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Cited by 34Neurological Disorders and TreatmentsCell death mechanisms and regulationAcute Kidney Injury Research

Protective effect of SGK1 in rat hippocampal neurons subjected to ischemia reperfusion

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Zhang, Wei, Qian, Chuan yun, Li, Shu qing·2014·Cellular Physiology and Biochemistry
DOI 10.1159/000363000
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Abstract

BACKGROUND/AIMS: To investigate the protective effect of SGK1 (serum- and glucocorticoid-inducible protein kinase 1) in rat hippocampal neurons in vitro and in vivo following ischemia reperfusion (I/R). METHODS: Isolated rat hippocampal neurons were subjected to 2 h of oxygen and glucose deprivation (OGD) then returned to normoxic conditions for 10, 30 or 60 min. Cell apoptosis and protein expression of SGK1 were analyzed. To examine SGK1 function, we overexpressed SGK1 in rat hippocampal neurons. Finally we examined the involvement of PI3K/Akt/GSK3β signaling by treating the cells (untransfected or transfected with expression vector encoding SGK1) with the PI3K inhibitor LY294002. Findings were confirmed in vivo in a rat model of middle cerebral artery occlusion. RESULTS: I/R caused a time-dependent increase in apoptosis, both in vitro and in vivo. SGK1 protein levels decreased significantly under the same conditions. Overexpression of SGK1 reduced apoptosis following OGD or I/R compared to cells transfected with empty vector and subjected to the same treatment, or sham-operated animals. Addition of LY294002 revealed that the action of SGK1 in suppressing apoptosis was mediated by the PI3K/Akt/GSK3β pathway. CONCLUSION: SGK1 plays a protective role in ischemia reperfusion in rat hippocampal neurons, exerting its effects via the PI3K/Akt/GSK3β pathway.

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  • SGK1 plays a positive role in neuronal apoptosis during cerebral ischemia.

    “Research indicates SGK1 plays a positive role in neuronal apoptosis during cerebral ischemia (Chaudhary et al., 2023; Zhang et al., 2014).”

    From Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain (2024) · cites this paper as Zhang et al., 2014

    The paper reports the opposite of a pro-apoptotic role: in its discussion of the cell experiments, SGK1 overexpression markedly reduced apoptosis after oxygen-glucose deprivation. Figure 6 also describes SGK1 transfection as protecting rats against ischemia/reperfusion-induced neuronal apoptosis. (LLM, conf=0.88)

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  • Overexpression of SGK1 partially restores activation of Akt and GSK-3β, reducing hippocampal neuronal apoptosis in rats following OGD or MCAO via PI3K/Akt/GSK-3β pathway.

    “Overexpression of SGK1 partially restores the activation of Akt and GSK-3β, reducing hippocampal neuronal apoptosis in rats following OGD or MCAO via the PI3K/Akt/GSK-3β pathway”

    From Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain (2024) · cites this paper as Zhang et al., 2014

    The paper reports that SGK1 overexpression partially restored Akt and GSK-3β activation and reduced apoptosis in cultured rat hippocampal neurons after OGD, with PI3K/Akt signaling implicated. Its MCAO experiment also found reduced neuronal apoptosis after SGK1 transfection, but measured apoptotic cells in the ischemic penumbral cortex, not the hippocampus (Fig. 6; page unavailable). Thus the claim's hippocampal-neuron specificity is not supported for MCAO. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Post-MCAO, SGK1 levels initially double compared to sham-operated rats at 6 hours before falling below control levels after 24 hours, accompanied by an increase in neuronal apoptosis.

    “post-MCAO, the levels initially double compared to sham-operated rats at 6 hours before falling below control levels after 24 hours, accompanied by an increase in neuronal apoptosis”

    From Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain (2024) · cites this paper as Zhang et al., 2014

    The discussion (page unavailable) reports that SGK1 levels rose transiently after MCAO and returned to control levels by 24 hours; it does not report that they fell below control. Figure 5 identifies a 6-hour measurement, but the supplied text does not establish a doubling at that time. The Results section reports increasing TUNEL-positive cells after reperfusion, supporting the apoptosis portion. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • In rat hippocampal neurons, SGK1 levels significantly drop following OGD and further decline over time.

    “In rat hippocampal neurons, SGK1 levels significantly drop following OGD and further decline over time”

    From Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain (2024) · cites this paper as Zhang et al., 2014

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Research works printed but not linked: 38

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Cited by

Sorted by citations

Authors
Zhang, W., Qian, C. Y., & Li, S. Q.
Affiliations
  • First Affiliated Hospital of Kunming Medical University (CN)
  • Kunming Medical University (CN)
ORCID
Zhang, Wei
Venue
Cellular Physiology and Biochemistry
Publisher
S. Karger AG
Published
2014
Volume
34
Issue
2
Pages
299-312
ISSN
  • 1015-8987 (ISSN-L)
  • 1421-9778
DOI
10.1159/000363000
OpenAlex
W2023971280
Cited by
34
References
2
Citations by year
2025: 2 · 2024: 2 · 2023: 4 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 8 · 2015: 7
FWCI
2.95
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Cellular Physiology and Biochemistry (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China (30971171)
  • Kunming Medical University
Topics
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
Keywords
SGK1, ischemia-reperfusion injury, hippocampal neurons, neuronal apoptosis, oxygen-glucose deprivation, PI3K/Akt/GSK-3β signaling, neuroprotection, middle cerebral artery occlusion, LY294002
MeSH terms
Serum-Glucocorticoid Regulated Kinases, Animals, Base Sequence, Cells, Cultured, Hippocampus, Male, Neurons, Reperfusion Injury, Rats, Sprague-Dawley, Protein Serine-Threonine Kinases, Immediate-Early Proteins, DNA Primers, In Situ Nick-End Labeling, Rats, Real-Time Polymerase Chain Reaction

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