当前位置: X-MOL 学术Mol. Cell. Biochem. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Berberine attenuates Aβ-induced neuronal damage through regulating miR-188/NOS1 in Alzheimer's disease.
Molecular and Cellular Biochemistry ( IF 4.3 ) Pub Date : 2020-08-10 , DOI: 10.1007/s11010-020-03852-1
Manman Chen 1 , Lu Li 1 , Chuanqin Liu 1 , Lina Song 1
Affiliation  

Alzheimer’s disease (AD) is a public health issue worldwide. Berberine (Ber) acts as the neuroprotective role in an animal experiment of AD. MicroRNA-188 (miRNA-188) was reported to be decreased in primary hippocampal neurons of mice. However, the roles and molecular basis of Ber and miRNA-188 in the treatment of AD need to be further explored. In this study, 5 μM Ber treatment has little effect on cell viability. Ber treatment or miR-188 overexpression expedited proliferation and inhibited caspase-3 activity and apoptotic rate in amyloid-beta (Aβ)-treated BV2 and N2a cells. MiR-188 was downregulated, and nitric oxide synthase 1 (NOS1) was upregulated in Aβ-induced BV2 and N2a cells. NOS1 worked as the target of miR-188. NOS1 overturned miR-188-induced effects on cell viability, caspase-3 activity, and apoptotic rate in Aβ-induced BV2 and N2a cells. Ber mitigated neuronal damage in Aβ-induced BV2 and N2a cells by miR-188/NOS1 axis. These results suggested that Ber accelerated cell viability and suppressed caspase-3 activity and apoptotic rate possible by miR-188/NOS1 pathway, implying the treatment of Ber as an underlying effective drug for AD patients.



中文翻译:

小ber碱通过调节阿尔茨海默氏病中的miR-188 / NOS1减轻Aβ诱导的神经元损伤。

阿尔茨海默氏病(AD)是世界范围内的公共卫生问题。小ber碱(Ber)在AD动物实验中起神经保护作用。据报道,MicroRNA-188(miRNA-188)在小鼠原代海马神经元中减少。但是,Ber和miRNA-188在AD治疗中的作用和分子基础还需要进一步探讨。在这项研究中,5μMBer处理对细胞生存力影响很小。Ber处理或miR-188过表达可加速增殖,并抑制淀粉样蛋白(Aβ)处理的BV2和N2a细胞的caspase-3活性和凋亡率。在Aβ诱导的BV2和N2a细胞中,MiR-188被下调,而一氧化氮合酶1(NOS1)被上调。NOS1作为miR-188的靶标。NOS1推翻了miR-188对细胞活力,caspase-3活性,Aβ诱导的BV2和N2a细胞的凋亡和凋亡率。Ber通过miR-188 / NOS1轴减轻了Aβ诱导的BV2和N2a细胞的神经元损伤。这些结果表明,通过miR-188 / NOS1途径,Ber可以加速细胞活力并抑制caspase-3活性和凋亡率,这暗示着Ber可以作为AD患者的基本有效药物。

更新日期:2020-08-11
down
wechat
bug