文献类型：期刊文献

英文题名：Neuroprotective effects of bacopaside I in ischemic brain injury

作者：Liu, Xiaojun[1];Yue, Rongcai[1];Zhang, Jigang[1];Shan, Lei[1];Wang, Rui[2];Zhang, Weidong[1,3]

机构：[1]Second Mil Med Univ, Sch Pharm, Shanghai 200433, Peoples R China;[2]E China Univ Sci & Technol, Sch Pharm, Dept Pharmaceut Sci, Shanghai Key Lab New Drug Design, Shanghai 200237, Peoples R China;[3]Shanghai Jiao Tong Univ, Sch Pharm, Shanghai 200030, Peoples R China

年份：2013

卷号：31

期号：2

起止页码：109

外文期刊名：RESTORATIVE NEUROLOGY AND NEUROSCIENCE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000316613700002)】；

基金：The work was supported by program NCET Foundation, NSFC (30972705, 81072627), the Special Program for New Drug Innovation of the Ministry of Science and Technology, China (2009ZX09103-319, 2008ZX09308-005), Shanghai Leading Academic Discipline Project (B906) and in part by the Scientific Foundation of Shanghai China (09DZ1975700, 09DZ1971500), Shanghai Committee of Science and Technology (11DZ2260600) and 111 Project (B07023), Key laboratory of drug research for special environments, PLA, Shanghai Engineering Research Center for the Preparation of Bioactive Natural Products (10DZ2251300).

语种：英文

外文关键词：Bacopaside I; stroke; ischemic injury; reactive oxygen radicals; energy metabolism

摘要：Purpose: Bacopa monnieri (L.) WETTST. is extensively used in traditional Indian medicine as a nerve tonic. The neuropharmacological properties of bacopaside I, an important component from B. monnieri, have not been studied so far. The present study investigated the effects and possible mechanisms of bacopaside I in a rat model of transient focal ischemia induced by middle cerebral artery occlusion (MCAO). Methods: Adult male Sprague-Dawley rats were divided into five groups: sham-operated group, ischemia group, and three bacopaside I-treated groups (3, 10 and 30 mg/kg) respectively. Bacopaside I or vehicle (0.5% CMC-Na) was administered orally once a day for 6 days. On the third day, the rats were subjected to 2 h right MCAO via the intraluminal filament technique and 70 h reperfusion. Assessment of behavioral deficits both at 22 and 70 h, and measurement of cerebral infarct volume, edema, cerebral energy metabolism, relative enzyme activities, malondialdehyde (MDA) content, nitric oxide (NO) level, and antioxidant enzyme activities at 70 h, performed after MCAO reperfusion. Results: Bacopaside I (10 and 30 mg/kg) treatment produced significant reduction in neurological deficits at 22 and 70 h, and significantly reduced cerebral infarct volume and edema at 70 h, when compared with the ischemia group. Animal, that were orally treated with bacopaside I (3, 10 and 30 mg/kg) showed increased the brain ATP content, energy charge (EC), total adenine nucleotides (TAN), nitric oxide (NO) level, Na+K+ ATPase and Ca2+Mg2+ ATPase activity. Bacopaside I (3, 10 and 30 mg/kg) treatment also improved antioxidant enzyme activities including brain superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), in varying degrees, compared with the ischemia group. In addition, three doses of bacopaside I (3, 10 and 30 mg/kg) markedly inhibited the increase in MDA content of the brain. Conclusions: These findings indicated that bacopaside I possess a neuroprotective effect against injury caused by cerebral ischemia. The protective mechanism might be related to improving cerebral energy metabolism and increasing antioxidant levels.