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目的研究鲁斯可皂苷元(Ruscogenin,Rus)对小鼠脑缺血缺氧的保护作用。方法采用小鼠断头致全脑缺血缺氧模型,通过观察小鼠断头呼吸维持时间,考察鲁斯可皂苷元抗脑缺氧活性及其量效时效关系;采用双侧颈总动脉结扎再灌注模型,考察鲁斯可皂苷元对脑组织含水量、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性及Na+-K+-ATP酶活性、Ca2+-ATP酶活性等生化指标的影响。结果 Rus 3～27 mg/kg灌胃给药1次,可显著延长小鼠断头后呼吸维持时间;给予Rus 9 mg/kg时,1 h即可明显延长小鼠断头后呼吸维持时间,2 h达到作用高峰,保护作用持续到8 h;Rus可明显降低反复缺血再灌注模型小鼠脑含水量,减少脑组织MDA含量,增加SOD活性、Na+-K+-ATPase活性和Ca2+-ATPase活性。结论 Rus在一定剂量范围内,明显改善小鼠脑缺血缺氧损伤,减轻缺血再灌注导致的脑水肿、氧化损伤和能量代谢障碍,具有起效较快,维持时间较长的作用特点。
Objective To study the protective effect of Ruscogenin (Rus) on cerebral ischemia and hypoxia in mice. Methods The model of global cerebral ischemia and hypoxia was induced by decapitation in mice. The duration of decapitation respiration in mice was observed. The anti-cerebral anoxia activity of russetapine and the dose-response relationship were investigated. The bilateral common carotid artery ligation Reperfusion model to investigate the effect of russetapine on biochemical indexes such as water content, malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, Na + -K + -ATPase activity and Ca2 + -ATPase activity Impact. Results The intragastric administration of Rus 3 ~ 27 mg / kg for one time significantly prolonged respiration maintenance after decapitation in mice. When resuscitated with Rus 9 mg / kg for 1 h, 2 h, the protective effect lasted for 8 h. Rus could significantly reduce brain water content, decrease MDA content, increase SOD activity, Na + -K + -ATPase activity and Ca2 + -ATPase activity in mice with repeated ischemia / reperfusion . Conclusion Rus can significantly improve cerebral ischemia-hypoxic injury in mice and relieve cerebral edema, oxidative damage and energy metabolism disorder induced by ischemia-reperfusion in a certain dose range. It has the characteristics of rapid onset of action and long-term maintenance.