Title:Breviscapine Combined with BMSCs Reduces Aβ Deposition in Rat
with Alzheimer's Disease by Regulating Circular RNA ciRS-7
Volume: 23
Issue: 1
Author(s): Fengqin Sun, Yulin Zhang, Xinran Wu, Xu Xu, Chaodie Zhu and Wei Huang*
Affiliation:
- Department of Neurology, The Third People’s Hospital of Yunnan Province, 292 Beijing Road, Kunming,
650011, China
Keywords:
Alzheimer's disease, breviscapine, bone marrow mesenchymal stem cells, circular RNA ciRS-7, Aβ deposition.
Abstract:
Aims: This study aimed to clarify that breviscapine combined with bone
marrow mesenchymal stem cells (BMSCs) treatment can reduce Aβ deposition in
Alzheimer's disease (AD) patients.
Background: AD is a common degenerative disease of the central nervous system. Aβ
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 Aβ deposition in AD.
Methods: The AD rat model was successfully induced by Aβ1-42. 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 β-amyloid precursor protein (APP), β-site APPcleaving
enzyme 1 (BAEC1), and Aβ 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 Aβ 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 Aβ, APP, and BAEC1 expression in
each group of rats compared with the control.
Conclusion: Breviscapine combined with BMSCs treatment can reduce Aβ deposition in
AD rats and promote the degradation of APP and BAEC1 by activating NF-kB to
promote UCHL1 expression.
