摘要
目的：观察隐丹参酮与多奈哌齐合用对Aβ42诱导大鼠皮层神经元凋亡的保护作用及其可能机制。方法通过Aβ42诱导体外培养的大鼠皮层神经元，建立阿尔茨海默病（Alzheimer＆#39;s disease，AD）细胞模型，MTT比色法检测细胞存活率，流式细胞仪检测细胞凋亡率，分光光度法测定SOD活性、MDA含量及LDH漏出量。结果成功建立大鼠皮层神经元AD细胞模型，经检测模型组MDA含量及LDH漏出量显著高于空白对照组且SOD活力明显低于空白对照组；隐丹参酮组、隐丹参酮加多奈哌齐组MDA含量及LDH漏出量均低于模型组，且SOD活力明显高于模型组，差异均有统计学意义（P〈0.05）；隐丹参酮与多奈哌齐合用在抑制神经元凋亡，降低MDA含量、LDH漏出量及提高SOD活性方面的效果显著强于隐丹参酮与多奈哌齐单用。结论隐丹参酮与多奈哌齐合用对Aβ损伤细胞有保护作用，其机制可能与协同抗氧化能力有关。
Objective To investigate the effect of the combination of cryptotanshinone and donepezil on Aβ-induced apoptosis in primary rat cortical neurons and to explore the mechanism. Methods AD cell models were established with Aβ-induced primary rat cortical neurons. Cell viability was detected by MTT assay. The cell apoptosis rate was measured by flow cytometry. The activities of superoxide dismutase（SOD）,the content of Malondialdehyde（MDA） and LDH level in neurons were measured with spectrophotometer. Results AD cell models were established,compared with control group,AD model significantly increased MDA and LDH level and decreased SOD activities. compared with model group,MDA and LDH levels were decreased in drug theraphy group and SOD activities increased. Compared with cryptotanshinone or donepezil group,the combination of cryptotanshinone and donepezil inhibited neurons apoptosis,decreased MDA content and increased the activities of SOD（P〈0.05）. Conclusion Cryptotanshinone and donepezil protect primary rat cortical neurons from Aβ-induced injury and the mechanism may be associated with synergistic improve antioxidation ability.
出处
《浙江临床医学》
2014年第5期691-693,共3页
Zhejiang Clinical Medical Journal
基金
广东省中医药强省基金项目（20111257）
关键词
阿尔茨海默病
隐丹参酮
氧化应激
凋亡
Alzheimer’s disease
Cryptotanshinone
Oxidative stress
Apoptosis
