Isoacteoside attenuates acute kidney injury induced by severe acute pancreatitis

Mol Med Rep. 2021 Apr;23(4):287. doi: 10.3892/mmr.2021.11926. Epub 2021 Mar 2.

Abstract

Severe acute pancreatitis (SAP) is a common acute abdominal disease accompanied by systemic inflammatory response syndrome, which may be complicated by acute kidney injury (AKI). Isoacteoside (ISO) is the active ingredient of Monochasma savatieri Franch. ex Maxim and has been reported to have anti‑inflammatory activities. The present study detected the effects of ISO on AKI induced by SAP in rat models, and the underlying mechanism. The optimum dose of ISO for treatment of AKI induced by SAP was determined. The serum levels of TNF‑α and IL‑6 were estimated using an ELISA. Kidney injury was evaluated by histopathological examination, and the expression levels of nitric oxide were also detected. The expression levels of Toll‑like receptor 4 (TLR4) and NF‑κB p65 were measured by immunohistochemistry and western blotting. The results revealed that ISO may serve a critical role in ameliorating AKI induced by SAP. These effects may be associated with the TLR4/NF‑κB signaling pathway.

Keywords: severe acute pancreatitis; acute kidney injury; Isoacteoside; TLR4; NF‑κB.

MeSH terms

  • Acute Kidney Injury / blood
  • Acute Kidney Injury / etiology
  • Acute Kidney Injury / prevention & control*
  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Glucosides / pharmacology*
  • Interleukin-6 / blood
  • Kidney / drug effects*
  • Kidney / metabolism
  • Kidney / pathology
  • Male
  • NF-kappa B / metabolism
  • Nitric Oxide / metabolism
  • Pancreatitis / complications*
  • Pancreatitis / pathology
  • Phenols / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Severity of Illness Index
  • Signal Transduction / drug effects
  • Toll-Like Receptor 4 / metabolism
  • Transcription Factor RelA / metabolism
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Anti-Inflammatory Agents
  • Glucosides
  • Interleukin-6
  • NF-kappa B
  • Phenols
  • Rela protein, rat
  • Toll-Like Receptor 4
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • isoacteoside