Translocator protein ligand, YL-IPA08, attenuates lipopolysaccharide-induced depression-like behavior by promoting neural regeneration
Translocator protein has received attention for its involvement in the pathogenesis of depression. This study assessed the effects of the new translocator protein ligand, YL-IPA08, on alleviating inflammation-induced depression-like behavior in mice and investigated its mechanism of action. Mice wer...
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| Veröffentlicht in: | Neural regeneration research Jg. 13; H. 11; S. 1937 - 1944 |
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Medknow Publications and Media Pvt. Ltd
01.11.2018
Medknow Publications & Media Pvt. Ltd Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing, China State Key Laboratory of Toxicology and Medical Countermeasures, Beijing, China%Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing, China%State Key Laboratory of Toxicology and Medical Countermeasures, Beijing, China Medknow Publications & Media Pvt Ltd |
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| ISSN: | 1673-5374, 1876-7958 |
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| Abstract | Translocator protein has received attention for its involvement in the pathogenesis of depression. This study assessed the effects of the new translocator protein ligand, YL-IPA08, on alleviating inflammation-induced depression-like behavior in mice and investigated its mechanism of action. Mice were intracerebroventricularly injected with 1, 10, 100 or 1000 ng lipopolysaccharide. The tail-suspension test and the forced swimming test confirmed that 100 ng lipopolysaccharide induced depression-like behavior. A mouse model was then established by intraventricular injection of 100 ng lipopolysaccharide. On days 16-24 after model establishment, mice were intragastrically administered 3 mg/kg YL-IPA08 daily. Immunohistochemistry was used to determine BrdU and NeuN expression in the hippocampus. YL-IPA08 effectively reversed the depression-like behavior of lipopolysaccharide-treated mice, restored body mass, increased the number of BrdU-positive cells, and the number and proportion of BrdU and NeuN double-positive cells. These findings indicate that YL-IPA08 can attenuate lipopolysaccharide-induced depression-like behavior in mice by promoting the formation of hippocampal neurons. |
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| AbstractList | Translocator protein has received attention for its involvement in the pathogenesis of depression. This study assessed the effects of the new translocator protein ligand, YL-IPA08, on alleviating inflammation-induced depression-like behavior in mice and investigated its mechanism of action. Mice were intracerebroventricularly injected with 1, 10, 100 or 1000 ng lipopolysaccharide. The tail-suspension test and the forced swimming test confirmed that 100 ng lipopolysaccharide induced depression-like behavior. A mouse model was then established by intraventricular injection of 100 ng lipopolysaccharide. On days 16–24 after model establishment, mice were intragastrically administered 3 mg/kg YL-IPA08 daily. Immunohistochemistry was used to determine BrdU and NeuN expression in the hippocampus. YL-IPA08 effectively reversed the depression-like behavior of lipopolysaccharide-treated mice, restored body mass, increased the number of BrdU-positive cells, and the number and proportion of BrdU and NeuN double-positive cells. These findings indicate that YL-IPA08 can attenuate lipopolysaccharide-induced depression-like behavior in mice by promoting the formation of hippocampal neurons. Translocator protein has received attention for its involvement in the pathogenesis of depression. This study assessed the effects of the new translocator protein ligand, YL-IPA08, on alleviating inflammation-induced depression-like behavior in mice and investigated its mechanism of action. Mice were intracerebroventricularly injected with 1, 10, 100 or 1000 ng lipopolysaccharide. The tail-suspension test and the forced swimming test confirmed that 100 ng lipopolysaccharide induced depression-like behavior. A mouse model was then established by intraventricular injection of 100 ng lipopolysaccharide. On days 16-24 after model establishment, mice were intragastrically administered 3 mg/kg YL-IPA08 daily. Immunohistochemistry was used to determine BrdU and NeuN expression in the hippocampus. YL-IPA08 effectively reversed the depression-like behavior of lipopolysaccharide-treated mice, restored body mass, increased the number of BrdU-positive cells, and the number and proportion of BrdU and NeuN double-positive cells. These findings indicate that YL-IPA08 can attenuate lipopolysaccharide-induced depression-like behavior in mice by promoting the formation of hippocampal neurons.Translocator protein has received attention for its involvement in the pathogenesis of depression. This study assessed the effects of the new translocator protein ligand, YL-IPA08, on alleviating inflammation-induced depression-like behavior in mice and investigated its mechanism of action. Mice were intracerebroventricularly injected with 1, 10, 100 or 1000 ng lipopolysaccharide. The tail-suspension test and the forced swimming test confirmed that 100 ng