Publication

Neuroprotection by Insulin-like Growth Factor-1 in Rats with Ischemic Stroke is Associated with Microglial Changes and a Reduction in Neuroinflammation

Serhan, A., Aerts, J. L., Boddeke, E. W. G. M. & Kooijman, R., 1-Feb-2020, In : Neuroscience. 426, p. 101-114 14 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Serhan, A., Aerts, J. L., Boddeke, E. W. G. M., & Kooijman, R. (2020). Neuroprotection by Insulin-like Growth Factor-1 in Rats with Ischemic Stroke is Associated with Microglial Changes and a Reduction in Neuroinflammation. Neuroscience, 426, 101-114. https://doi.org/10.1016/j.neuroscience.2019.11.035

Author

Serhan, Ahmad ; Aerts, Joeri L. ; Boddeke, Erik W. G. M. ; Kooijman, Ron. / Neuroprotection by Insulin-like Growth Factor-1 in Rats with Ischemic Stroke is Associated with Microglial Changes and a Reduction in Neuroinflammation. In: Neuroscience. 2020 ; Vol. 426. pp. 101-114.

Harvard

Serhan, A, Aerts, JL, Boddeke, EWGM & Kooijman, R 2020, 'Neuroprotection by Insulin-like Growth Factor-1 in Rats with Ischemic Stroke is Associated with Microglial Changes and a Reduction in Neuroinflammation', Neuroscience, vol. 426, pp. 101-114. https://doi.org/10.1016/j.neuroscience.2019.11.035

Standard

Neuroprotection by Insulin-like Growth Factor-1 in Rats with Ischemic Stroke is Associated with Microglial Changes and a Reduction in Neuroinflammation. / Serhan, Ahmad; Aerts, Joeri L.; Boddeke, Erik W. G. M.; Kooijman, Ron.

In: Neuroscience, Vol. 426, 01.02.2020, p. 101-114.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Serhan A, Aerts JL, Boddeke EWGM, Kooijman R. Neuroprotection by Insulin-like Growth Factor-1 in Rats with Ischemic Stroke is Associated with Microglial Changes and a Reduction in Neuroinflammation. Neuroscience. 2020 Feb 1;426:101-114. https://doi.org/10.1016/j.neuroscience.2019.11.035


BibTeX

@article{64722297e35a4618994b05cb8a47c480,
title = "Neuroprotection by Insulin-like Growth Factor-1 in Rats with Ischemic Stroke is Associated with Microglial Changes and a Reduction in Neuroinflammation",
abstract = "We and others have shown that insulin-like growth factor-1 (IGF-1) is neuroprotective when administered systemically shortly following stroke. In the current study, we addressed the hypothesis that microglia mediate neuroprotection by IGF-1 following ischemic stroke. Furthermore, we investigated whether IGF-1 modulates pro- and anti-inflammatory mediators in ischemic brain with a special reference to microglia. Ischemic stroke was induced in normal conscious Wistar rats by infusing the vasoconstrictor, endothelin-1 (Et-1), next to middle cerebral artery (MCA). IGF-1 (300 mu g) was injected subcutaneously (SC) at 30 and 120 min following stroke. Microglial inhibitor, minocycline, was injected intraperitoneally (IP) at 1 h before stroke (25 mg/kg) and 11 h after stroke (45 mg/kg). Post-stroke IGF-1 treatment reduced the infarct size and increased the sensorimotor function which coincided with an increase in the number of ameboid microglia in the ischemic cortex. Minocycline treatment abrogated the increase in ameboid microglia by IGF-1, while the effect of IGF-1 in the reduction of infarct size was only partially affected. IGF-1 suppressed mRNA expression of inducible nitric oxide synthase (iNOS) and interleukin (IL)-1 beta in the ischemic hemisphere, while in purified microglia, only iNOS expression levels were reduced. Our findings show that microglia are a target for IGF-1 and that neuroprotection by IGF-1 coincides with down-regulation of inflammatory mediators which could be instrumental to the beneficial effects. (C) 2019 IBRO. Published by Elsevier Ltd. All rights reserved.",
keywords = "inflammation, neuroprotection, microglia, ischemic stroke, IGF-1, FOCAL CEREBRAL-ISCHEMIA, IGF-I, ACTIVATED MICROGLIA, BRAIN-DAMAGE, NEUTROPHILS, RECEPTOR, INFLAMMATION, IMPAIRMENT, ALTEPLASE, INVASION",
author = "Ahmad Serhan and Aerts, {Joeri L.} and Boddeke, {Erik W. G. M.} and Ron Kooijman",
year = "2020",
month = "2",
day = "1",
doi = "10.1016/j.neuroscience.2019.11.035",
language = "English",
volume = "426",
pages = "101--114",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "PERGAMON-ELSEVIER SCIENCE LTD",

}

RIS

TY - JOUR

T1 - Neuroprotection by Insulin-like Growth Factor-1 in Rats with Ischemic Stroke is Associated with Microglial Changes and a Reduction in Neuroinflammation

AU - Serhan, Ahmad

AU - Aerts, Joeri L.

