Nicotinamide Improves Cognitive Function in Mice With Chronic Cerebral Hypoperfusion
Normal brain function requires steady blood supply to maintain stable energy state. When blood supply to the brain becomes suboptimal for a long period of time, chronic cerebral hypoperfusion (CCH) and a variety of brain changes may occur. CCH causes white matter injury and cognitive impairment. The...
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| Published in | Frontiers in neurology Vol. 12; p. 596641 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
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Frontiers Media S.A
25.01.2021
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| ISSN | 1664-2295 1664-2295 |
| DOI | 10.3389/fneur.2021.596641 |
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| Abstract | Normal brain function requires steady blood supply to maintain stable energy state. When blood supply to the brain becomes suboptimal for a long period of time, chronic cerebral hypoperfusion (CCH) and a variety of brain changes may occur. CCH causes white matter injury and cognitive impairment. The present study investigated the effect of nicotinamide (NAM) on CCH-induced cognitive impairment and white matter damage in mice. Male C57Bl/6J mice aged 10–12 weeks (mean age = 11 ± 1 weeks) and weighing 24 - 29 g (mean weight = 26.5 ± 2.5 g) were randomly assigned to three groups (eight mice/group): sham group, CCH group and NAM group. Chronic cerebral hypoperfusion (CCH) was induced using standard methods. The treatment group mice received intraperitoneal injection of NAM at a dose of 200 mg/kg body weight (bwt) daily for 30 days. Learning, memory, anxiety, and depression-like behaviors were measured using Morris water maze test (MWMT), open field test (OFT), sucrose preference test (SPT), and forced swim test (FST), respectively. White matter damage and remodeling were determined via histological/ immunohistochemical analyses, and western blotting, respectively. The results showed that the time spent in target quadrant, number of crossings and escape latency were significantly lower in CCH group than in sham group, but they were significantly increased by NAM (
p
< 0.05). Mice in NAM group moved significantly faster and covered longer distances, when compared with those in CCH group (
p
< 0.05). The percentage of time spent in open arms and the number of entries to the open arms were significantly lower in CCH group than in NAM group (
p
< 0.05). Moreover, anhedonia and histologic scores (index of myelin injury) were significantly higher in CCH group than in sham group, but they were significantly reduced by NAM (
p
< 0.05). The results of immunohistochemical staining and Western blotting showed that the protein expressions of 2′, 3′-cyclic-nucleotide 3′-phosphodiesterase (CNPase) and synaptophysin were significantly downregulated in CCH group, relative to sham group, but they were significantly upregulated by NAM (
p
< 0.05). These results indicate that NAM improves cognitive function in mice with CCH. |
|---|---|
| AbstractList | Normal brain function requires steady blood supply to maintain stable energy state. When blood supply to the brain becomes suboptimal for a long period of time, chronic cerebral hypoperfusion (CCH) and a variety of brain changes may occur. CCH causes white matter injury and cognitive impairment. The present study investigated the effect of nicotinamide (NAM) on CCH-induced cognitive impairment and white matter damage in mice. Male C57Bl/6J mice aged 10–12 weeks (mean age = 11 ± 1 weeks) and weighing 24 - 29 g (mean weight = 26.5 ± 2.5 g) were randomly assigned to three groups (eight mice/group): sham group, CCH group and NAM group. Chronic cerebral hypoperfusion (CCH) was induced using standard methods. The treatment group mice received intraperitoneal injection of NAM at a dose of 200 mg/kg body weight (bwt) daily for 30 days. Learning, memory, anxiety, and depression-like behaviors were measured using Morris water maze test (MWMT), open field test (OFT), sucrose preference test (SPT), and forced swim test (FST), respectively. White matter damage and remodeling were determined via histological/ immunohistochemical analyses, and western blotting, respectively. The results showed that the time spent in target quadrant, number of crossings and escape latency were significantly lower in CCH group than in sham group, but they were significantly increased by NAM (
p
