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Carnosic Acid Attenuates Cadmium Induced Nephrotoxicity by Inhibiting Oxidative Stress, Promoting Nrf2/HO-1

Sonjit Das1, Saikat Dewanjee1, Tarun K Dua1

  • 1Advanced Pharmacognosy Research Laboratory, Department of Pharmaceutical Technology, Jadavpur University, Kolkata 700032, India.

Molecules (Basel, Switzerland)
|November 23, 2019
PubMed

Insights

Carnosic acid (CA) protects kidneys from cadmium toxicity by reducing oxidative stress, apoptosis, and fibrosis. This natural antioxidant shows potential as a therapeutic agent against cadmium-induced kidney damage.

Area of Science:

  • Toxicology
  • Pharmacology
  • Biochemistry

Background:

  • Cadmium (Cd) exposure causes kidney damage (nephrotoxicity) through oxidative stress and cellular signaling.
  • Natural compounds are being investigated for protective effects against heavy metal toxicity.

Purpose of the Study:

  • To investigate the protective mechanism of carnosic acid (CA) against cadmium chloride (CdCl2)-induced nephrotoxicity.
  • To evaluate CA's efficacy in both in vitro and in vivo models.

Main Methods:

  • In vitro assays using normal kidney epithelial (NKE) cells and in vivo studies in mice.
  • Assessment of cell viability, oxidative stress markers, apoptosis, fibrosis, and renal function parameters.
  • Molecular docking to predict interactions between CA and key signaling molecules.

Main Results:

  • CdCl2 induced oxidative stress, apoptosis, and fibrosis in renal cells by inhibiting Nrf2 and activating TGF-β1/Smad/collagen IV pathways.
  • CA treatment attenuated CdCl2-induced nephrotoxicity by reducing free radicals, enhancing redox defense, suppressing apoptosis, and inhibiting fibrosis.
  • CA improved blood and urine parameters in mice and showed protective effects in histological analyses.
  • Molecular docking suggested interactions between CA and Nrf2, TGF-β1, Smad, and collagen IV.

Conclusions:

  • Carnosic acid exhibits significant protective effects against cadmium-induced nephrotoxicity.
  • CA acts by mitigating oxidative stress, apoptosis, and fibrosis through modulation of key signaling pathways.
  • CA is a promising therapeutic candidate for treating cadmium-mediated kidney damage.
Keywords:
antioxidantcadmium chloridecarnosic acidmolecular dockingoxidative stress

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