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Systemic administration of catalpol prevents D-galactose induced mitochondrial dysfunction in mice
Xiuli Zhang1, Weidong Liu, Xinhua Niu
1School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, Shandong 264003, China. zhangxiuli2008@163.com
Abstract:
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.
Insights
Catalpol improves mitochondrial function in aging brains by reducing nitric oxide synthase (NOS) activity and reactive oxygen species (ROS) production. It also enhances respiratory complex activities and mitochondrial membrane potential (MMP) in senescent mice.
Area of Science:
- Neuroscience
- Mitochondrial Biology
- Pharmacology
Background:
- Aging is associated with mitochondrial dysfunction, including decreased respiratory complex activities and increased reactive oxygen species (ROS) production.
- Nitric oxide synthase (NOS) activity and mitochondrial membrane potential (MMP) are also affected during senescence.
- Understanding the mechanisms behind these age-related changes is crucial for developing interventions.
Purpose of the Study:
- To investigate the effects of catalpol on mitochondrial function in a mouse model of aging.
- To evaluate the impact of catalpol on nitric oxide synthase (NOS) activity, reactive oxygen species (ROS) production, respiratory complex activities, and mitochondrial membrane potential (MMP).
- To elucidate the underlying mechanisms of catalpol's neuroprotective effects.
Main Methods:
- Senescence was induced in mice using d-galactose injections over 6 weeks.
- Mice were treated with varying doses of catalpol (2.5, 5, 10 mg/kg) or piracetam (300 mg/kg) for the final 2 weeks.
- Mitochondrial function parameters, including NOS activity, ROS production, respiratory complex activities, and MMP, were measured in brain mitochondria.
Main Results:
- D-galactose induced decreased respiratory complex activities, increased NOS activity, elevated ROS production, and collapsed MMP in mouse brains.
- Catalpol administration significantly reduced ROS production and NOS activity.
- Catalpol treatment also increased respiratory complex activities and restored MMP levels in senescent mice.
Conclusions:
- Catalpol demonstrates neuroprotective effects by improving mitochondrial function in aging brains.
- Its mechanisms involve the inhibition of NOS activity and ROS production.
- Catalpol also enhances mitochondrial respiration and preserves mitochondrial membrane potential, suggesting therapeutic potential for age-related cognitive decline.