< 0.05). Mice in NAM group moved significantly faster and covered longer distances, when compared with those in CCH group (
p
< 0.05). The percentage of time spent in open arms and the number of entries to the open arms were significantly lower in CCH group than in NAM group (
p
< 0.05). Moreover, anhedonia and histologic scores (index of myelin injury) were significantly higher in CCH group than in sham group, but they were significantly reduced by NAM (
p
< 0.05). The results of immunohistochemical staining and Western blotting showed that the protein expressions of 2′, 3′-cyclic-nucleotide 3′-phosphodiesterase (CNPase) and synaptophysin were significantly downregulated in CCH group, relative to sham group, but they were significantly upregulated by NAM (
p
< 0.05). These results indicate that NAM improves cognitive function in mice with CCH. Normal brain function requires steady blood supply to maintain stable energy state. When blood supply to the brain becomes suboptimal for a long period of time, chronic cerebral hypoperfusion (CCH) and a variety of brain changes may occur. CCH causes white matter injury and cognitive impairment. The present study investigated the effect of nicotinamide (NAM) on CCH-induced cognitive impairment and white matter damage in mice. Male C57Bl/6J mice aged 10-12 weeks (mean age = 11 ± 1 weeks) and weighing 24 - 29 g (mean weight = 26.5 ± 2.5 g) were randomly assigned to three groups (eight mice/group): sham group, CCH group and NAM group. Chronic cerebral hypoperfusion (CCH) was induced using standard methods. The treatment group mice received intraperitoneal injection of NAM at a dose of 200 mg/kg body weight (bwt) daily for 30 days. Learning, memory, anxiety, and depression-like behaviors were measured using Morris water maze test (MWMT), open field test (OFT), sucrose preference test (SPT), and forced swim test (FST), respectively. White matter damage and remodeling were determined via histological/ immunohistochemical analyses, and western blotting, respectively. The results showed that the time spent in target quadrant, number of crossings and escape latency were significantly lower in CCH group than in sham group, but they were significantly increased by NAM (p < 0.05). Mice in NAM group moved significantly faster and covered longer distances, when compared with those in CCH group (p < 0.05). The percentage of time spent in open arms and the number of entries to the open arms were significantly lower in CCH group than in NAM group (p < 0.05). Moreover, anhedonia and histologic scores (index of myelin injury) were significantly higher in CCH group than in sham group, but they were significantly reduced by NAM (p < 0.05). The results of immunohistochemical staining and Western blotting showed that the protein expressions of 2', 3'-cyclic-nucleotide 3'-phosphodiesterase (CNPase) and synaptophysin were significantly downregulated in CCH group, relative to sham group, but they were significantly upregulated by NAM (p < 0.05). These results indicate that NAM improves cognitive function in mice with CCH.Normal brain function requires steady blood supply to maintain stable energy state. When blood supply to the brain becomes suboptimal for a long period of time, chronic cerebral hypoperfusion (CCH) and a variety of brain changes may occur. CCH causes white matter injury and cognitive impairment. The present study investigated the effect of nicotinamide (NAM) on CCH-induced cognitive impairment and white matter damage in mice. Male C57Bl/6J mice aged 10-12 weeks (mean age = 11 ± 1 weeks) and weighing 24 - 29 g (mean weight = 26.5 ± 2.5 g) were randomly assigned to three groups (eight mice/group): sham group, CCH group and NAM group. Chronic cerebral hypoperfusion (CCH) was induced using standard methods. The treatment group mice received intraperitoneal injection of NAM at a dose of 200 mg/kg body weight (bwt) daily for 30 days. Learning, memory, anxiety, and depression-like behaviors were measured using Morris water maze test (MWMT), open field test (OFT), sucrose preference test (SPT), and forced swim test (FST), respectively. White matter damage and remodeling were determined via histological/ immunohistochemical analyses, and western blotting, respectively. The results showed that the time spent in target quadrant, number of crossings and escape latency were significantly lower in CCH group than in sham group, but they were significantly increased by NAM (p < 0.05). Mice in NAM group moved significantly faster and covered longer distances, when