» Articles » PMID: 25422636

Inflammatory Response and Neuronal Necrosis in Rats with Cerebral Ischemia

Overview
Date 2014 Nov 26
PMID 25422636
Citations 9
Authors
Affiliations
Soon will be listed here.
Abstract

In the middle cerebral artery occlusion model of ischemic injury, inflammation primarily occurs in the infarct and peripheral zones. In the ischemic zone, neurons undergo necrosis and apoptosis, and a large number of reactive microglia are present. In the present study, we investigated the pathological changes in a rat model of middle cerebral artery occlusion. Neuronal necrosis appeared 12 hours after middle cerebral artery occlusion, and the peak of neuronal apoptosis appeared 4 to 6 days after middle cerebral artery occlusion. Inflammatory cytokines and microglia play a role in damage and repair after middle cerebral artery occlusion. Serum intercellular cell adhesion molecule-1 levels were positively correlated with the permeability of the blood-brain barrier. These findings indicate that intercellular cell adhesion molecule-1 may be involved in blood-brain barrier injury, microglial activation, and neuronal apoptosis. Inhibiting blood-brain barrier leakage may alleviate neuronal injury following ischemia.

Citing Articles

Rutaecarpine Attenuates Oxidative Stress-Induced Traumatic Brain Injury and Reduces Secondary Injury the PGK1/KEAP1/NRF2 Signaling Pathway.

Xu M, Li L, Liu H, Lu W, Ling X, Gong M Front Pharmacol. 2022; 13:807125.

PMID: 35529443 PMC: 9070303. DOI: 10.3389/fphar.2022.807125.


The Effect of the -ε4 Allele on the Cholinergic Circuitry for Subjects With Different Levels of Cognitive Impairment.

Lai Y, Chen K, Lee T, Tso C, Lin H, Kuo L Front Neurol. 2021; 12:651388.

PMID: 34721251 PMC: 8548434. DOI: 10.3389/fneur.2021.651388.


Pathways Involved in Remyelination after Cerebral Ischemia.

Garcia-Martin G, Alcover-Sanchez B, Wandosell F, Cubelos B Curr Neuropharmacol. 2021; 20(4):751-765.

PMID: 34151767 PMC: 9878953. DOI: 10.2174/1570159X19666210610093658.


Cholinergic Modulation of Glial Function During Aging and Chronic Neuroinflammation.

Gamage R, Wagnon I, Rossetti I, Childs R, Niedermayer G, Chesworth R Front Cell Neurosci. 2020; 14:577912.

PMID: 33192323 PMC: 7594524. DOI: 10.3389/fncel.2020.577912.


Hypoxia-inducible factor-1 alpha is involved in RIP-induced necroptosis caused by in vitro and in vivo ischemic brain injury.

Yang X, Yi T, Zhang S, Xu Z, Yu Z, Sun H Sci Rep. 2017; 7(1):5818.

PMID: 28724891 PMC: 5517428. DOI: 10.1038/s41598-017-06088-0.


References
1.
Muir K, Tyrrell P, Sattar N, Warburton E . Inflammation and ischaemic stroke. Curr Opin Neurol. 2007; 20(3):334-42. DOI: 10.1097/WCO.0b013e32813ba151. View

2.
Peng H, Du J, Zhang G, Kuang X, Liu Y, Qian Z . Neuroprotective effect of Z-ligustilide against permanent focal ischemic damage in rats. Biol Pharm Bull. 2007; 30(2):309-12. DOI: 10.1248/bpb.30.309. View

3.
Kettenmann H, Hanisch U, Noda M, Verkhratsky A . Physiology of microglia. Physiol Rev. 2011; 91(2):461-553. DOI: 10.1152/physrev.00011.2010. View

4.
Horky M, Wurzer G, Kotala V, Anton M, Vojtesek B, Vacha J . Segregation of nucleolar components coincides with caspase-3 activation in cisplatin-treated HeLa cells. J Cell Sci. 2001; 114(Pt 4):663-70. DOI: 10.1242/jcs.114.4.663. View

5.
Lawson C, Wolf S . ICAM-1 signaling in endothelial cells. Pharmacol Rep. 2009; 61(1):22-32. DOI: 10.1016/s1734-1140(09)70004-0. View