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Pathways of apoptosis regulation in hepatocytes induced by first-line antitubercular drugs

E D Bazhanova1, D S Sukhanov, D L Teplyi

  • 1I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia, bazhanove@mail.ru.

Bulletin of Experimental Biology and Medicine
|March 18, 2015
PubMed

Insights

Antitubercular drugs trigger liver cell apoptosis via external and p53 pathways. Some drugs reduce liver damage, while ademetionine and reamberin offer distinct hepatoprotective and apoptosis-protective effects.

Area of Science:

  • Hepatology
  • Pharmacology
  • Molecular Biology

Background:

  • Antitubercular drug treatment can cause experimental hepatopathy.
  • Understanding apoptosis regulation is crucial for managing drug-induced liver injury.

Purpose of the Study:

  • To investigate apoptosis regulation pathways in drug-induced hepatopathy.
  • To evaluate the effects of hepatoprotectors and immunomodulators on hepatocyte apoptosis.

Main Methods:

  • Assessing apoptosis intensity and expression of apoptosis-associated molecules.
  • Evaluating the impact of specific drugs (Runihol, remaxol, cycloferon, ademetionine, reamberin) on liver tissue.

Main Results:

  • Antitubercular drugs induce hepatocyte apoptosis via external and p53-dependent pathways, decreasing Bcl-2 protein.
  • Runihol, remaxol, and cycloferon mitigated liver degeneration but apoptosis persisted.
  • Ademetionine and reamberin inhibited both apoptotic pathways, demonstrating hepatoprotective and apoptosis-protective effects.

Conclusions:

  • Antitubercular drugs induce hepatocyte apoptosis through specific molecular pathways.
  • Ademetionine and reamberin exhibit significant hepatoprotective and apoptosis-protective properties, particularly beneficial in later developmental stages.

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