Decrease of intracellular ROS by arbutin is associated with apoptosis induction and downregulation of IL-1β and TNF-α

Hajar Safari1, Ebrahim Zabihi2, Mahdi Pouramir2

  • 1Student Research Committee, Babol University of Medical Sciences, Babol, Iran.

Insights

Arbutin, an antioxidant, reduced reactive oxygen species (ROS) and inflammation in prostate cancer cells. This study suggests arbutin

Area of Science:

  • Oncology
  • Biochemistry
  • Pharmacology

Background:

  • Prostate cancer (PCa) is associated with increased reactive oxygen species (ROS) and inflammation.
  • Arbutin, a natural antioxidant, has demonstrated anti-inflammatory and anti-melanoma properties.
  • Investigating arbutin's effects on PCa provides potential complementary therapeutic strategies.

Purpose of the Study:

  • To investigate the molecular mechanisms of arbutin's antioxidant effects on the LNCap prostate cancer cell line.
  • To evaluate arbutin's impact on ROS levels, cell death, and inflammatory gene expression in PCa cells.

Main Methods:

  • In vitro study using the LNCap prostate cancer cell line.
  • Measurement of intracellular reactive oxygen species (ROS) levels.
  • Assessment of cell death profiles (apoptosis and necrosis) and gene/protein expression of inflammatory markers (IL-1β, TNF-α).

Main Results:

  • Arbutin significantly decreased intracellular ROS levels in a dose-dependent manner.
  • Arbutin (1,000 μM) induced apoptosis, whereas tert-butyl hydroperoxide (tBHP) induced necrosis.
  • Arbutin reduced the expression of pro-inflammatory genes (IL-1β, TNF-α) and IL-1β protein levels.

Conclusions:

  • Arbutin exhibits antioxidant and anti-inflammatory effects in prostate cancer cells by reducing ROS and pro-inflammatory cytokines.
  • Arbutin promotes apoptosis in PCa cells, suggesting a potential role in cancer therapy.
  • These findings highlight arbutin's potential as a complementary medicine approach for prostate cancer treatment.