AU - Boddeke, Erik W. G. M.

AU - Kooijman, Ron

PY - 2020/2/1

Y1 - 2020/2/1

N2 - We and others have shown that insulin-like growth factor-1 (IGF-1) is neuroprotective when administered systemically shortly following stroke. In the current study, we addressed the hypothesis that microglia mediate neuroprotection by IGF-1 following ischemic stroke. Furthermore, we investigated whether IGF-1 modulates pro- and anti-inflammatory mediators in ischemic brain with a special reference to microglia. Ischemic stroke was induced in normal conscious Wistar rats by infusing the vasoconstrictor, endothelin-1 (Et-1), next to middle cerebral artery (MCA). IGF-1 (300 mu g) was injected subcutaneously (SC) at 30 and 120 min following stroke. Microglial inhibitor, minocycline, was injected intraperitoneally (IP) at 1 h before stroke (25 mg/kg) and 11 h after stroke (45 mg/kg). Post-stroke IGF-1 treatment reduced the infarct size and increased the sensorimotor function which coincided with an increase in the number of ameboid microglia in the ischemic cortex. Minocycline treatment abrogated the increase in ameboid microglia by IGF-1, while the effect of IGF-1 in the reduction of infarct size was only partially affected. IGF-1 suppressed mRNA expression of inducible nitric oxide synthase (iNOS) and interleukin (IL)-1 beta in the ischemic hemisphere, while in purified microglia, only iNOS expression levels were reduced. Our findings show that microglia are a target for IGF-1 and that neuroprotection by IGF-1 coincides with down-regulation of inflammatory mediators which could be instrumental to the beneficial effects. (C) 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

AB - We and others have shown that insulin-like growth factor-1 (IGF-1) is neuroprotective when administered systemically shortly following stroke. In the current study, we addressed the hypothesis that microglia mediate neuroprotection by IGF-1 following ischemic stroke. Furthermore, we investigated whether IGF-1 modulates pro- and anti-inflammatory mediators in ischemic brain with a special reference to microglia. Ischemic stroke was induced in normal conscious Wistar rats by infusing the vasoconstrictor, endothelin-1 (Et-1), next to middle cerebral artery (MCA). IGF-1 (300 mu g) was injected subcutaneously (SC) at 30 and 120 min following stroke. Microglial inhibitor, minocycline, was injected intraperitoneally (IP) at 1 h before stroke (25 mg/kg) and 11 h after stroke (45 mg/kg). Post-stroke IGF-1 treatment reduced the infarct size and increased the sensorimotor function which coincided with an increase in the number of ameboid microglia in the ischemic cortex. Minocycline treatment abrogated the increase in ameboid microglia by IGF-1, while the effect of IGF-1 in the reduction of infarct size was only partially affected. IGF-1 suppressed mRNA expression of inducible nitric oxide synthase (iNOS) and interleukin (IL)-1 beta in the ischemic hemisphere, while in purified microglia, only iNOS expression levels were reduced. Our findings show that microglia are a target for IGF-1 and that neuroprotection by IGF-1 coincides with down-regulation of inflammatory mediators which could be instrumental to the beneficial effects. (C) 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

KW - inflammation

KW - neuroprotection

KW - microglia

KW - ischemic stroke

KW - IGF-1

KW - FOCAL CEREBRAL-ISCHEMIA

KW - IGF-I

KW - ACTIVATED MICROGLIA

KW - BRAIN-DAMAGE

KW - NEUTROPHILS

KW - RECEPTOR

KW - INFLAMMATION

KW - IMPAIRMENT

KW - ALTEPLASE

KW - INVASION

U2 - 10.1016/j.neuroscience.2019.11.035

DO - 10.1016/j.neuroscience.2019.11.035

M3 - Article

VL - 426

SP - 101

EP - 114

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

ER -

ID: 116877444