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Leonurine alleviates vancomycin nephrotoxicity via activating PPARγ and inhibiting the TLR4/NF-κB/TNF-α pathway

Xuedong Yin1, Qian Gao1, Chensuizi Li1

  • 1Department of Pharmacy, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China; School of Medicine, Shanghai Jiao Tong University, Shanghai 200125, China.

International Immunopharmacology
|March 21, 2024
PubMed

Insights

Leonurine (Leo) protects against vancomycin (VCM)-induced kidney damage by reducing oxidative stress and inflammation. This study reveals Leo activates PPARγ, offering a potential therapeutic strategy for VCM nephrotoxicity.

Area of Science:

  • Pharmacology
  • Nephrology
  • Cell Biology

Background:

  • Vancomycin (VCM) is a critical antibiotic for severe infections but causes dose-limiting nephrotoxicity.
  • Leonurine (Leo) demonstrates potential renoprotective properties, yet its mechanism against VCM-induced kidney injury is not fully understood.

Purpose of the Study:

  • To investigate the protective effects and underlying mechanisms of Leonurine (Leo) against vancomycin (VCM)-induced nephrotoxicity in vivo and in vitro.
  • To elucidate the role of PPARγ activation and inflammatory pathways in Leo's renoprotective action.

Main Methods:

  • Mice and HK-2 cells were exposed to VCM and treated with Leo.
  • Evaluated renal injury using biochemical assays, pathological analysis, and fluorescence probes.
  • Mechanisms were explored via immunohistochemistry, q-PCR, western blot, FACS, and molecular docking (Autodock).

Main Results:

  • Leo significantly mitigated VCM-induced renal injury, morphological damage, and oxidative stress.
  • Leo reversed increased reactive oxygen species (ROS) and restored mitochondrial numbers in affected cells and tissues.
  • Molecular docking confirmed Leo's high-affinity binding to PPARγ, with mechanistic studies showing Leo activates PPARγ and inhibits the TLR4/NF-κB/TNF-α inflammatory pathway.

Conclusions:

  • Leonurine (Leo) effectively alleviates vancomycin (VCM)-induced nephrotoxicity.
  • The renoprotective effects are mediated by activating the PPARγ pathway and suppressing the TLR4/NF-κB/TNF-α inflammatory cascade.
  • Leo represents a promising therapeutic candidate for managing VCM-associated kidney injury.
Keywords:
InflammationLeonurineNephrotoxicityPPARγVancomycin

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