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Pranoprofen inhibits endoplasmic reticulum stress-mediated apoptosis of chondrocytes

Yuqing Gong1, Wanqiang Zhang2, Peipei Yan3

  • 1Department of Pharmacy, Guangrao People's Hospital, Dongying, China.

Panminerva Medica
|July 2, 2020
PubMed
Abstract

Insights

Pranoprofen (PF) inhibits endoplasmic reticulum stress (ERS) and apoptosis in human chondrocytes, offering a new therapeutic approach for osteoarthritis (OA) by reducing prostaglandin E2 (PGE2) levels.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Pharmacology

Background:

  • Endoplasmic reticulum stress (ERS) is a pathway implicated in apoptosis.
  • Limited research exists on non-steroidal anti-inflammatory drugs (NSAIDs) and chondrocyte apoptosis.
  • Osteoarthritis (OA) is characterized by cartilage degeneration and chondrocyte apoptosis.

Purpose of the Study:

  • To investigate the anti-apoptotic effects of pranoprofen (PF), a prostaglandin E2 (PGE2) inhibitor, on human chondrocytes (CHs).
  • To explore the role of ERS in chondrocyte apoptosis and the potential of PF in mitigating this process.

Main Methods:

  • Compared levels of PGE2, ERS, and apoptosis in OA versus healthy cartilage.
  • Induced ERS in isolated human CHs using hydrogen peroxide (H2O2) or tunicamycin (TM).
  • Assessed the impact of PF treatment on chondrocyte markers, ERS indicators, oxidative stress, and apoptosis.

Main Results:

  • OA cartilage exhibited elevated oxidative stress, PGE2, ERS, and apoptosis.
  • H2O2 and TM treatments increased PGE2, ERS markers (GRP78, CHOP, caspase-12), and reactive oxygen species (ROS), leading to chondrocyte degeneration.
  • PF treatment significantly reduced PGE2, suppressed ERS and apoptosis induced by H2O2/TM, and protected chondrocytes from degeneration.

Conclusions:

  • PF exhibits anti-apoptotic effects by abrogating ERS-mediated apoptosis in human chondrocytes.
  • This study suggests a novel mechanism for PF in the treatment of osteoarthritis (OA).
  • PF demonstrates chondroprotective properties against ERS-induced apoptosis.

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