School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, Shandong 264003, China.
Neurosci Lett. 2010 Apr 12;473(3):224-8. doi: 10.1016/j.neulet.2010.02.054. Epub 2010 Feb 26.
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.
本工作旨在通过测定衰老小鼠大脑皮质和海马线粒体中一氧化氮合酶（NOS）活性、活性氧（ROS）产生、呼吸复合物活性和线粒体膜电位（MMP），来评估梓醇对线粒体功能的影响机制。除对照组外，其余小鼠均经皮下注射半乳糖（150mg/kg 体重）6 周。同时，在最后 2 周，药物组小鼠用梓醇（2.5、5、10mg/kg 体重）和吡拉西坦（300mg/kg 体重）进行治疗。结果表明，半乳糖处理小鼠大脑中呼吸复合物活性降低，NOS 活性升高。半乳糖诱导的衰老小鼠大脑中 ROS 生成显著增加，MMP 崩溃。梓醇治疗 2 周可显著降低 ROS 生成和 NOS 活性，同时增加复合物活性和 MMP 水平。我们的结果表明，梓醇对线粒体功能的体内作用可能通过不同的机制发生，包括抑制 NOS 活性和 ROS 生成，增加呼吸复合物活性和 MMP 水平。
