雌二醇对海马神经元和隔区胆碱能神经元损伤的保护作用比较

Comparison between the protection of estradiol against the injury of hippocampal neurons and cholinergic neuron in septal area

目的:研究雌二醇在体外原代培养条件下对淀粉样β25～35肽(amyloid-β25-35,Aβ25-35)诱导的海马神经元和胆碱能神经元损伤的保护作用,探讨其可能的机制。方法:实验于2002-03/2003-03在中山大学医学院解剖教研室完成。采用SD大鼠海马神经元原代培养,用终浓度为10μmol/L的Aβ25-35诱导体外海马和隔胆碱能神经元损伤,MTT法比色微量分析较雌二醇对这两种神经元的存活率的影响,并检测超氧化物歧化酶(superoxidedismutase,SOD活性的变化。将两种培养细胞分为3组,分)别为Aβ处理组、雌二醇组、空白对照组。结果:雌二醇可提高海马和胆碱能神经元存活率与Aβ处理组比较,P(<0.05),经雌激素作用后,两种神经元的存活率分别为103.52%和85.90%,它对海马神经元的保护作用优于胆碱能神经元两者存活率(比较,P<0.05),并可诱导两种神经元Mn-SOD的活性增加(与Aβ处理组比较,P<0.05),分别比Aβ处理组提高了63.76%和131.38%,对隔胆碱能神经元的诱导作用较强(两者活性比较,P<0.05),对CuZn-SOD的活性无明显影响(P>0.05)。结论:雌二醇对Aβ25～35诱导毒性损伤的海马和隔胆碱能神经元有相似程度的保护作用,其机制可能与提高Mn-SOD活性,促进聚集型的Aβ溶解有关。

AIM:To study the protective role of estradiol in the injury of primary culture d hippocampal neurons and cholinergic neuron in septal area induced by amyloid beta 25-35(Aβ25-35) in vitro,and probe into its probable mechanism. METHODS:The experiment was done in the Department of Anatomy, the Medical Coll ege of Sun Yat sen University from March 2002 to March 2003.After primary cultu re of hippocampal neurons of SD rats,10 μmol/L Aβ25-35 was used to induce the damage to hippocampal neurons and cholinergic neuron in septal area in vitro.Th e different effect of estradiol on neuron survival and the activity of superoxid e dismutase(SOD) were observed and measured with MTT.These two kinds of cultured cells were divided into three groups:Aβpretreated group,estradiol group and co ntrol group respectively. RESULTS:Compared with the Aβ25-35,estradiol increased the survival rate of n eurons which was 103.52%and 85.90%respectively(P< 0.05). Estraiol had a better role in protecting hippocampal neurons than cholinergic neuron in septal area(P < 0.05),and increased the activity of Mn SOD by 63.76%and 131.38%respectively as compared with the Aβ25-35(P< 0.05),and had a stronger inducible effect on cholinergic neuron in septal area (P< 0.05),but not on CuZu SOD activity(P >0.0 5). CONCLUSION:Estradiol has the same effect in protecting hipocampal neurons and cholinergic neuron in septal area from cytotoxic injury induced by Aβ25-35.The mechanism is likely involved to activate the Mn SOD activity and dissolve conc entrated Aβ.