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

The aim of the present study is to investigate the protective effect of bilberry extract on liver damage in restraint stressed mice. A remarkable increase in alanine aminotransferase (ALT) and reactive oxygen species (ROS) levels was observed in stressed mice. Treatment with bilberry extract restored ALT and ROS to normal levels, and enhanced mitochondrial complex II activity that was lowered in restraint stressed mice. The mitochondrial electron transfer chain (ETC)-related gene expression was measured by RT-PCR, and a significant up-regulation of complex II mRNA was observed for SDHA, B, C and D mRNA in bilberry extract-treated group compared with that in stressed group. Bilberry extract administration also profoundly elevated the Na(+)-K(+)-ATPase activity and mitochondria membrane potential (∆Ψ(m)), which was reduced in the stressed group. Bilberry extract exhibited protective effect by scavenging free radicals and attenuating mitochondrial dysfunction in the liver of restraint stressed mice. It may be used as a promising therapeutic agent in preventing and delaying the life-related disease.