Systemic administration of catalpol prevents D-galactose induced mitochondrial dysfunction in mice.

The aim of this work was to evaluate the mechanisms involved in the effects of catalpol on mitochondrial function through the measurements of nitric oxide synthase (NOS) activity, reactive oxygen species (ROS) production, respiratory complex activities and mitochondrial membrane potential (MMP) in the brain cortex and hippocampus mitochondria of senescent mice induced by d-galactose. Except control group, mice were subcutaneously injected with d-galactose (150 mg/kg body weight) for 6 weeks. Meanwhile, drug group mice were treated with catalpol (2.5, 5, 10mg/kg body weight) and piracetam (300 mg/kg body weight) for the last 2 weeks. The results indicated that respiratory complex activities decreased while NOS activities increased in d-galactose treated mice brain. The production of ROS increased remarkably and MMP collapsed in the brain of senescent mice induced by d-galactose. Administration of catalpol for 2 weeks significantly decreased ROS production and NOS activities, in accordance with its increase on complex activities and MMP level. Our results suggest that in vivo effects of catalpol on mitochondrial function can occur through different mechanisms, involving inhibiting NOS activity and ROS production, increasing respiratory complex activities and MMP level.