Sinapine suppresses ROS-induced C2C12 myoblast cell death through MAPK and autophagy pathways

Area of Science:

• Biochemistry
• Cell Biology
• Pharmacology

Background:

• Oxidative stress from reactive oxygen species (ROS) contributes to skeletal muscle atrophy and cell death.
• tert-Butyl hydroperoxide (TBHP) is a common inducer of oxidative stress and cellular damage.
• The protective effects of sinapine, a cruciferous plant phytochemical, against ROS-induced muscle cell death are not well understood.

Purpose of the Study:

• To investigate the protective role of sinapine against TBHP-induced oxidative stress and cell death in skeletal muscle cells.
• To elucidate the underlying molecular mechanisms, including the involvement of mitogen-activated protein kinase (MAPK) pathways and autophagy.

Main Methods:

• Skeletal muscle cells were pretreated with varying doses of sinapine followed by exposure to TBHP.
• Cell viability assays and reactive oxygen species (ROS) measurements were performed.
• Western blotting was used to analyze the phosphorylation status of MAPK pathway proteins (Akt, p38, JNK) and autophagy markers (LC3B-II).
• The effects of MAPK inhibitors in combination with TBHP were assessed.

Main Results:

• Sinapine pretreatment dose-dependently reduced TBHP-induced cell death and ROS accumulation.
• TBHP activated Akt, p38, and JNK pathways and induced autophagy, indicated by increased LC3B-II levels.
• Sinapine suppressed the phosphorylation of key MAPK proteins and modulated autophagy markers.
• MAPK inhibitors partially reversed TBHP-induced cell death and LC3B-II accumulation.

Conclusions:

• Sinapine exhibits significant protective effects against oxidative stress-induced skeletal muscle cell death.
• The protective mechanism involves the suppression of MAPK signaling pathways and modulation of autophagy.
• Sinapine represents a potential therapeutic agent for managing muscle injury and maintaining skeletal muscle health.