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Psoralen Inhibited Apoptosis of Osteoporotic Osteoblasts by Modulating IRE1-ASK1-JNK Pathway

Shuqing Chen1, Yongqian Wang2, Yubin Yang1

  • 1Department of Traditional Chinese Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.

Biomed Research International
|March 29, 2017
PubMed

Insights

Psoralen and estradiol inhibit osteoblast apoptosis, a key factor in osteoporosis. These compounds regulate the IRE1-ASK1-JNK pathway, offering a potential therapeutic strategy for osteoporosis treatment.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Pharmacology

Background:

  • Osteoporosis is a prevalent condition in aging populations, characterized by fractures.
  • Abnormal osteoblast apoptosis (programmed cell death) is a primary driver of osteoporosis.
  • Targeting osteoblast apoptosis presents a viable therapeutic avenue for osteoporosis prevention.

Purpose of the Study:

  • To investigate the effects of psoralen and estradiol on osteoblast proliferation and apoptosis.
  • To elucidate the molecular mechanisms underlying psoralen's anti-apoptotic effects in osteoblasts.

Main Methods:

  • Osteoblast isolation from osteoporotic patients and healthy subjects.
  • MTT assay for cell proliferation assessment.
  • Annexin V/PI assay for apoptosis determination.
  • Western blot analysis for protein expression (IRE1, ASK1, JNK, Bax, Bcl-2).

Main Results:

  • Osteoporotic osteoblasts exhibited reduced proliferation and increased apoptosis compared to healthy controls.
  • Psoralen and estradiol significantly enhanced proliferation and reduced apoptosis in osteoporotic osteoblasts.
  • Psoralen and estradiol downregulated IRE1, p-ASK1, p-JNK, and Bax, while upregulating Bcl-2.
  • IRE1 and JNK agonists diminished the protective effects of psoralen.

Conclusions:

  • Psoralen effectively inhibits osteoblast apoptosis in osteoporosis.
  • The mechanism involves the regulation of the IRE1-ASK1-JNK signaling pathway.
  • Psoralen demonstrates therapeutic potential for managing osteoporosis by preserving osteoblast function.

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