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Madecassoside ameliorates cisplatin-induced nephrotoxicity by inhibiting activation of the mitogen activated protein

Hui Yuan1, Yingying Zhao2,3,4, Shumin Li2,3,4

  • 1Department of Children's Health Care, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Maternal and Child Health Care Hospital, Nanjing, China.

Environmental Toxicology
|April 23, 2023
PubMed

Insights

Madecassoside (MA) protects against cisplatin-induced kidney injury by reducing apoptosis, inflammation, and oxidative stress. MA inhibits the MAPK signaling pathway, offering potential for acute kidney injury (AKI) treatment.

Area of Science:

  • Pharmacology
  • Nephrology
  • Molecular Biology

Background:

  • Cisplatin is a widely used chemotherapy agent, but its use is limited by significant nephrotoxicity.
  • Cisplatin-induced acute kidney injury (AKI) involves apoptosis, oxidative stress, inflammation, and MAPK signaling pathway activation.
  • Madecassoside (MA), derived from Centella asiatica, possesses known anti-oxidative and anti-inflammatory properties.

Purpose of the Study:

  • To investigate the protective mechanisms of Madecassoside (MA) against cisplatin-induced nephrotoxicity.
  • To evaluate the efficacy of MA in ameliorating cisplatin-induced kidney damage in a mouse model.
  • To elucidate the molecular pathways targeted by MA in preventing cisplatin nephrotoxicity.

Main Methods:

  • Mice were pretreated with MA before cisplatin administration to assess in vivo effects.
  • Kidney function, morphology, and injury biomarkers (KIM-1, NGAL) were evaluated.
  • In vitro studies on renal cells were performed to confirm MA's effects on apoptosis, oxidative stress, and inflammation.
  • RNA-sequencing was utilized for transcriptome analysis to identify affected signaling pathways.

Main Results:

  • MA pretreatment significantly improved kidney function and morphology in cisplatin-treated mice.
  • MA blocked the upregulation of kidney injury biomarkers KIM-1 and NGAL.
  • MA treatment attenuated cisplatin-induced renal cell apoptosis, oxidative stress, and inflammation both in vivo and in vitro.
  • Transcriptome analysis revealed that the MAPK signaling pathway was significantly affected, and MA inhibited its activation by cisplatin.

Conclusions:

  • Madecassoside (MA) demonstrates significant protective effects against cisplatin-induced nephrotoxicity.
  • MA ameliorates kidney damage by suppressing apoptosis, inflammation, oxidative stress, and inhibiting the MAPK signaling pathway.
  • MA shows potential as a therapeutic agent for preventing or treating acute kidney injury (AKI) caused by cisplatin.
Keywords:
AKIMAPK signaling pathwaycisplatinmadecassosidenephrotoxicity

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