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Icariin modulates mitochondrial function and apoptosis in high glucose-induced glomerular podocytes through G

Chen Qiao1, Wenjuan Ye1, Sai Li1

  • 1China Pharmaceutical University, School of Basic Medicine and Clinical Pharmacy, Nanjing, 211198, China.

Molecular and Cellular Endocrinology
|January 27, 2018
PubMed

Insights

Icariin protects kidney podocytes from high glucose-induced apoptosis by reducing oxidative stress and stabilizing mitochondria via G protein-coupled estrogen receptor 1 (GPER) activation. This mechanism involves promoting Bcl-2 expression and translocation, preventing caspase activation in diabetic nephropathy.

Area of Science:

  • Nephrology
  • Cell Biology
  • Pharmacology

Background:

  • Diabetic nephropathy progression is linked to podocyte apoptosis.
  • High glucose levels exacerbate podocyte apoptosis and increase reactive oxygen species (ROS).

Purpose of the Study:

  • To investigate the protective effects of icariin on diabetic podocytes.
  • To elucidate the mechanism of icariin's action on podocyte apoptosis.

Main Methods:

  • High glucose treatment to induce podocyte apoptosis.
  • Assessment of ROS levels and mitochondrial membrane integrity.
  • G protein-coupled estrogen receptor 1 (GPER) knockdown experiments.
  • Analysis of caspase cascade and Bcl-2 expression/translocation.

Main Results:

  • Icariin significantly inhibited high glucose-induced podocyte apoptosis.
  • Icariin reduced ROS levels and maintained mitochondrial membrane integrity.
  • GPER knockdown reversed icariin's protective effects on mitochondria.
  • Icariin promoted Bcl-2 expression and its translocation to mitochondria, inhibiting the caspase cascade.

Conclusions:

  • Icariin exerts a protective effect on diabetic podocytes.
  • Icariin's mechanism involves GPER activation, ROS reduction, and mitochondrial stabilization.
  • Icariin prevents podocyte apoptosis by inducing Bcl-2 mitochondrial translocation and inhibiting caspase activation.
Keywords:
Bcl-2GPERIcariinTranslocation

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