CI  - Copyright (c) 2019 Elsevier Ltd. All rights reserved.
FAU - Zhong, Xiongxiong
AU  - Zhong X
AD  - Department of Physiology and Pain Research Center, Zhongshan School of Medicine, 
      Sun Yat-sen University, Guangzhou, Guangdong, PR China.
FAU - Wang, Wei
AU  - Wang W
AD  - Department of Physiology and Pain Research Center, Zhongshan School of Medicine, 
      Sun Yat-sen University, Guangzhou, Guangdong, PR China.
FAU - Mao, Zuchao
AU  - Mao Z
AD  - Department of Physiology and Pain Research Center, Zhongshan School of Medicine, 
      Sun Yat-sen University, Guangzhou, Guangdong, PR China. Electronic address: 
      maozch@mail2.sysu.edu.cn.
FAU - Gao, Feng
AU  - Gao F
AD  - Department of Physiology and Pain Research Center, Zhongshan School of Medicine, 
      Sun Yat-sen University, Guangzhou, Guangdong, PR China.
FAU - Guo, Ruixian
AU  - Guo R
AD  - Department of Physiology and Pain Research Center, Zhongshan School of Medicine, 
      Sun Yat-sen University, Guangzhou, Guangdong, PR China; Guangdong Provincial Key 
      Laboratory of Brain Function and Disease, Guangzhou, Guangdong, PR China.
FAU - Wei, Xuxia
AU  - Wei X
AD  - Department of Surgery ICU, The Third Affliated Hospital of Sun Yat-sen 
      University, Guangzhou, Guangdong, PR China. Electronic address: 
      weixuxia06@163.com.
FAU - Liu, Xianguo
AU  - Liu X
AD  - Department of Physiology and Pain Research Center, Zhongshan School of Medicine, 
      Sun Yat-sen University, Guangzhou, Guangdong, PR China; Guangdong Provincial Key 
      Laboratory of Brain Function and Disease, Guangzhou, Guangdong, PR China. 
      Electronic address: liuxg@mail.sysu.edu.cn.
FAU - Wei, Xuhong
AU  - Wei X
AD  - Department of Physiology and Pain Research Center, Zhongshan School of Medicine, 
      Sun Yat-sen University, Guangzhou, Guangdong, PR China; Guangdong Provincial Key 
      Laboratory of Brain Function and Disease, Guangzhou, Guangdong, PR China. 
      Electronic address: weixhong@mail.sysu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190421
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide)
RN  - 0 (Carbazoles)
RN  - 0 (Hydrocarbons, Fluorinated)
RN  - 0 (Liver X Receptors)
RN  - 0 (NF-kappa B)
RN  - 0 (Sulfonamides)
RN  - 0 (T0901317)
RN  - EC 3.5.1.- (Sirt1 protein, rat)
RN  - EC 3.5.1.- (Sirtuin 1)
SB  - IM
MH  - Animals
MH  - Carbazoles/pharmacology
MH  - Hydrocarbons, Fluorinated/pharmacology
MH  - Liver X Receptors/agonists/*metabolism
MH  - Long-Term Potentiation/drug effects/*physiology
MH  - Male
MH  - Muscle, Skeletal/metabolism/surgery
MH  - NF-kappa B/*biosynthesis
MH  - Posterior Horn Cells/drug effects/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sirtuin 1/antagonists & inhibitors/*biosynthesis
MH  - Skin/metabolism
MH  - Sulfonamides/pharmacology
MH  - Surgical Wound/*metabolism
OTO - NOTNLM
OT  - Acetylated nuclear factor kappaB
OT  - Liver X receptor
OT  - Long term potentiation
OT  - Silent information regulator 1
OT  - Tumor necrosis factor-alpha
EDAT- 2019/04/25 06:00
MHDA- 2020/04/25 06:00
CRDT- 2019/04/25 06:00
PHST- 2019/01/15 00:00 [received]
PHST- 2019/04/03 00:00 [revised]
PHST- 2019/04/05 00:00 [accepted]
PHST- 2019/04/25 06:00 [pubmed]
PHST- 2020/04/25 06:00 [medline]
PHST- 2019/04/25 06:00 [entrez]
AID - S0197-0186(19)30034-8 [pii]
AID - 10.1016/j.neuint.2019.04.002 [doi]
PST - ppublish
SO  - Neurochem Int. 2019 Sep;128:106-114. doi: 10.1016/j.neuint.2019.04.002. Epub 2019 
      Apr 21.