
浏览全部资源
扫码关注微信
纸质出版日期:2017
移动端阅览
张志慧, 贾振华, 康健生, 等. A损伤人脑微血管内皮细胞培养液对正常神经元凋亡的影响及通心络胶囊的干预作用[J]. 中国实验方剂学杂志, 2017,23(17):166-171.
ZHANG Zhi-hui, JIA Zhen-hua, KANG Jian-sheng, et al. Effect of AInjury-based Human Brain Microvascular Endothelial Cell Culture Solution on Apoptosis of Normal Neurons and Intervention Effect of Tongxinluo Capsule[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(17): 166-171.
张志慧, 贾振华, 康健生, 等. A损伤人脑微血管内皮细胞培养液对正常神经元凋亡的影响及通心络胶囊的干预作用[J]. 中国实验方剂学杂志, 2017,23(17):166-171. DOI: 10.13422/j.cnki.syfjx.2017170166.
ZHANG Zhi-hui, JIA Zhen-hua, KANG Jian-sheng, et al. Effect of AInjury-based Human Brain Microvascular Endothelial Cell Culture Solution on Apoptosis of Normal Neurons and Intervention Effect of Tongxinluo Capsule[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(17): 166-171. DOI: 10.13422/j.cnki.syfjx.2017170166.
目的:通过β淀粉样蛋白(amyloid β-protien,Aβ)损伤人脑微血管内皮细胞(human brain microvascular endothelial cells,HBMEC)培养液对正常神经元凋亡的影响及通心络胶囊的干预作用研究,探讨通心络对HBMEC及脑神经元的保护作用及其可能作用机制。方法:实验分为空白组,正常组,模型组,Aβ损伤组,通心络组,石杉碱甲组,空白组为正常神经元组,正常组为正常HBMEC培养液培养神经元组,其余4组采用20 μmol · L-1Aβ诱导HBMEC损伤,其中通心络组提前干预(400 mg · L-1通心络预处理6 h),石杉碱甲组提前干预(100 mg · L-1石杉碱甲预处理6 h),取其损伤后的细胞培养液加到正常脑神经元中进行培养,实验结束检测神经元的凋亡情况及凋亡蛋白、基因表达。结果:Aβ损伤HBMEC后的培养液可加速脑神经元的凋亡,且较Aβ直接导致脑神经元凋亡严重,提前通过通心络干预的HBMEC培养液诱导脑神经元凋亡细胞减少,凋亡蛋白、基因表达均有降低(P<0.05,P<0.01),且优于西药石杉碱甲组(P<0.05)。结论:老年性痴呆(AD)中HBMEC损伤可以进一步加速神经元的凋亡,而通心络保护HBMEC同时可起到保护脑神经元的作用,通心络胶囊对AD脑神经元及HBMEC具有双重保护作用。
Objective: To study the effect of amyloid beta (Aβ) injury-based human brain microvascular endothelial cell culture solution on normal neuronal apoptosis and the intervention effect of Tongxinluo capsule
in order to investigate the protective effect of Tongxinluo on brain microvascular and brain neurons and its possible mechanism. Method: The experiment was divided into blank group
normal group
model group
Aβ injury group
Tongxinluo group
Huperzine A group. The blank group was normal neuron group
The normal group was normal human brain microvascular endothelial cells-cultured neuron group. In the other 4 groups
20 mol · L-1 Aβ was used to induce damage in brain microvascular endothelial cells. Among them
the early intervention was made for the Tongxinluo group (pretreatment with 400 g · mL-1 Tongxinluo for 6 h) and the huperzine A group (pretreatment with 100 g · mL-1 huperzine A for 6 h). The damaged cell culture fluid was cultured in normal brain neurons. At the end of experiment
neuron apoptosis and apoptosis protein and gene expressions were detected. Result: The culture fluid of brain microvascular endothelial cells after Aβ damage could increase apoptosis rate of neurons in the brain
and directly cause severer cerebral neuron apoptosis than Aβ. After the early intervention with Tongxinluo
human brain microvascular endothelial cells-induced cerebral neuron apoptosis rate decreased
and apoptosis gene and protein expressions reduced (P<0.05
P<0.01)
with a better effect than western medicine huperzine A (P<0.05). Conclusion: The apoptosis of neurons could be further accelerated in Alzheimer's disease(AD)
and Tongxinluo protects brain microvascular endothelial cells and brain neurons. This suggests that Tongxinluo capsule has a double protective effect on AD neurons in the brain and brain microvascular endothelial cells.
0
浏览量
5
下载量
6
CSCD
关联资源
相关文章
相关作者
相关机构
京公网安备11010802024621