Adiponectin attenuates H2O2-induced apoptosis in chicken skeletal myoblasts through the lysosomal-mitochondrial axis

Area of Science:

• Cell Biology
• Biochemistry
• Molecular Biology

Background:

• Adiponectin is known for its protective roles against myocardial injury via anti-apoptotic and anti-oxidative mechanisms.
• Hydrogen peroxide (H₂O₂) is a common inducer of oxidative stress and apoptosis in various cell types, including skeletal muscle cells.

Purpose of the Study:

• To investigate how adiponectin inhibits H₂O₂-induced apoptosis in chicken skeletal myoblasts.
• To elucidate the underlying molecular mechanisms, focusing on oxidative stress, lysosomal, and mitochondrial pathways.

Main Methods:

• Chicken skeletal myoblasts were treated with H₂O₂ and/or adiponectin.
• Assays included CCK-8 for cytotoxicity, TUNEL and ROS staining for apoptosis and oxidative damage, AO staining for lysosomal permeability, and JC-1 for mitochondrial membrane potential.
• Real-time quantitative PCR and western blot were used to analyze apoptosis-related gene and protein expression (Bax, Bcl-2, cathepsin B, chymotrypsin B, cytochrome-c, caspase-8).

Main Results:

• Adiponectin treatment significantly reduced H₂O₂-induced cytotoxicity and oxidative stress in skeletal myoblasts.
• Apoptosis, reactive oxygen species (ROS) levels, and lysosomal membrane damage were decreased by adiponectin.
• Adiponectin increased mitochondrial membrane potential and modulated the expression of key apoptosis-related proteins (Bax, Bcl-2, cytochrome-c, caspase-8).

Conclusions:

• Adiponectin effectively attenuates H₂O₂-induced apoptosis in chicken skeletal myoblasts.
• The protective effect is mediated by the inhibition of oxidative stress and the regulation of the lysosomal-mitochondrial apoptotic pathway.