Curcumin suppresses AGEs induced apoptosis in tubular epithelial cells via protective autophagy

Ying Wei1,2,3, Jiaqi Gao1,2,3, Lingling Qin2,3

  • 1School of Chinese Pharmacy, Beijing University of Chinese Medicine, Beijing, Chaoyang 100102, P.R. China.

Insights

Curcumin protects kidney cells from damage caused by advanced glycation end-products (AGEs) by promoting autophagy, a cellular recycling process. This suggests curcumin may be a novel therapeutic strategy for diabetic nephropathy.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Nephrology

Background:

  • Diabetic nephropathy (DN) involves renal tubular cell apoptosis and dysfunction.
  • Understanding renal tubular epithelial cell survival mechanisms is crucial for preventing kidney damage from glucotoxicity.
  • Curcumin exhibits anti-apoptotic properties, but its role in renal epithelial cells requires definition.

Purpose of the Study:

  • To investigate the effects of advanced glycation or glycoxidation end-products (AGEs) on renal tubular epithelial cells.
  • To determine the protective mechanisms of curcumin in AGE-induced renal tubular cell toxicity.
  • To explore curcumin's impact on autophagy and related signaling pathways.

Main Methods:

  • Utilized the NRK-52E rat kidney tubular epithelial cell line.
  • Assessed cell viability, apoptosis, and autophagy following AGEs and curcumin treatment.
  • Investigated the involvement of the phosphoinositide 3-kinase/AKT signaling pathway.

Main Results:

  • AGEs significantly increased apoptosis in NRK-52E cells.
  • Curcumin reversed AGE-induced apoptosis.
  • Curcumin promoted autophagy via the phosphoinositide 3-kinase/AKT signaling pathway.

Conclusions:

  • Curcumin exerts a renoprotective effect against AGEs in NRK-52E cells, partly by activating autophagy.
  • Curcumin's mechanism involves promoting autophagy through the PI3K/AKT pathway.
  • Curcumin shows potential as a novel therapeutic strategy for diabetic nephropathy.

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