lipopolysaccharide induced depression-like behavior. A mouse model was then established by intraventricular injection of 100 ng lipopolysaccharide. On days 16-24 after model establishment, mice were intragastrically administered 3 mg/kg YL-IPA08 daily. Immunohistochemistry was used to determine BrdU and NeuN expression in the hippocampus. YL-IPA08 effectively reversed the depression-like behavior of lipopolysaccharide-treated mice, restored body mass, increased the number of BrdU-positive cells, and the number and proportion of BrdU and NeuN double-positive cells. These findings indicate that YL-IPA08 can attenuate lipopolysaccharide-induced depression-like behavior in mice by promoting the formation of hippocampal neurons. Translocator protein has received attention for its involvement in the pathogenesis of depression. This study assessed the effects of the new translocator protein ligand, YL-IPA08, on alleviating inflammation-induced depression-like behavior in mice and investigated its mecha-nism of action. Mice were intracerebroventricularly injected with 1, 10, 100 or 1000 ng lipopolysaccharide. The tail-suspension test and the forced swimming test confirmed that 100 ng lipopolysaccharide induced depression-like behavior. A mouse model was then established by intraventricular injection of 100 ng lipopolysaccharide. On days 16–24 after model establishment, mice were intragastrically administered 3 mg/kg YL-IPA08 daily. Immunohistochemistry was used to determine BrdU and NeuN expression in the hippocampus. YL-IPA08 effec-tively reversed the depression-like behavior of lipopolysaccharide-treated mice, restored body mass, increased the number of BrdU-positive cells, and the number and proportion of BrdU and NeuN double-positive cells. These findings indicate that YL-IPA08 can attenuate lipo-polysaccharide-induced depression-like behavior in mice by promoting the formation of hippocampal neurons. |
| Audience | Academic |
| Author | Mi, Wei-Dong Zhang, Xiao-Ying Li, Yun-Feng Zhang, Li-Ming |
| AuthorAffiliation | Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing, China;State Key Laboratory of Toxicology and Medical Countermeasures, Beijing, China%Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing, China%State Key Laboratory of Toxicology and Medical Countermeasures, Beijing, China |
| AuthorAffiliation_xml | – name: Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing, China;State Key Laboratory of Toxicology and Medical Countermeasures, Beijing, China%Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing, China%State Key Laboratory of Toxicology and Medical Countermeasures, Beijing, China – name: 1 Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing, China – name: 2 State Key Laboratory of Toxicology and Medical Countermeasures, Beijing, China |
| Author_xml | – sequence: 1 givenname: Xiao-Ying surname: Zhang fullname: Zhang, Xiao-Ying – sequence: 2 givenname: Li-Ming surname: Zhang fullname: Zhang, Li-Ming – sequence: 3 givenname: Wei-Dong surname: Mi fullname: Mi, Wei-Dong – sequence: 4 givenname: Yun-Feng surname: Li fullname: Li, Yun-Feng |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30233067$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1134_S1068162021030122 crossref_primary_10_1007_s11011_025_01565_2 crossref_primary_10_1016_j_neuint_2024_105728 |
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| Keywords | dentate gyrus neural regeneration translocator protein hippocampus neuroinflammation nerve regeneration depression lipopolysaccharide YL-IPA08 |
| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Author contributions: XYZ conceived the study, carried out the study execution and data analysis and contributed to the manuscript draft. LMZ participated in the study design, the construction of recombinant lentiviruses and the draft of manuscript. WDM and YFL contributed to the study design, data analysis and manuscript revision. All authors approved the final version of this paper. |
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| PublicationTitle | Neural regeneration research |
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| Publisher | Medknow Publications and Media Pvt. Ltd Medknow Publications & Media Pvt. Ltd Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing, China State Key Laboratory of Toxicology and Medical Countermeasures, Beijing, China%Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing, China%State Key Laboratory of Toxicology and Medical Countermeasures, Beijing, China Medknow Publications & Media Pvt Ltd |
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| Snippet | Translocator protein has received attention for its involvement in the pathogenesis of depression. This study assessed the effects of the new translocator... |
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| StartPage | 1937 |
| SubjectTerms | Analysis Behavior Brain Depression, Mental Inflammation Laboratory animals Ligands Ligands (Biochemistry) Lipopolysaccharides Medical research Mental depression Mice Nervous system Neurogenesis Regeneration |
| Title | Translocator protein ligand, YL-IPA08, attenuates lipopolysaccharide-induced depression-like behavior by promoting neural regeneration |
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