Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway

Lan Xian-wu; Cui Liang; Gui Wen-shan

doi:doi:10.11648/j.ajim.20170504.11

| Peer-Reviewed

Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway

Lan Xian-wu, Cui Liang, Gui Wen-shan

Published in American Journal of Internal Medicine (Volume 5, Issue 4)

Received: 28 March 2017 Accepted: 10 April 2017 Published: 15 June 2017

Views: Downloads:

Download PDF

Share This Article

Twitter
Linked In
Facebook

Abstract

Objective To observe the abnormal expression of IL-1βin hippocampus after bilateral common carotid artery ligation and to evaluate its effects on memory impairment induced by chronic cerebral ischemia. Methods Bilateral common carotid artery ligation (2-vessel occlusion, 2VO) was performed in wild type (Wild Type WT) and interleukin -1 receptor knock-out (IL-1 Resept Knock Out, IL-1R KO) C57 mice (male) to produce chronic cerebral ischemia mouse models. After the operation, their memory was detected with eight-arm radial maze test and the novel object recognition test, and the level of IL-1β and BDNF in hippocampus was detected with Western Blot. Results The average number of working memory errors of the KO-2VO mice was significantly decreased (P<0.05), and the recognition index was significantly increased (P<0.05) compared with those of the WT-2VO mice. Dramatic decrease in IL-1β in hippocampus (P<0.05) and substantial increase in BDNF (P<0.05) were observed in the KO-2VO mice. In the behavioral experiment and Western Blot, there was no significant difference between the KO-sham mice and the WT-sham controls. Conclusion Increase in the level of the IL-1β in hippocampus after bilateral common carotid artery ligation can lead to decrease in the level of the BDNF, which may cause memory impairment.

Published in	American Journal of Internal Medicine (Volume 5, Issue 4)
DOI	10.11648/j.ajim.20170504.11
Page(s)	52-56
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Chronic Cerebral Ischemia, Bilateral Common Carotid Artery Ligation, Microglia, Interleukin-1β,Brain-Derived Neurotrophic Factor (BDNF), Working Memory Impairment

References

[1]	Sivakumar L, Camicioli R, Butcher K. Factors associated with cognitive decline in transient ischemic attack patients. Can J Neurol Sci, 2014, 41(3):303-13.
[2]	Amantea D, Nappi G, Bernardi G, Bagetta G, Corasaniti MT. Post-ischemic brain damage: pathophysiology and role of inflammatory mediators. Febs Journal, 2009, 276(1):13-26.
[3]	Zhou Y, Zhang J, Wang L, Chen Y, Wan Y, He Y, et al. Interleukin-1β impedes oligodendrocyte progenitor cell recruitment and white matter repair following chronic cerebral hypoperfusion. Brain Behav Immun, 2017, 60:93-105.
[4]	Leal G, Afonso PM, Salazar IL, Duarte. Regulation of hippocampal synaptic plasticity by BDNF. Brain Research, 2014, 1621:82-101.
[5]	Chen G, FU Q, Cao J, Mi W. Effect of propofol on brain-derived neurotrophic factor and tyrosine kinase receptor B in the hippocampus of aged rats with chronic cerebral ischemia. Neural Regen Res, 2012,7(21):1645-9.
[6]	Tanila H. The role of BDNF in Alzheimer's disease. Neurobiol Dis, 2017,97(Pt B):114-118.
[7]	Toyama K, Koibuchi N, Uekawa K, Hasegawa Y, Kataoka K, Katayama T, et al. Apoptosis signal regulating kinase 1 is a novel target molecule for cognitive impairment induced by chronic cerebral hypoperfusion. Arterioscler Tthromb Vvasc Biol, 2014,34( 3): 616-625.
[8]	Wang M, Norman JE, Srinivasan VJ, Rutledge JC. Metabolic, inflammatory, and microvascular determinants of white matter disease and cognitive decline. Am J Neurodegener Dis, 2016, 5(5):171-177.
[9]	Brassai A, Suvanjeiev RG, Bán EG, Lakatos M. Role of synaptic and nonsynaptic glutamate receptors in ischaemia induced neurotoxicity. Brain Res Bull, 2015, 112:1-6.
[10]	Shukla V, Shakya AK, Perez-Pinzon MA, Dave KR. Cerebral ischemic damage in diabetes: an inflammatory perspective. J Neuroinflammation, 2017,14(1):21.
[11]	Alawieh A, Elvington A, Tomlinson S. Complement in the Homeostatic and Ischemic Brain. Front Immunol, 2015,6:417.
[12]	Xiong XY, Liu L, Yang QW. Functions and mechanisms of microglia/macrophages in neuroinflammation and neurogenesis after stroke. Prog Neurobiol, 2016, 142:23-44.
[13]	Udeochu JC, Shea JM, Villeda SA. Microglia communication: Parallels between aging and Alzheimer's disease. Clin Exp Neuroimmunol, 2016, 7(2):114-125.
[14]	Ransohoff RM. How neuroinflammation contributes to neurodegeneration. Science, 2016, 353(6301):777-83.
[15]	Mizui T, Ishikawa Y, Kumanogoh H, Kojima M. Neurobiological actions by three distinct subtypes of brain-derived neurotrophic factor: Multi-ligand model of growth factor signaling. Pharmacol Res, 2016, 105:93-8.
[16]	Zhang ZH, Wu LN, Song JG, Li WQ. Correlations between cognitive impairment and brain?derived neurotrophic factor expression in the hippocampus of post-stroke depression rats. Mol Med Rep, 2012, 6(4):889-93.
[17]	Patterson SL. Immune dysregulation and cognitive vulnerability in the aging brain: Interactions of microglia, IL-1β, BDNF and synaptic plasticity. Neuropharmacology, 2015, 96(Pt A):11-8.

