The Neuroprotective Effect of Byu d Mar 25 in LPS-Induced Alzheimer's Disease Mice Model.

Xiumin Li,Lan Liu,Shanling Liu,Liang Tang,Yongcang Zhang,Dunzhu Danzeng,Hua Zhong,Cuiting Liang

doi:10.1155/2021/8879014

Abstract

Inflammatory factors play an important role in the pathogenesis of Alzheimer's disease (AD). Byu d Mar 25 (BM25) has been suggested to have protective effects in the central nervous system. However, the effect of BM25 on AD has not been determined. This study aims to investigate the neuroprotective effect of BM25 in AD. A total of 40 AD model mice were randomly assigned to the following five groups (n = 8 per group): the AD + NS group, the AD + donepezil group, and three AD + BM25 groups treated with either 58.39 mg/kg (AD + BM25-L), 116.77 mg/kg (AD + BM25-M), or 233.54 mg/kg BM25 (AD + BM25-H). The Morris water maze test was performed to assess alterations in spatial learning and memory deficits. Nissl staining was performed to detect Nissl bodies and neuronal damage. The expression of IL-1β and TNF-α was evaluated by ELISA. The protein expression of P-P38, P38, P-IκBα, caspase 1, COX2, and iNOS was determined by western blotting. The expression of Aβ, p-Tau, and CD11b was measured by immunohistochemistry. The mRNA expression levels of IL-1β, TNF-α, COX2, and iNOS were measured by qRT-PCR. Spatial memory significantly improved in the AD + BM25-M and AD + BM25-H groups compared with the AD + NS group (p < 0.05). The expression of Aβ and p-Tau significantly decreased in the AD + BM25-M and AD + BM25-H groups (p < 0.05). The neuron density and hierarchy and number of pyramidal neurons significantly increased in the AD + BM25-M and AD + BM25-H groups (p < 0.05). In addition, the expression levels of CD11b, IL-1β, TNF-α, COX2, iNOS, caspase 1, p-IκBα, and p-P38 significantly decreased in the AD + BM25-M and AD + BM25-H groups (p < 0.05). In conclusion, our findings suggest that BM25 may exert anti-inflammatory and neuroprotective effects in AD model mice by suppressing the activity of microglia and inhibiting the phosphorylation of IκBα and p38 MAPK.

Highlights

Alzheimer’s disease (AD) is a common neurodegenerative disease in the elderly population that causes declines in learning and memory [1,2,3,4]. e incidence of AD in people over the age of 65 is approximately 5% [5]
Animals and Drug Administration. is experiment followed the ethical standards of the Declaration of Helsinki as well as national and international guidelines. e research procedures were approved by the Ethics Committee of Tibet University, China (EC20190018). e LPS-induced AD mouse model was established according to our previous study [15]
E expression of IL-1β and tumor necrosis factor-α (TNF-α) was evaluated by Enzyme-Linked Immunosorbent Assay (ELISA). e expression of P-P38, P38, P-IκBα, Caspase1, COX2, and iNOS proteins was determined by western blotting. e expression of Aβ, p-Tau, and CD11b was measured by immunohistochemistry. e mRNA expression levels of IL1β, TNF-α, COX2, and iNOS were measured by qRT-PCR

Summary

Introduction

Alzheimer’s disease (AD) is a common neurodegenerative disease in the elderly population that causes declines in learning and memory [1,2,3,4]. e incidence of AD in people over the age of 65 is approximately 5% [5]. Alzheimer’s disease (AD) is a common neurodegenerative disease in the elderly population that causes declines in learning and memory [1,2,3,4]. Neuroinflammation has been suggested to play an important role in the development of AD [6, 7]. The role of glial cell activation, especially microglial cells, in neuroinflammation has been widely confirmed [8, 9]. Byu d Mar 25 (BM25) was developed by the Tibetan Medicine Master Dima Danzeng Peng Cuo in the 18th century and is still used today for multiple neurological disorders [10]. BM25 is composed of 25 rare herbs, such as saffron, calamus, and musk.

Objectives

Methods

Results

Conclusion