ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2025
[Hypertension exacerbates postoperative learning and memory impairment in rats possibly due to UCP2 downregulation-mediated mitochondrial dysfunction].
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Metabolic syndrome and perioperative neurocognitive disorders: epidemiology, mechanisms, and interventions.Frontiers in neuroscience · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
objectivesTo explore the correlation of hypertension with postoperative cognitive dysfunction and its possible mechanism.
methodsTwelve-week-old spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats were both randomized into control group and surgical group (
resultsThe SHRs exhibited exacerbated learning and memory deficits following the surgery as shown by significantly reduced performance in novel object recognition tests and context-related and tone-related fear conditioning experiments. Compared with WKY rats, the SHRs had significantly decreased mitochondrial UCP2 expression and MMP in the hippocampus, increased hippocampal ATP level, and markedly increased serum levels of ROS and inflammatory factors, showing also increased activation of hippocampal astrocytes and microglia and reduced number of neurons positive for Nissl staining.
conclusionsHypertension can exacerbate major postoperative learning and memory impairment in rats possibly as a result of UCP2-mediated mitochondrial dysfunction and oxidative stress damage, which further leads to astrocyte overactivation and neuronal damage.
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