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Amelioration of muscle wasting by gintonin in cancer cachexia

Yoseph Toni Wijaya1, Tania Setiawan1, Ita Novita Sari2

  • 1Department of Integrated Biomedical Science, Soonchunhyang University, Cheonan-si 31151, Republic of Korea.

Neoplasia (New York, N.Y.)
|November 19, 2021
PubMed

Insights

Gintonin (GT), a compound from ginseng, combats cancer cachexia by preventing muscle loss. It works by targeting specific receptors to reduce inflammation and oxidative stress, showing promise as a therapeutic agent.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Cancer cachexia is a debilitating condition marked by systemic inflammation and severe muscle loss.
  • Current treatments for cancer cachexia are limited, necessitating the development of novel therapeutic strategies.
  • Lysophosphatidic acid receptors (LPARs) and their signaling pathways are implicated in muscle atrophy.

Purpose of the Study:

  • To investigate the potential of gintonin (GT), a ginseng-derived LPAR ligand, as a therapeutic agent against cancer cachexia.
  • To elucidate the molecular mechanisms underlying GT's protective effects on skeletal muscle.

Main Methods:

  • Utilized C2C12 myotubes and primary human skeletal myoblasts to assess GT's anti-atrophic effects.
  • Investigated the role of LPAR/Gαi2 signaling in GT's activity using an LPAR antagonist and siRNA.
  • Evaluated GT's impact on oxidative stress and inflammation markers (ROS, IL-6, NOX-2) in vitro.
  • Assessed GT's efficacy in a Lewis lung carcinoma cell line (LLC1)-induced mouse model of cancer cachexia.

Main Results:

  • Gintonin (GT) protected C2C12 myotubes and human myoblasts against tumor necrosis factor α (TNFα)/interferon γ (IFNγ)-induced muscle wasting.
  • GT's anti-atrophic effects were dependent on LPAR/Gαi2 signaling, as confirmed by LPAR antagonist and Gαi2 siRNA.
  • GT suppressed TNFα-induced oxidative stress by reducing reactive oxygen species (ROS) and key inflammation-related genes (IL-6, NOX-2).
  • In vivo, GT treatment improved grip strength, hanging ability, and muscle cross-sectional area in a mouse model of LLC1-induced cancer cachexia.

Conclusions:

  • Gintonin (GT) demonstrates significant anti-atrophic properties in skeletal muscle cells, both in vitro and in vivo.
  • The therapeutic effects of GT are mediated through the LPAR/Gαi2 signaling pathway.
  • GT effectively mitigates key pathological features of cancer cachexia, including inflammation and oxidative stress.
  • Gintonin presents a promising therapeutic candidate for the prevention and treatment of cancer cachexia.
Keywords:
Cancer cachexiaGintoninMuscle atrophyOxidative stress

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