In vivo antioxidative activivty of a Pueraria lobata root extract in a diabetic rat model
Oxidative stress has been associated with many pathological disorders such as atherosclerosis, diabetes and cancer. Oxidative stress is caused by a disturbance of the balance between the antioxidant defence mechanisms of the human organism and the level of Reactive Oxygen Species (ROS). Supplementation with exogenous antioxidants, such as phenolic compounds from plant sources, may help to restore this balance. Even a range of in vitro antioxidative assays cannot truely reflect in vivo activity because of the influence of absorption, metabolisation, binding to plasma proteins, distribution, and elimination. Therefore antioxidative research should also be extended to in vivo models.
Because of the increasing interest for Oriental Medicine in the Western world, Pueraria lobata (Fabaceae) was selected, among other plants, for our investigations. Roots of Pueraria lobata are included in the Chinese Pharmacopoeia (“Gegen“; Radix Puerariae Lobatae). The genus Pueraria is a rich source of isoflavonoids, the most abundant isoflavonoid in the root being puerarin, and in the flowers tectorigenin and its glycosides . We have investigated the roots as well as the flowers of P. lobata, and developed and validated analytical HPLC methods for their main constituents. The in vivo antioxidative activity of a quantified root extract was evaluated in a diabetic rat model, where diabetes and the accompanying oxidative stress were induced by IP administration of streptozotocin. This root extract was found to contain 10.42±0.15% puerarin as the main constituent and smaller amounts of 3'-hydroxypuerarin, 3'-methoxypuerarin, 6“-xylosylpuerarin, daidzin, genistin, daidzein and genistein. After oral administration at a dose of 500mg/kg root extract, corresponding to 50mg/kg puerarin, during 3 weeks, the level of malondialdehyde (MDA) in plasma, used as a marker of oxidative damage to lipids, was reduced to the same level as in healthy control animals, and to the same level as in the positive control group treated with 50mg/kg α-tocopherol acetate.
References: 1. Bebrevska, L. et al. (2007) Planta Med. 73: 1606–1613.