ArticleInternational journal of clinical and experimental pathology2018
Protective effects of the AKT activator SC79 on renal ischemia-reperfusion injury.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 4 citations in OpenAlex.
- Apoptosis, Pyroptosis, and Necroptosis (PANoptosis) may be Present in Renal Ischemic Injury.Current medicinal chemistry · 2026Article
- Targeting the Inositol Pyrophosphate Biosynthetic Enzymes in Metabolic Diseases.Molecules (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsSC79, an AKT activator, has been reported to protect experimental ischemia-elicited neuronal death, brain injury, and myocardiocyte hypoxia/reoxygenation (H/R) injury. However, the protection of SC79 from renal ischemia-reperfusion (I/R) injury and the precise mechanisms involved are unknown. Here, we investigated the effects of SC79 in renal tubular epithelial cells
methodsThe kidneys of Sprague-Dawley rats were subjected to 30 min of warm ischemia followed by 24 h of reperfusion. Murine renal tubular epithelial NRK-52E cells were subjected to hypoxia for 6 h and reoxygenation for 24 h. The NRK-52E cells and the renal I/R injury model were treated with SC79 and/or LY294002 at different times and concentrations. Serum creatinine (Cr) concentration, renal histology, cellular viability, and cell apoptosis were assessed. Levels of phospho-Akt, bad, Bim, bax, bcl-2, and bcl-XL in NRK-52E cells and renal tissues were determined by western blotting.
resultsSC79 improved viability and inhibited apoptosis in NRK-52E cells following H/R. SC79 decreased serum Cr and markedly improved pathology and decreased cell apoptosis in kidneys following I/R. In addition, SC79 promoted the expression of phospho-Akt, bcl-2, and bcl-XL, and decreased the expression levels of bid, bax, and bim. PI3K inhibitor (LY294002) pre-treatment completely abolished these effects of SC79.
conclusionsThe protective role of SC79 against H/R of NRK-52E cells or renal I/R injury is related to activation of phosphorylation of AKT, resulting in a decrease in the pro-apoptotic proteins bim, bax, and bad and an increase in the anti-apoptotic proteins bcl-2 and bcl-XL induced by cell H/R and renal I/R injury.
Indexed as
Identifiers
31949855PMC6962971W3027560050What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.