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目的:研究毛蕊花糖苷对β淀粉样蛋白(Aβ_(1-42))损伤神经元的保护作用及可能机制。方法:从新生乳鼠大脑皮层中分离纯化得到神经元,与Aβ_(1-42)、不同浓度的毛蕊花糖苷分别孵育24 h,利用CCK-8法检测神经元存活率;利用免疫荧光染色法检测突触素-1(Synapsin-1,SYN)的表达量;利用原位末端标记法(Terminaldeoxynucleoitidyl Transferase Mediated Nick End Labeling,TUNEL)检测神经元凋亡;利用Real-time及Western blot法检测Bcl-2、Bax和Caspase-3 m RNA及蛋白的表达量。结果:毛蕊花糖苷能显著提高Aβ_(1-42)损伤后神经元的存活率,能增加SYN的表达,抑制其凋亡,并且能提高神经元Bcl-2 m RNA及蛋白,降低Bax和Caspase-3 m RNA及蛋白的表达量。结论:促进抗凋亡因子、抑制促凋亡因子表达可能是毛蕊花糖苷拮抗Aβ_(1-42)神经毒性的机制之一。
Objective: To study the protective effect of verbascoside on the neurons damaged by β-amyloid protein (Aβ 1-42) and its possible mechanism. Methods: Neurons were isolated and purified from neonate neonatal rat cerebral cortex. The cells were incubated with Aβ 1-42 and verbascoside at different concentrations for 24 h. The survival rate of neurons was detected by CCK-8 assay. The immunofluorescence staining The expression of synapsin-1 (SYN) was detected by flow cytometry. Neuronal apoptosis was detected by Terminal deoxynucleotidyl transferase Mediated Nick End Labeling (TUNEL). Real-time and Western blot were used to detect the expression of Bcl-2, Bax and Caspase-3 m RNA and protein expression levels. Results: Verbascoside significantly increased the survival rate of neurons after Aβ 1-42 injury, increased the expression of SYN and inhibited the apoptosis of neurons, increased the expression of Bcl-2 mRNA and protein, decreased the expression of Bax and Caspase- 3 m RNA and protein expression levels. CONCLUSION: Promoting anti-apoptotic factor and inhibiting the expression of pro-apoptotic factor may be one of the mechanisms of verbascoside antagonizing the neurotoxicity of Aβ 1-42.