Carnosine Protects Mouse Podocytes from High Glucose Induced Apoptosis through PI3K/AKT and Nrf2 Pathways

Kunxiao Zhao1, Ying Li1, Ziqiang Wang2

  • 1Department of Nephrology, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei Province 050051, China.

Insights

Carnosine protects kidney cells from diabetes complications by reducing oxidative stress and apoptosis. It activates PI3K/AKT and Nrf2 pathways, offering a potential treatment for diabetic nephropathy.

Area of Science:

  • Nephrology
  • Diabetology
  • Molecular Biology

Background:

  • Diabetic nephropathy, a diabetes complication, can cause chronic renal failure.
  • Reactive oxygen species (ROS) are key players in diabetic nephropathy's pathology.
  • Carnosine exhibits antioxidant properties, but its precise mechanism in diabetic nephropathy is unclear.

Purpose of the Study:

  • To investigate carnosine's protective effects on high glucose-induced injury in mouse podocytes (MPC5).
  • To elucidate the molecular mechanisms underlying carnosine's antioxidant and anti-apoptotic actions.

Main Methods:

  • MPC5 cells were exposed to high glucose (HG) with varying carnosine concentrations.
  • Cell viability was assessed using the Cell Counting Kit-8 assay.
  • ROS levels and apoptosis were measured using quantitative real-time PCR, Western blotting, and immunofluorescence staining.

Main Results:

  • Carnosine (5-20mM) protected MPC5 cells against HG-induced injury.
  • High glucose-induced ROS production and podocyte apoptosis were significantly downregulated by carnosine.
  • These protective effects were mediated through the activation of the PI3K/AKT and Nrf2 signaling pathways.

Conclusions:

  • Carnosine demonstrates protective effects against diabetic nephropathy-related kidney cell injury.
  • Carnosine reduces ROS levels and podocyte apoptosis by activating PI3K/AKT and Nrf2 signaling pathways.
  • Carnosine represents a potential therapeutic agent for managing diabetic nephropathy.

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