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Taurochenodeoxycholic acid induces NR8383 cells apoptosis via PKC/JNK-dependent pathway

Xu Wang1, Ziying Zhang2, Xiuling He1

  • 1College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, China; Key Laboratory of Clinical Diagnosis and Treatment Techniques for Animal Disease, Ministry of Agriculture, Hohhot, China.

European Journal of Pharmacology
|June 9, 2016
PubMed

Insights

Taurochenodeoxycholic acid (TCDCA) promotes apoptosis in NR8383 cells by activating caspase cascades. The protein kinase C (PKC)/Jun N-terminal kinase (JNK) pathway is implicated, suggesting TCDCA

Area of Science:

  • Cell Biology
  • Immunology
  • Pharmacology

Background:

  • Taurochenodeoxycholic acid (TCDCA) is recognized for its anti-inflammatory and immune-regulating functions.
  • Previous research suggests TCDCA acts as a signaling molecule with potential therapeutic applications.

Purpose of the Study:

  • To investigate the effects of TCDCA on apoptosis in NR8383 cells.
  • To elucidate the underlying molecular mechanisms, including the involvement of the PKC/JNK pathway and caspase activation.

Main Methods:

  • Flow cytometry was used to assess apoptosis rates.
  • Quantitative PCR (qPCR) determined gene expression levels.
  • Western Blot analyzed protein kinase C (PKC) and Jun N-terminal kinase (JNK) expression and phosphorylation.
  • Caspase-Glo® reagent measured caspase-3 and caspase-8 activities.

Main Results:

  • TCDCA significantly increased NR8383 cell apoptosis in a concentration-dependent manner.
  • TCDCA upregulated PKC mRNA levels and activity.
  • TCDCA enhanced JNK, caspase-3, and caspase-8 mRNA expression and activity, which were reversed by specific inhibitors.

Conclusions:

  • TCDCA induces apoptosis in NR8383 cells via caspase cascade activation.
  • The PKC/JNK signaling pathway plays a role in TCDCA-mediated apoptosis.
  • TCDCA shows potential as a therapeutic agent for apoptosis-related diseases.
Keywords:
ApoptosisCaspaseJNKMacrophagePKCTCDCA

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