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Related Experiment Video

Updated: Jun 20, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

JNK and p38 inhibitors increase and decrease apoptosis, respectively, in pyrogallol-treated calf pulmonary arterial

Yong Hwan Han1, Hwa Jin Moon, Bo Ra You

  • 1Department of Physiology, Medical School, Centers for Healthcare Technology Development Institute for Medical Sciences, Chonbuk National University, JeonJu 561-180, Korea.

International Journal of Molecular Medicine
|September 30, 2009
PubMed
Summary

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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Pyrogallol induces cell death in pulmonary artery cells by disrupting mitochondrial function and depleting glutathione. MAPK inhibitors differentially modulate these effects, impacting apoptosis and cell viability.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Pharmacology

Background:

  • Pyrogallol (PG), a polyphenol, is known to induce apoptosis in various cell types.
  • Calf pulmonary artery endothelial cells (CPAEC) are crucial for lung function and susceptible to oxidative stress.
  • Mitogen-activated protein kinase (MAPK) pathways play significant roles in cellular responses to stress and apoptosis.

Purpose of the Study:

  • To investigate the impact of MAPK inhibitors on Pyrogallol-induced apoptosis in CPAEC.
  • To analyze the effects of these inhibitors on cell death, reactive oxygen species (ROS), and glutathione (GSH) levels.
  • To elucidate the specific roles of JNK and p38 pathways in PG-mediated cellular responses.

Main Methods:

  • CPAEC were treated with Pyrogallol (PG) and various MAPK inhibitors (JNK, p38, MEK).

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Last Updated: Jun 20, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

  • Cell viability, mitochondrial membrane potential (MMP), ROS production, and GSH depletion were assessed.
  • Differential effects of inhibitors on PG-treated and control cells were analyzed.

    • Main Results:

    • PG inhibited CPAEC growth, induced cell death, and decreased mitochondrial membrane potential (MMP).
    • PG treatment led to reduced ROS levels and an increased number of GSH-depleted cells.
    • JNK inhibitor enhanced PG's growth inhibition and CPAEC death, correlating with GSH depletion.
    • p38 inhibitor attenuated PG's growth inhibition and CPAEC death, decreasing GSH depletion.
    • MEK and p38 inhibitors reduced PG-induced CPAEC death, while JNK inhibitor increased it.

    Conclusions:

    • Pyrogallol induces apoptosis in CPAEC through MMP loss and GSH depletion.
    • JNK and p38 MAPK pathways differentially regulate PG-induced apoptosis in CPAEC.
    • MAPK inhibitors modulate PG's effects on cell viability, death, ROS, and GSH, offering potential therapeutic insights.