compared with those in CCH group (p < 0.05). The percentage of time spent in open arms and the number of entries to the open arms were significantly lower in CCH group than in NAM group (p < 0.05). Moreover, anhedonia and histologic scores (index of myelin injury) were significantly higher in CCH group than in sham group, but they were significantly reduced by NAM (p < 0.05). The results of immunohistochemical staining and Western blotting showed that the protein expressions of 2', 3'-cyclic-nucleotide 3'-phosphodiesterase (CNPase) and synaptophysin were significantly downregulated in CCH group, relative to sham group, but they were significantly upregulated by NAM (p < 0.05). These results indicate that NAM improves cognitive function in mice with CCH. Normal brain function requires steady blood supply to maintain stable energy state. When blood supply to the brain becomes suboptimal for a long period of time, chronic cerebral hypoperfusion (CCH) and a variety of brain changes may occur. CCH causes white matter injury and cognitive impairment. The present study investigated the effect of nicotinamide (NAM) on CCH-induced cognitive impairment and white matter damage in mice. Male C57Bl/6J mice aged 10-12 weeks (mean age = 11 ± 1 weeks) and weighing 24 - 29 g (mean weight = 26.5 ± 2.5 g) were randomly assigned to three groups (eight mice/group): sham group, CCH group and NAM group. Chronic cerebral hypoperfusion (CCH) was induced using standard methods. The treatment group mice received intraperitoneal injection of NAM at a dose of 200 mg/kg body weight (bwt) daily for 30 days. Learning, memory, anxiety, and depression-like behaviors were measured using Morris water maze test (MWMT), open field test (OFT), sucrose preference test (SPT), and forced swim test (FST), respectively. White matter damage and remodeling were determined via histological/ immunohistochemical analyses, and western blotting, respectively. The results showed that the time spent in target quadrant, number of crossings and escape latency were significantly lower in CCH group than in sham group, but they were significantly increased by NAM ( < 0.05). Mice in NAM group moved significantly faster and covered longer distances, when compared with those in CCH group ( < 0.05). The percentage of time spent in open arms and the number of entries to the open arms were significantly lower in CCH group than in NAM group ( < 0.05). Moreover, anhedonia and histologic scores (index of myelin injury) were significantly higher in CCH group than in sham group, but they were significantly reduced by NAM ( < 0.05). The results of immunohistochemical staining and Western blotting showed that the protein expressions of 2', 3'-cyclic-nucleotide 3'-phosphodiesterase (CNPase) and synaptophysin were significantly downregulated in CCH group, relative to sham group, but they were significantly upregulated by NAM ( < 0.05). These results indicate that NAM improves cognitive function in mice with CCH. Normal brain function requires steady blood supply to maintain stable energy state. When blood supply to the brain becomes suboptimal for a long period of time, chronic cerebral hypoperfusion (CCH) and a variety of brain changes may occur. CCH causes white matter injury and cognitive impairment. The present study investigated the effect of nicotinamide (NAM) on CCH-induced cognitive impairment and white matter damage in mice. Male C57Bl/6J mice aged 10–12 weeks (mean age = 11 ± 1 weeks) and weighing 24 - 29 g (mean weight = 26.5 ± 2.5 g) were randomly assigned to three groups (eight mice/group): sham group, CCH group and NAM group. Chronic cerebral hypoperfusion (CCH) was induced using standard methods. The treatment group mice received intraperitoneal injection of NAM at a dose of 200 mg/kg body weight (bwt) daily for 30 days. Learning, memory, anxiety, and depression-like behaviors were measured using Morris water maze test (MWMT), open field test (OFT), sucrose preference test (SPT), and forced swim test (FST), respectively. White matter damage and remodeling were determined via histological/ immunohistochemical analyses, and western blotting, respectively. The results showed that the time spent in target quadrant, number of crossings and escape latency were significantly lower in CCH group than in sham group, but they were significantly increased by NAM (p < 0.05). Mice in NAM group moved significantly faster and covered longer distances, when compared with those in CCH group (p < 0.05). The percentage