PMID- 27366867
OWN - NLM
STAT- MEDLINE
DCOM- 20171225
LR  - 20180309
IS  - 1473-558X (Electronic)
IS  - 0959-4965 (Linking)
VI  - 27
IP  - 13
DP  - 2016 Sep 7
TI  - Infliximab ameliorating depression-like behavior through inhibiting the 
      activation of the IDO-HAAO pathway mediated by tumor necrosis factor-alpha in a rat 
      model.
PG  - 953-9
LID - 10.1097/WNR.0000000000000637 [doi]
AB  - In recent years, some studies have suggested that the activation of inflammatory 
      system plays a role in the occurrence of depression. Tumor necrosis factor-alpha 
      (TNF-alpha), as one of the preinflammatory cytokines, has been reported to be 
      involved in the occurrence of various diseases including depression. Infliximab, 
      an antagonist of TNF-alpha, is usually used to treat some autoimmune diseases such as 
      Crohn's disease and can perhaps be used to treat other diseases. In this study, 
      the antidepressant effect and a possible mechanism of infliximab were 
      investigated by studying the depression-like behavior and expression of TNF-alpha, 
      indoleamine 2, 3-dioxygenase (IDO), and 3-hydroxyl amino acid oxygenase (HAAO) 
      from the cortex and hippocampus in rat exposed to chronic unpredicted stress. 
      Forty male Sprague-Dawley rats were divided into a control group (CG), an 
      infliximab-treated control group, a model group (MG), and an infliximab-treated 
      model group (IFXM). Infliximab (5 mg/kg once week) was administered to the 
      infliximab-treated control group and IFXM rats by an intraperitoneal injection, 
      whereas an equivalent volume of vehicle was administered to CG and MG rats. Rat 
      behaviors and the expression of TNF-alpha, IDO, and HAAO in the cortex and 
      hippocampus were determined. It was found that a significant relief in 
      depression-like behaviors was observed with a downregulation of TNF-alpha, IDO, and 
      HAAO expression in the IFXM rats compared with MG rats. The results show the 
      antidepressant effect of infliximab and suggest that its mechanism is partly 
      related to inhibition of IDO-HAAO pathway activation mediated by TNF-alpha in rat 
      brain.
FAU - Fu, Xiao-Yan
AU  - Fu XY
AD  - aKey Laboratory of Biochemistry and Molecular Pharmacology, Department of 
      Pharmacology bKey Laboratory of Biochemistry and Molecular Pharmacology, 
      Department of Drug Analysis, School of Pharmacy of Chongqing Medical University, 
      Yixueyuan Lu, Chongqing, China.
FAU - Li, Hai-Yan
AU  - Li HY
FAU - Jiang, Qing-Song
AU  - Jiang QS
FAU - Cui, Ting
AU  - Cui T
FAU - Jiang, Xin-Hui
AU  - Jiang XH
FAU - Zhou, Qi-Xin
AU  - Zhou QX
FAU - Qiu, Hong-Mei
AU  - Qiu HM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Neuroreport
JT  - Neuroreport
JID - 9100935
RN  - 0 (Antidepressive Agents)
RN  - 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - B72HH48FLU (Infliximab)
SB  - IM
MH  - Animals
MH  - Antidepressive Agents/*administration & dosage
MH  - Cerebral Cortex/drug effects/*metabolism
MH  - Depression/metabolism/*prevention & control
MH  - Disease Models, Animal
MH  - Hippocampus/drug effects/*metabolism
MH  - Indoleamine-Pyrrole 2,3,-Dioxygenase/*metabolism
MH  - Inflammation/metabolism
MH  - Infliximab/*administration & dosage/therapeutic use
MH  - Male
MH  - Motor Activity/drug effects
MH  - RNA, Messenger/metabolism
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction/drug effects
MH  - Stress, Psychological/metabolism
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 2016/07/02 06:00
MHDA- 2017/12/26 06:00
CRDT- 2016/07/02 06:00
PHST- 2016/07/02 06:00 [entrez]
PHST- 2016/07/02 06:00 [pubmed]
PHST- 2017/12/26 06:00 [medline]
AID - 10.1097/WNR.0000000000000637 [doi]
PST - ppublish
SO  - Neuroreport. 2016 Sep 7;27(13):953-9. doi: 10.1097/WNR.0000000000000637.