Lu Jun, Zheng Yuan-Lin, Wu Dong-Mei, Luo Lan, Sun Dong-Xu, Shan Qun
Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, Xuzhou Normal University, Xuzhou 221116, PR China.
Biochem Pharmacol. 2007 Oct 1;74(7):1078-90. doi: 10.1016/j.bcp.2007.07.007. Epub 2007 Jul 10.
Ursolic acid (UA), a pentracyclic triterpene, is reported to have an antioxidant activity. Here we assessed the protective effect of UA against the d-galactose (D-gal)-induced neurotoxicity. We found that UA markedly reversed the D-gal induced learning and memory impairment by behavioral tests. The following antioxidant defense enzymes were measured: superoxide dismutases (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR). The content of the lipid peroxidation product malondialdehyde (MDA) was also analyzed. Our results indicated that the neuroprotective effect of UA against D-gal induced neurotoxicity might be caused, at least in part, by the increase in the activity of antioxidant enzymes with a reduction in lipid peroxidation. And UA also inhibited the activation of caspase-3 induced by D-gal. Furthermore, we found that UA significantly increased the level of growth-associated protein GAP43 in the brain of D-gal-treated mice. These results suggest that the pharmacological action of UA may offer a novel therapeutic strategy for the treatment of age-related conditions.
熊果酸（UA）是一种五环三萜，据报道具有抗氧化活性。在此，我们评估了UA对D-半乳糖（D-gal）诱导的神经毒性的保护作用。通过行为测试，我们发现UA显著逆转了D-gal诱导的学习和记忆损伤。检测了以下抗氧化防御酶：超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）和谷胱甘肽还原酶（GR）。还分析了脂质过氧化产物丙二醛（MDA）的含量。我们的结果表明，UA对D-gal诱导的神经毒性的神经保护作用可能至少部分是由于抗氧化酶活性增加以及脂质过氧化减少所致。并且UA还抑制了D-gal诱导的caspase-3的激活。此外，我们发现UA显著提高了D-gal处理小鼠大脑中生长相关蛋白GAP43的水平。这些结果表明，UA的药理作用可能为治疗与年龄相关的疾病提供一种新的治疗策略。
