Bilberry extract protect restraint stress-induced liver damage through attenuating mitochondrial dysfunction

Area of Science:

• Biochemistry
• Pharmacology
• Toxicology

Background:

• Restraint stress induces liver damage, characterized by increased alanine aminotransferase (ALT) and reactive oxygen species (ROS).
• Mitochondrial dysfunction plays a critical role in stress-induced liver injury.

Purpose of the Study:

• To investigate the protective effects of bilberry extract against restraint stress-induced liver damage in mice.
• To elucidate the underlying mechanisms of bilberry extract's hepatoprotective action, focusing on oxidative stress and mitochondrial function.

Main Methods:

• Mice were subjected to restraint stress, and liver damage markers (ALT, ROS) were assessed.
• Mitochondrial complex II activity, Na(+)-K(+)-ATPase activity, and mitochondrial membrane potential (ΔΨm) were measured.
• Gene expression of mitochondrial electron transfer chain (ETC) complex II subunits was analyzed using RT-PCR.

Main Results:

• Bilberry extract treatment normalized elevated ALT and ROS levels in stressed mice.
• The extract enhanced mitochondrial complex II activity and elevated mitochondrial membrane potential (ΔΨm).
• Bilberry extract upregulated the mRNA expression of mitochondrial ETC complex II subunits (SDHA, B, C, D).

Conclusions:

• Bilberry extract demonstrates significant hepatoprotective effects against restraint stress.
• These protective effects are attributed to free radical scavenging and the attenuation of mitochondrial dysfunction.
• Bilberry extract shows potential as a therapeutic agent for preventing and delaying life-related diseases associated with oxidative stress and mitochondrial damage.