Abstract Title:

Berberine attenuates Aβ-induced neuronal damage through regulating miR-188/NOS1 in Alzheimer's disease.

Abstract Source:

Mol Cell Biochem. 2020 Nov ;474(1-2):285-294. Epub 2020 Aug 10. PMID: 32779043

Abstract Author(s):

Manman Chen, Lu Li, Chuanqin Liu, Lina Song

Article Affiliation:

Manman Chen


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 upregulatedin 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.

Study Type : In Vitro Study

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