4.4 Article

Breviscapine Combined with BMSCs Reduces Aß Deposition in Rat with Alzheimer's Disease by Regulating Circular RNA ciRS-7

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CURRENT MOLECULAR MEDICINE
卷 23, 期 1, 页码 76-86

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BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1566524022666220113151044

关键词

Alzheimer's disease; breviscapine; bone marrow mesenchymal stem cells; circular RNA ciRS-7; A ss deposition

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The aim of this study was to investigate the effect of breviscapine combined with bone marrow mesenchymal stem cells (BMSCs) treatment on reducing Aβ deposition in Alzheimer's disease (AD) patients. The results showed that the combination treatment was more effective in reducing Aβ deposition compared to single treatment.
Aims: This study aimed to clarify that breviscapine combined with bone marrow mesenchymal stem cells ( BMSCs) treatment can reduce A ss deposition in Alzheimer's disease (AD) patients. Background: AD is a common degenerative disease of the central nervous system. A ss protein deposition in the cerebral cortex and hippocampus causes neuronal peroxidation damage, synaptic dysfunction, neuroinflammation, and nerve cell apoptosis, and ultimately leads to AD. Objective: To investigate whether breviscapine combined with BMSCs treatment can reduce A ss deposition in AD. Methods: The AD rat model was successfully induced by A ss 1-42. The expression of protein and mRNA was detected by western blot and reverse transcription-quantitative PCR (RT-qPCR), respectively. Results: In AD rat brain tissue, the expression of circular RNA ciRS-7 (ciRS-7), ubiquitin carboxyl-terminal hydrolase L1 (UCHL1), and NF-kappaB p65 was significantly downregulated, and the expression of ss-amyloid precursor protein (APP), ss-site APPcleaving enzyme 1 (BAEC1), and A ss was upregulated. The expression of ciRS- 7, UCHL1, and p65 was significantly upregulated after breviscapine or BMSCs treatment, and there was increased APP and BAEC1 degradation. Notably, breviscapine combined with BMSCs treatment was more effective than either treatment alone. In SH-SY5Y cells, overexpression of ciRS-7 reduced A ss deposition by upregulating UCHL1 to degrade APP and BAEC1, but these effects were reversed with inhibition of NF-kB signaling. Finally, knockdown of ciRS-7 elevated A ss, APP, and BAEC1 expression in each group of rats compared with the control. Conclusion: Breviscapine combined with BMSCs treatment can reduce A ss deposition in AD rats and promote the degradation of APP and BAEC1 by activating NF-kB to promote UCHL1 expression.

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