摘要
目的观察人参皂苷Rg1对大鼠海马神经元缺糖氧／复糖氧（OGD—R）后神经元型一氧化氮合酶（nNOS）活性和细胞凋亡的影响，并探讨其可能的脑保护机制。方法建立大鼠海马神经元OGD—R模型，随机分为正常对照组、模型组和人参皂苷Rg1干预组（5、20、60μmol／L）。复糖氧后24h以生物化学法观察各组海马nNOS活性的变化，并以Hochest染色法检测细胞凋亡。结果与模型组比较，人参皂苷Rg1中、高剂量组海马神经元nNOS活性下降，凋亡减少，人参皂苷Rg1低剂量组变化不明显。结论人参皂苷Rg1可通过降低缺糖氧nNOS活性，减少一氧化氮生成，发挥脑保护作用。
Objective To demonstrate the effect of Ginsenoside Rgl against neuronal nitric oxide synthase （nNOS） activity and cell apoptosis after oxygen - glucose deprivation/reperfusion in cultured hippocampal cells, and to explore its possible mechanisms. Methods Rat hippocampal neurons were cultured and set up the model of oxygen - glucose deprivation and reperfusion. They were randomly divided into control group, model group and Ginsenoside Rgl treatment groups （5, 20, 60 μmol/L）. The nNOS activity and cell apoptosis were measured 24 h after reperfusion. Results Compared with model group, the nNOS activity and the cell apoptosis was decreased in the groups receiving middle and high dose of Ginsenoside Rgl, but not in the tow dose Ginsenoside Rgl group. Conclusion Ginsenoside Rgl has neuroprotective effect due to decreasing the nNOS activity after cerebral ischemia.
出处
《中国急救医学》
CAS
CSCD
北大核心
2013年第12期1127-1130,I0010,共5页
Chinese Journal of Critical Care Medicine
基金
基金项目：国家自然科学基金项目（30901578）
江苏高校优势学科建设工程项目（PAPD,Jx10231081）
江苏省高校“青蓝工程”中青年学术带头人培养对象项目（JX2161015003）
