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Protective effects of simvastatin on endotoxin-induced acute kidney injury through activation of tubular epithelial cells’ survival and hindering cytochrome c-mediated apoptosis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62690094%3A18470%2F20%3A50017160" target="_blank" >RIV/62690094:18470/20:50017160 - isvavai.cz</a>

  • Result on the web

    <a href="https://www.mdpi.com/1422-0067/21/19/7236" target="_blank" >https://www.mdpi.com/1422-0067/21/19/7236</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3390/ijms21197236" target="_blank" >10.3390/ijms21197236</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Protective effects of simvastatin on endotoxin-induced acute kidney injury through activation of tubular epithelial cells’ survival and hindering cytochrome c-mediated apoptosis

  • Original language description

    Increasing evidence suggests that apoptosis of tubular cells and renal inflammation mainly determine the outcome of sepsis-associated acute kidney injury (AKI). The study aim was to investigate the molecular mechanism involved in the renoprotective effects of simvastatin in endotoxin (lipopolysaccharide, LSP)-induced AKI. A sepsis model was established by intraperitoneal injection of a single non-lethal LPS dose after short-term simvastatin pretreatment. The severity of the inflammatory injury was expressed as renal damage scores (RDS). Apoptosis of tubular cells was detected by Terminal deoxynucleotidyl transferase-mediated dUTP Nick End Labeling (TUNEL assay) (apoptotic DNA fragmentation, expressed as an apoptotic index, AI) and immunohistochemical staining for cleaved caspase-3, cytochrome C, and anti-apoptotic Bcl-xL and survivin. We found that endotoxin induced severe renal inflammatory injury (RDS = 3.58 ± 0.50), whereas simvastatin dose-dependently prevented structural changes induced by LPS. Furthermore, simvastatin 40 mg/kg most profoundly attenuated tubular apoptosis, determined as a decrease of cytochrome C, caspase-3 expression, and AIs (p &lt; 0.01 vs. LPS). Conversely, simvastatin induced a significant increase of Bcl-XL and survivin, both in the strong inverse correlations with cleaved caspase-3 and cytochrome C. Our study indicates that simvastatin has cytoprotective effects against LPS-induced tubular apoptosis, seemingly mediated by upregulation of cell-survival molecules, such as Bcl-XL and survivin, and inhibition of the mitochondrial cytochrome C and downstream caspase-3 activation. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10608 - Biochemistry and molecular biology

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2020

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    International journal of molecular sciences

  • ISSN

    1661-6596

  • e-ISSN

  • Volume of the periodical

    21

  • Issue of the periodical within the volume

    19

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    18

  • Pages from-to

    "Article number 7236"

  • UT code for WoS article

    000587175500001

  • EID of the result in the Scopus database

    2-s2.0-85091960370