Galectin-3 ablation does not affect infarct size or inflammatory cytokines after experimental stroke in 24-month-old female mice
Manouchehrian, Oscar LU ; Andersson, Emelie LU
; Eriksson Hallberg, Björn
and Deierborg, Tomas
LU
(2022)
In NeuroReport
33(6).
p.266-271
- Abstract
- Background: The tissue damage following a focal stroke causes an inflammatory response that is thought to aggravate the disease state. Galectin-3 is a proinflammatory molecule that has been shown to play a significant role in the inflammatory responses in brain diseases and following experimental stroke. In most animal experiments, young animals are used, although attempts are often made to model diseases that affect the elderly. Therefore, in this project, we intended to investigate the role of Galectin-3 in experimental stroke in older mice.
Methods: In this project, 24-month-old (aged) female mice were subjected to an experimental stroke (permanent middle cerebral artery occlusion) 7 days before sacrifice. We wanted to investigate... (More) - Background: The tissue damage following a focal stroke causes an inflammatory response that is thought to aggravate the disease state. Galectin-3 is a proinflammatory molecule that has been shown to play a significant role in the inflammatory responses in brain diseases and following experimental stroke. In most animal experiments, young animals are used, although attempts are often made to model diseases that affect the elderly. Therefore, in this project, we intended to investigate the role of Galectin-3 in experimental stroke in older mice.
Methods: In this project, 24-month-old (aged) female mice were subjected to an experimental stroke (permanent middle cerebral artery occlusion) 7 days before sacrifice. We wanted to investigate whether the absence of the inflammatory protein Galectin-3 could affect motor phenotype, neuroinflammation and infarct size. Number of mice without Galectin-3 (Galectin-3 KO) = 9, number of wildtype controls of the same age = 6.
Results: In our aged female mice, we could not observe any significant differences between Galectin-3 KO and wildtype regarding the inclined plane test or cylinder test. We could not observe different infarct sizes between the two genotypes. In brain homogenates, we measured levels of 10 inflammatory cytokines, but we could not see any significant differences in any of them.
Conclusion: In summary, it can be said that the absence of the inflammatory mediator Galectin-3 does not seem to have a strong poststroke effect in aged females. Unfortunately, we could not analyze these mice with immunohistochemistry, which limited our study.
(Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/f5c312de-4d81-417d-96fd-c66fa95a1dca
- author
- Manouchehrian, Oscar
LU
; Andersson, Emelie
LU
; Eriksson Hallberg, Björn
and Deierborg, Tomas
LU
- organization
- publishing date
- 2022-04-06
- type
- Contribution to journal
- publication status
- published
- subject
- in
- NeuroReport
- volume
- 33
- issue
- 6
- pages
- 266 - 271
- publisher
- Lippincott Williams & Wilkins
- external identifiers
-
- pmid:35352699
- scopus:85128245319
- ISSN
- 1473-558X
- DOI
- 10.1097/WNR.0000000000001778
- language
- English
- LU publication?
- yes
- id
- f5c312de-4d81-417d-96fd-c66fa95a1dca
- date added to LUP
- 2022-04-13 14:06:48
- date last changed
- 2022-05-14 05:09:48
@article{f5c312de-4d81-417d-96fd-c66fa95a1dca,
abstract = {{Background: The tissue damage following a focal stroke causes an inflammatory response that is thought to aggravate the disease state. Galectin-3 is a proinflammatory molecule that has been shown to play a significant role in the inflammatory responses in brain diseases and following experimental stroke. In most animal experiments, young animals are used, although attempts are often made to model diseases that affect the elderly. Therefore, in this project, we intended to investigate the role of Galectin-3 in experimental stroke in older mice.<br/>Methods: In this project, 24-month-old (aged) female mice were subjected to an experimental stroke (permanent middle cerebral artery occlusion) 7 days before sacrifice. We wanted to investigate whether the absence of the inflammatory protein Galectin-3 could affect motor phenotype, neuroinflammation and infarct size. Number of mice without Galectin-3 (Galectin-3 KO) = 9, number of wildtype controls of the same age = 6.<br/>Results: In our aged female mice, we could not observe any significant differences between Galectin-3 KO and wildtype regarding the inclined plane test or cylinder test. We could not observe different infarct sizes between the two genotypes. In brain homogenates, we measured levels of 10 inflammatory cytokines, but we could not see any significant differences in any of them.<br/>Conclusion: In summary, it can be said that the absence of the inflammatory mediator Galectin-3 does not seem to have a strong poststroke effect in aged females. Unfortunately, we could not analyze these mice with immunohistochemistry, which limited our study.<br/>}},
author = {{Manouchehrian, Oscar and Andersson, Emelie and Eriksson Hallberg, Björn and Deierborg, Tomas}},
issn = {{1473-558X}},
language = {{eng}},
month = {{04}},
number = {{6}},
pages = {{266--271}},
publisher = {{Lippincott Williams & Wilkins}},
series = {{NeuroReport}},
title = {{Galectin-3 ablation does not affect infarct size or inflammatory cytokines after experimental stroke in 24-month-old female mice}},
url = {{http://dx.doi.org/10.1097/WNR.0000000000001778}},
doi = {{10.1097/WNR.0000000000001778}},
volume = {{33}},
year = {{2022}},
}