Cite This Article

Plain Text BibTeX RIS

APA Style

Lan Xian-wu, Cui Liang, Gui Wen-shan. (2017). Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway. American Journal of Internal Medicine, 5(4), 52-56. https://doi.org/10.11648/j.ajim.20170504.11

Copy | Download

ACS Style

Lan Xian-wu; Cui Liang; Gui Wen-shan. Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway. Am. J. Intern. Med. 2017, 5(4), 52-56. doi: 10.11648/j.ajim.20170504.11

Copy | Download

AMA Style

Lan Xian-wu, Cui Liang, Gui Wen-shan. Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway. Am J Intern Med. 2017;5(4):52-56. doi: 10.11648/j.ajim.20170504.11

Copy | Download

@article{10.11648/j.ajim.20170504.11,
  author = {Lan Xian-wu and Cui Liang and Gui Wen-shan},
  title = {Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway},
  journal = {American Journal of Internal Medicine},
  volume = {5},
  number = {4},
  pages = {52-56},
  doi = {10.11648/j.ajim.20170504.11},
  url = {https://doi.org/10.11648/j.ajim.20170504.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajim.20170504.11},
  abstract = {Objective To observe the abnormal expression of IL-1βin hippocampus after bilateral common carotid artery ligation and to evaluate its effects on memory impairment induced by chronic cerebral ischemia. Methods Bilateral common carotid artery ligation (2-vessel occlusion, 2VO) was performed in wild type (Wild Type WT) and interleukin -1 receptor knock-out (IL-1 Resept Knock Out, IL-1R KO) C57 mice (male) to produce chronic cerebral ischemia mouse models. After the operation, their memory was detected with eight-arm radial maze test and the novel object recognition test, and the level of IL-1β and BDNF in hippocampus was detected with Western Blot. Results The average number of working memory errors of the KO-2VO mice was significantly decreased (P<0.05), and the recognition index was significantly increased (P<0.05) compared with those of the WT-2VO mice. Dramatic decrease in IL-1β in hippocampus (P<0.05) and substantial increase in BDNF (P<0.05) were observed in the KO-2VO mice. In the behavioral experiment and Western Blot, there was no significant difference between the KO-sham mice and the WT-sham controls. Conclusion Increase in the level of the IL-1β in hippocampus after bilateral common carotid artery ligation can lead to decrease in the level of the BDNF, which may cause memory impairment.},
 year = {2017}
}

Copy | Download

TY  - JOUR
T1  - Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway
AU  - Lan Xian-wu
AU  - Cui Liang
AU  - Gui Wen-shan
Y1  - 2017/06/15
PY  - 2017
N1  - https://doi.org/10.11648/j.ajim.20170504.11
DO  - 10.11648/j.ajim.20170504.11
T2  - American Journal of Internal Medicine
JF  - American Journal of Internal Medicine
JO  - American Journal of Internal Medicine
SP  - 52
EP  - 56
PB  - Science Publishing Group
SN  - 2330-4324
UR  - https://doi.org/10.11648/j.ajim.20170504.11
AB  - Objective To observe the abnormal expression of IL-1βin hippocampus after bilateral common carotid artery ligation and to evaluate its effects on memory impairment induced by chronic cerebral ischemia. Methods Bilateral common carotid artery ligation (2-vessel occlusion, 2VO) was performed in wild type (Wild Type WT) and interleukin -1 receptor knock-out (IL-1 Resept Knock Out, IL-1R KO) C57 mice (male) to produce chronic cerebral ischemia mouse models. After the operation, their memory was detected with eight-arm radial maze test and the novel object recognition test, and the level of IL-1β and BDNF in hippocampus was detected with Western Blot. Results The average number of working memory errors of the KO-2VO mice was significantly decreased (P<0.05), and the recognition index was significantly increased (P<0.05) compared with those of the WT-2VO mice. Dramatic decrease in IL-1β in hippocampus (P<0.05) and substantial increase in BDNF (P<0.05) were observed in the KO-2VO mice. In the behavioral experiment and Western Blot, there was no significant difference between the KO-sham mice and the WT-sham controls. Conclusion Increase in the level of the IL-1β in hippocampus after bilateral common carotid artery ligation can lead to decrease in the level of the BDNF, which may cause memory impairment.
VL  - 5
IS  - 4
ER  -

