ArticleNeurocritical care2018
The Effect of Therapeutic Mild Hypothermia on Brain Microvascular Endothelial Cells During Ischemia-Reperfusion Injury.
Article in Neurocritical care, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Hypothermia improves neuronal network recovery in a human-derived in vitro model of oxygen-deprivation.PloS one · 2024Article
- The Effects of Temperature Management on Brain Microcirculation, Oxygenation and Metabolism.Brain sciences · 2022Article
- The Role of Sphingomyelin Metabolism in the Protection of Rat Brain Microvascular Endothelial Cells by Mild Hypothermia.Neurocritical care · 2022Article
- Propofol Mediated Protection of the Brain From Ischemia/Reperfusion Injury Through the Regulation of Microglial Connexin 43.Frontiers in cell and developmental biology · 2021Article
- X-Ray Causes mRNA Transcripts Change to Enhance Orai2-Mediated CaFrontiers in molecular biosciences · 2021Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundTo determine the cerebral protective effects of mild hypothermia (MH) on cerebral microcirculation.
methodsWe established ischemia-reperfusion (I/R) injury and MH treatment models with rat brain microvascular endothelial cells (RBMECs) in vitro and examined the apoptotic changes. The cultured RBMECs were randomly divided into the control group, I/R group, and MH group, which was further divided into two subgroups: intra-ischemia hypothermia (IIH) and post-ischemia hypothermia (PIH). Cell morphological changes were assessed using fluorescence microscopy. Apoptotic rates were obtained by flow cytometry. Expressions of caspase-3, Bax, and Bcl-2 were analyzed by Western blot.
resultsI/R injury in vitro induced apoptosis of RBMECs. The apoptotic rates in the control group, I/R group, and MH group were 0.13, 19.04, and 13.13%, respectively (P < 0.01). Compared with the I/R group, the MH group showed a significant decrease in the number of apoptotic cells, mainly in stage I apoptotic cells (P < 0.0083). The caspase-3 and Bax expressions were significantly enhanced (P < 0.05) in RBMECs after I/R injury, while substantial decreases in Bcl-2 expression were noted (P < 0.05). Following MH intervention, the increase in caspase-3 and Bax expression was suppressed (P < 0.05), while Bcl-2 expression significantly increased. The apoptotic rates or protein expressions between the two subgroups were not different significantly (P > 0.05).
conclusionsThese results indicate that MH could inhibit RBMEC apoptosis by preventing pro-apoptotic cells and early apoptotic cells from progressing to intermediate and advanced stages. This may be due to the effect of MH on I/R-induced apoptotic gene expression changes.
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Registered trials
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