of time spent in open arms and the number of entries to the open arms were significantly lower in CCH group than in NAM group (p < 0.05). Moreover, anhedonia and histologic scores (index of myelin injury) were significantly higher in CCH group than in sham group, but they were significantly reduced by NAM (p < 0.05). The results of immunohistochemical staining and Western blotting showed that the protein expressions of 2′, 3′-cyclic-nucleotide 3′-phosphodiesterase (CNPase) and synaptophysin were significantly downregulated in CCH group, relative to sham group, but they were significantly upregulated by NAM (p < 0.05). These results indicate that NAM improves cognitive function in mice with CCH. |
| Author | Liu, Bin Shi, Jingping Jin, Ling Zhao, Guifeng |
| AuthorAffiliation | 3 Department of Neurology, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing Brain Hospital , Nanjing , China 1 Department of Geriatrics, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing Brain Hospital , Nanjing , China 2 Key Laboratory of Research and Application of Animal Models for Environmental and Metabolic Diseases, Sheng Jing Hospital of China Medical University , Shenyang , China |
| AuthorAffiliation_xml | – name: 2 Key Laboratory of Research and Application of Animal Models for Environmental and Metabolic Diseases, Sheng Jing Hospital of China Medical University , Shenyang , China – name: 3 Department of Neurology, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing Brain Hospital , Nanjing , China – name: 1 Department of Geriatrics, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing Brain Hospital , Nanjing , China |
| Author_xml | – sequence: 1 givenname: Bin surname: Liu fullname: Liu, Bin – sequence: 2 givenname: Guifeng surname: Zhao fullname: Zhao, Guifeng – sequence: 3 givenname: Ling surname: Jin fullname: Jin, Ling – sequence: 4 givenname: Jingping surname: Shi fullname: Shi, Jingping |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33569040$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_3390_nu14153231 crossref_primary_10_3389_fimmu_2023_1273570 crossref_primary_10_1038_s41467_023_37286_2 crossref_primary_10_3389_fmed_2024_1379335 crossref_primary_10_3390_bioengineering10070871 crossref_primary_10_3390_cells14020074 |
| Cites_doi | 10.1016/S1474-4422(19)30079-1 10.4103/bc.bc_15_18 10.1097/01.WCB.0000122746.72175.0e 10.1155/2018/2413841 10.1126/science.aal0092 10.3389/fnagi.2019.00378 10.1002/jnr.23777 10.1016/j.neuroscience.2014.12.054 10.3389/fnins.2018.00339 10.1177/0271678X17743670 10.1212/WNL.0000000000009890 10.1007/s11357-020-00164-6 10.1007/978-3-7091-6139-5_3 10.1177/1178646918776658 10.1159/000147098 10.1007/s12035-016-9915-1 10.1089/neu.2016.4486 10.1016/j.brainres.2019.146337 10.3390/ijms21031095 10.1016/j.neuroscience.2016.02.058 10.1016/S0091-3057(02)00939-5 10.3390/ijms20246176 10.1016/j.neuroscience.2019.04.044 10.1016/j.brainres.2006.10.019 10.1016/j.cmet.2016.05.006 10.1212/wnl.0000000000007654 10.1161/STROKEAHA.115.011679 10.1111/jnc.14271 10.1042/CS20160380 10.1039/C9FO01780A 10.1002/jnr.21925 10.1007/s11306-019-1604-4 10.1016/j.pbb.2013.10.021 10.1177/0271678X17736963 10.1016/j.brainres.2019.01.017 10.3233/JAD-190369 10.2174/156720512800107555 10.1016/j.arr.2016.09.007 10.1182/blood-2013-09-512749 10.1002/dneu.22627 10.1007/s11845-020-02385-2 10.5935/0004-2749.20170019 10.3390/ijms20174196 10.1155/2017/7019803 10.1097/00004647-200201000-00012 10.1007/s10072-014-2014-z |
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| Copyright | Copyright © 2021 Liu, Zhao, Jin and Shi. Copyright © 2021 Liu, Zhao, Jin and Shi. 2021 Liu, Zhao, Jin and Shi |
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| Keywords | white matter cognitive impairment memory chronic cerebral hypoperfusion nicotinamide |
| Language | English |
| License | Copyright © 2021 Liu, Zhao, Jin and Shi. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 This article was submitted to Neuropharmacology, a section of the journal Frontiers in Neurology Edited by: Santiago Perez-Lloret, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina Reviewed by: Lucas Daniel Udovin, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina; Vinod Tiwari, Indian Institute of Technology (BHU), India These authors share first authorship |
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| Title | Nicotinamide Improves Cognitive Function in Mice With Chronic Cerebral Hypoperfusion |
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