Copy | Download

Author Information

Lan Xian-wu

Department of Cardiology, The First Affiliated Hospital of Jinan University, Guangzhou, People’s Republic of China
Cui Liang

Department of Cardiology, The First Affiliated Hospital of Jinan University, Guangzhou, People’s Republic of China
Gui Wen-shan

Department of Cardiology, The First Affiliated Hospital of Jinan University, Guangzhou, People’s Republic of China

Download PDF

Sections

Plain Text BibTeX RIS

APA Style

Lan Xian-wu, Cui Liang, Gui Wen-shan. (2017). Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway. American Journal of Internal Medicine, 5(4), 52-56. https://doi.org/10.11648/j.ajim.20170504.11

Copy | Download

ACS Style

Lan Xian-wu; Cui Liang; Gui Wen-shan. Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway. Am. J. Intern. Med. 2017, 5(4), 52-56. doi: 10.11648/j.ajim.20170504.11

Copy | Download

AMA Style

Lan Xian-wu, Cui Liang, Gui Wen-shan. Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway. Am J Intern Med. 2017;5(4):52-56. doi: 10.11648/j.ajim.20170504.11

Copy | Download

@article{10.11648/j.ajim.20170504.11,
  author = {Lan Xian-wu and Cui Liang and Gui Wen-shan},
  title = {Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway},
  journal = {American Journal of Internal Medicine},
  volume = {5},
  number = {4},
  pages = {52-56},
  doi = {10.11648/j.ajim.20170504.11},
  url = {https://doi.org/10.11648/j.ajim.20170504.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajim.20170504.11},
  abstract = {Objective To observe the abnormal expression of IL-1βin hippocampus after bilateral common carotid artery ligation and to evaluate its effects on memory impairment induced by chronic cerebral ischemia. Methods Bilateral common carotid artery ligation (2-vessel occlusion, 2VO) was performed in wild type (Wild Type WT) and interleukin -1 receptor knock-out (IL-1 Resept Knock Out, IL-1R KO) C57 mice (male) to produce chronic cerebral ischemia mouse models. After the operation, their memory was detected with eight-arm radial maze test and the novel object recognition test, and the level of IL-1β and BDNF in hippocampus was detected with Western Blot. Results The average number of working memory errors of the KO-2VO mice was significantly decreased (P<0.05), and the recognition index was significantly increased (P<0.05) compared with those of the WT-2VO mice. Dramatic decrease in IL-1β in hippocampus (P<0.05) and substantial increase in BDNF (P<0.05) were observed in the KO-2VO mice. In the behavioral experiment and Western Blot, there was no significant difference between the KO-sham mice and the WT-sham controls. Conclusion Increase in the level of the IL-1β in hippocampus after bilateral common carotid artery ligation can lead to decrease in the level of the BDNF, which may cause memory impairment.},
 year = {2017}
}

Copy | Download

TY  - JOUR
T1  - Chronic Cerebral Ischemia-Induced Memory Impairment After Inhibition of BDNF by Interleukin-1 Signaling Pathway
AU  - Lan Xian-wu
AU  - Cui Liang
AU  - Gui Wen-shan
Y1  - 2017/06/15
PY  - 2017
N1  - https://doi.org/10.11648/j.ajim.20170504.11
DO  - 10.11648/j.ajim.20170504.11
T2  - American Journal of Internal Medicine
JF  - American Journal of Internal Medicine
JO  - American Journal of Internal Medicine
SP  - 52
EP  - 56
PB  - Science Publishing Group
SN  - 2330-4324
UR  - https://doi.org/10.11648/j.ajim.20170504.11
AB  - Objective To observe the abnormal expression of IL-1βin hippocampus after bilateral common carotid artery ligation and to evaluate its effects on memory impairment induced by chronic cerebral ischemia. Methods Bilateral common carotid artery ligation (2-vessel occlusion, 2VO) was performed in wild type (Wild Type WT) and interleukin -1 receptor knock-out (IL-1 Resept Knock Out, IL-1R KO) C57 mice (male) to produce chronic cerebral ischemia mouse models. After the operation, their memory was detected with eight-arm radial maze test and the novel object recognition test, and the level of IL-1β and BDNF in hippocampus was detected with Western Blot. Results The average number of working memory errors of the KO-2VO mice was significantly decreased (P<0.05), and the recognition index was significantly increased (P<0.05) compared with those of the WT-2VO mice. Dramatic decrease in IL-1β in hippocampus (P<0.05) and substantial increase in BDNF (P<0.05) were observed in the KO-2VO mice. In the behavioral experiment and Western Blot, there was no significant difference between the KO-sham mice and the WT-sham controls. Conclusion Increase in the level of the IL-1β in hippocampus after bilateral common carotid artery ligation can lead to decrease in the level of the BDNF, which may cause memory impairment.
VL  - 5
IS  - 4
ER  -

Copy | Download