Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Remote ischemic conditioning (RIC) has attracted considerable attention as a brain protection strategy, although its impact remains unclear. Hypothermia is the most effective strategy in experimental transient cerebral ischemia. Therefore, we compared the efficacy of RIC, hypothermia, and no treatment on cerebral ischemia. We assessed the effects of both permanent and transient middle cerebral artery occlusion (MCAO) for 45 min in male mice. Brain hemodynamics were monitored during and after the procedure via 2D color-coded ultrasound imaging. Ischemic lesions on magnetic resonance imaging (MRI)-diffusion-weighted imaging (DWI), early breakdown of microtubule-associated protein 2 (MAP2), expression levels of inflammatory cytokines by reverse transcriptase quantitative polymerase chain reaction (RT-qPCR), and neurological signs and infarct volume were examined. In permanent MCAO, RIC increased cerebral blood flow (CBF) in the peri-infarct area, reduced early lesions on MRI-DWI, decreased early MAP2 breakdown, and lowered infarct volume compared with no treatment. However, hypothermia only showed a protective effect against neurological signs. In contrast, in transient MCAO, both RIC and hypothermia reduced the expression of inflammatory cytokines, mitigated MAP2 breakdown, and reduced infarct volume to a similar extent compared with no treatment. In conclusion, although RIC proved to be more effective than hypothermia in permanent MCAO, the protective effects of RIC and hypothermia were comparable in transient cerebral ischemia. Thus, RIC could be a promising strategy for brain protection against cerebral ischemia.

Download full-text PDF

Source
http://dx.doi.org/10.1002/jnr.70003DOI Listing

Publication Analysis

Top Keywords

cerebral ischemia
20
transient cerebral
12
ric hypothermia
12
infarct volume
12
remote ischemic
8
ischemic conditioning
8
hypothermia permanent
8
permanent transient
8
male mice
8
brain protection
8

Similar Publications

The GPR120 agonist TUG-891 mitigates ischemic brain injury by attenuating endoplasmic reticulum stress and apoptosis via the PI3K/AKT signaling pathway.

Neurotherapeutics

September 2025

Department of Neurology, Peking University Third Hospital, Beijing, 100191, China; Beijing Key Laboratory of Biomarker and Translational Research in Neurodegenerative Diseases, Beijing, 100191, China; Key Laboratory for Neuroscience, National Health Commission/Ministry of Education, Peking Universit

Extensive research has confirmed that omega-3 fatty acids provide cardiovascular protection primarily by activating the G protein-coupled receptor 120 (GPR120) signaling pathway. However, natural activators of this receptor often lack sufficient strength and precision. TUG-891, a recently synthesized selective GPR120 activator, has displayed significant therapeutic potential in multiple disease.

View Article and Find Full Text PDF

Effect of Celsior Cold Storage on Warm Ischemia-Induced Myocardial Plasma Membrane Damage and Pyroptosis in Human Hearts from Circulatory Death Donors.

J Thorac Cardiovasc Surg

September 2025

, Michael E. DeBakey Department of Surgery, Division of Cardiothoracic Transplantation and Circulatory Support, Baylor College of Medicine, Houston, Texas, USA; , Department of Regenerative Medicine Research, Texas Heart Institute, Houston, Texas, USA. Electronic address:

Objective: Celsior solution (CS) is used for cold preservation of hearts from brain death donors but not for those from circulatory death donors (DCD). Plasma membrane repair proteins are crucial for maintaining myocardial integrity during ischemia. We compared the effects of CS cold preservation with normal saline (NS) on myocardial membrane disruption and pyroptosis in human DCD hearts, with varying warm ischemia times (WIT) and cold storage durations.

View Article and Find Full Text PDF

The molecular mechanisms and therapeutic implications of PANoptosis in ischemic diseases.

Apoptosis

September 2025

Key Laboratory of Emergency and Trauma of the Ministry of Education, Department of Interventional Radiology and Vascular Surgery, First Affiliated Hospital of Hainan Medical University, Hainan Medical University, 31 Longhua Road, Longhua District, Haikou City, Hainan Province, China.

The singular forms of programmed cell death (PCD), including pyroptosis, apoptosis, and necroptosis, are inadequate for comprehensively elucidating the complex pathological mechanisms underlying ischemic diseases. PANoptosis is a unique lytic, innate immune, and inflammatory cell death pathway, initiated by innate immune sensors and driven by caspases and RIPKs through PANoptosome complexes. In diseases like cerebral ischemia, retinal ischemia, myocardial ischemia, renal ischemia, and spinal cord ischemia, targeting key regulatory factors of PANoptosis can help mitigate tissue damage.

View Article and Find Full Text PDF

Background: Current neurovascular unit isolation requires processing brain microvascular endothelial cells (BMECs) and neurons from separate animals, preventing concurrent analysis of neurovascular crosstalk within identical genetic/physiological contexts.

New Methods: We developed an enzymatic digestion/bovine serum albumin density gradient technique that enables the simultaneous isolation of neural tissue and microvascular segments from individual mice. The neural tissue was filtered and centrifuged for primary cortical neuron culture on poly-L-lysine-coated plates.

View Article and Find Full Text PDF

Glutamate-mediated excitotoxicity represents a common pathomechanism in neurological disorders. As the predominant glutamate transporter in the central nervous system, glutamate transporter 1 (GLT-1, known as EAAT2 in humans) plays a crucial role in maintaining glutamate homeostasis and preventing excitotoxicity through its Na⁺-dependent transport mechanism. Key functions of GLT-1 include reducing extracellular glutamate concentration, regulating calcium homeostasis, suppressing oxidative stress, preserving mitochondrial integrity, and modulating neuroinflammatory processes by limiting microglial activation.

View Article and Find Full Text PDF