ArticleJournal of inflammation research2023
Effects of Cooling Interventions with Different Target Temperatures on Heat Stroke Rats.
Article in Journal of inflammation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed, 0 citations in OpenAlex.
- Histopathological and molecular mechanisms of multi-organ damage in heat stroke: Endothelial failure, immune crosstalk, and regulated cell death pathways.Histology and histopathology · 2026Review
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Purpose: To investigate the optimal target temperature of cooling intervention in heat stroke (HS) rats and explore the potential mechanisms of cooling intervention in alleviating heat stroke-induced damage. Materials and Methods: A total of 32 Sprague-Dawley rats were randomly divided into 4 groups (n=8/group), including control, HS[core body temperature (Tc)], HS(Tc-1°C) and HS(Tc+1°C) group. Heat stroke model was established in rats of HS(Tc), HS(Tc-1°C) and HS(Tc+1°C) group. Rats in HS(Tc) group were cooled to baseline core body temperature after establishing heat stroke model, HS(Tc-1°C) group to baseline core body temperature minus 1°C and HS(Tc+1°C) group to baseline core body temperature plus 1°C. We compared the histopathological changes of lung, liver and renal tissue, as well as cell apoptosis and expression of critical proteins in phosphatidylinositol 3´-kinase (PI3K)/Akt signaling pathway. Results: Heat stroke caused the histopathological damage and cell apoptosis of lung, liver and renal tissue, which could be alleviated by cooling intervention to a certain extent. Notably, HS(Tc+1°C) group demonstrated a better effect on alleviating cell apoptosis although the differences were not significant. Heat stroke lead to the elevated expression of p-Akt, which subsequently induced the elevated expression of Caspase-3 and Bax, as well as the decreased expression of Bcl-2. Cooling intervention could reverse this trend. Notably, the expression level of Bax in lung tissue of HS(Tc+1°C) group was significantly lower than that of HS(Tc) and HS(Tc-1°C) group. Conclusion: The mechanisms of cooling intervention in alleviating heat stroke-induced damage were associated with the expression changes of p-Akt, Caspase-3, Bax and Bcl-2. The better effect of Tc+1°C might be associated with low expression of Bax.
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