中国中医药信息杂志
中國中醫藥信息雜誌
중국중의약신식잡지
CHINESE JOURNAL OF INFORMATION ON TRADITIONAL CHINESE MEDICINE
2014年
8期
57-59
,共3页
杨丽鹍%玛娜璐璐%朱海燕%马涛%孙逸坤%赵一舟%高永红
楊麗鹍%瑪娜璐璐%硃海燕%馬濤%孫逸坤%趙一舟%高永紅
양려곤%마나로로%주해연%마도%손일곤%조일주%고영홍
三七总皂苷%阿尔茨海默病%β-淀粉样蛋白42%ZO-1蛋白
三七總皂苷%阿爾茨海默病%β-澱粉樣蛋白42%ZO-1蛋白
삼칠총조감%아이자해묵병%β-정분양단백42%ZO-1단백
Panax Notoginseng Saponins%Alzheimer’s disease%β-amyloid42%ZO-1
目的:观察三七总皂苷对β-淀粉样蛋白(Aβ)42损伤脑微血管内皮细胞ZO-1表达的影响,为阿尔茨海默病的对因治疗提供新的依据。方法细胞分为正常对照组、模型组和三七总皂苷低、中、高剂量组,37℃、5%CO2培养箱中培养24 h后,采用MTT比色法检测细胞活力,Western blot检测ZO-1蛋白表达。结果 Aβ42刺激后微血管内皮细胞活力降低(P<0.01),ZO-1蛋白表达被抑制(P<0.01);与模型组比较,三七总皂苷低、中、高剂量组微血管内皮细胞活力增加,其中三七总皂苷中、高剂量组增加较为明显,差异有统计学意义(P<0.05),ZO-1蛋白表达增加。结论三七总皂苷通过抑制Aβ42所致微血管内皮细胞活力降低,恢复血脑屏障的部分屏障功能。
目的:觀察三七總皂苷對β-澱粉樣蛋白(Aβ)42損傷腦微血管內皮細胞ZO-1錶達的影響,為阿爾茨海默病的對因治療提供新的依據。方法細胞分為正常對照組、模型組和三七總皂苷低、中、高劑量組,37℃、5%CO2培養箱中培養24 h後,採用MTT比色法檢測細胞活力,Western blot檢測ZO-1蛋白錶達。結果 Aβ42刺激後微血管內皮細胞活力降低(P<0.01),ZO-1蛋白錶達被抑製(P<0.01);與模型組比較,三七總皂苷低、中、高劑量組微血管內皮細胞活力增加,其中三七總皂苷中、高劑量組增加較為明顯,差異有統計學意義(P<0.05),ZO-1蛋白錶達增加。結論三七總皂苷通過抑製Aβ42所緻微血管內皮細胞活力降低,恢複血腦屏障的部分屏障功能。
목적:관찰삼칠총조감대β-정분양단백(Aβ)42손상뇌미혈관내피세포ZO-1표체적영향,위아이자해묵병적대인치료제공신적의거。방법세포분위정상대조조、모형조화삼칠총조감저、중、고제량조,37℃、5%CO2배양상중배양24 h후,채용MTT비색법검측세포활력,Western blot검측ZO-1단백표체。결과 Aβ42자격후미혈관내피세포활력강저(P<0.01),ZO-1단백표체피억제(P<0.01);여모형조비교,삼칠총조감저、중、고제량조미혈관내피세포활력증가,기중삼칠총조감중、고제량조증가교위명현,차이유통계학의의(P<0.05),ZO-1단백표체증가。결론삼칠총조감통과억제Aβ42소치미혈관내피세포활력강저,회복혈뇌병장적부분병장공능。
Objective To study the effects of Panax Notoginseng Saponins (PNS) on the damaged expression of ZO-1 of brain microvascular endothelial cells caused by Aβ42.MethodsBrain microvascular endothelial cells were divided into normal control group, model group, PNS low-, medium- and high concentration groups. They were incubated for 24h in 5% CO2 incubator at 37℃ . Then cell vitality was detected by MTT colorimetric method and ZO-1 protein expression was tested by Western blot.Results Stimulation of Aβ42 reduced the activity of microvascular endothelial cells (P<0.01) and suppressed the expression of ZO-1 protein (P<0.01). Compared with the model group, the activity of microvascular endothelial cells of PNS groups, especially the high and medium dose groups (P<0.05), and increased the ZO-1 protein expression. Conclusion PNS can partly recover the barrier function of blood brain barrier through inhibiting the decrease of the activity of microvascular endothelial cells caused by Aβ42.