Abstract
Alzheimer's disease (AD) is a serious neurodegenerative disease. While the main pathological characteristic of AD is widely believed to be the accumulation of amyloid-beta (Aβ) in neurons around neurofibrillary plaques, the molecular mechanism of pathological changes is not clear. Traditional Chinese medicine offers many treatments for AD. Among these, Danggui Shaoyao San (DSS) is a classic prescription. In this study, an AD model was established by injecting Aβ 1–42 into the brains of rats, which were then treated with different concentrations of Danggui Shaoyao San (sham operation; model; and Danggui Shaoyao San high-dose, medium-dose, and low-dose intervention groups). The Morris water maze test was used to assess the learning and memory abilities of the animals in each group. Nissl staining was used to detect neurons. Mitophagy was evaluated by transmission electron microscopy and immunofluorescence colocalization. Apoptosis was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expression levels of autophagy- and apoptosis-related proteins were measured by western blot. Compared to the model group, the groups of AD rats administered medium and high doses of Danggui Shaoyao San showed significantly increased learning and memory abilities (P < 0.05), as well as significantly increased autophagosomes in the hippocampus. Moreover, the expression of PTEN-induced kinase 1 (PINK1), Parkin, and microtubule-associated protein light chain 3 (LC3-I/LC3-II) was increased, while that of p62 was significantly decreased (P < 0.05). The neuronal apoptosis rate was also significantly decreased, the Bcl-2/Bax ratio was significantly increased, and the cleaved caspase-3 protein expression was significantly decreased (P < 0.05). Therefore, Danggui Shaoyao San inhibited neuronal apoptosis in AD rats via a mechanism that may be related to the activation of the PINK1-Parkin-mediated mitophagy signaling pathway.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disease, the clinical symptoms of which include cognitive decline, declining living ability, and aberrant mental behavior
The drug treatments were administered continuously for 14 days. e results of place navigation in the Morris water maze showed that compared to the sham operation group, AD rats in the model group required a significantly longer time to find a platform (P < 0.05) and showed chaotic trajectories
In the space exploration experiment, compared to the sham operation group, the AD rats in the model group showed a significantly reduced number of times reaching the shuttle platform and time spent in the first quadrant (P < 0.05)
Summary
Alzheimer’s disease (AD) is a neurodegenerative disease, the clinical symptoms of which include cognitive decline, declining living ability, and aberrant mental behavior. E burden of AD on Chinese socioeconomic costs and the global economy is substantial and increasing. China were US$167.74 billion and are expected to increase to US$2.54 trillion in 2030 [2]. E main characteristic of AD is the hyperphosphorylation of the tau protein, which causes nerve fiber masses called tau tangles inside neurons, which are diagnostic biomarkers and new targets for drug discovery [3]. Aβ and nerve fiber tangles can affect microglial cells (MGC), induce inflammation, and are related to Evidence-Based Complementary and Alternative Medicine abnormal glucose metabolism. Inflammatory responses and abnormal glucose metabolism impair mitochondrial function. E accumulation of impaired mitochondria leads to a series of cascade reactions, eventually resulting in neuronal death, which might be the main pathological factors of AD [4]. Mitophagy can identify and eradicate damaged mitochondria to maintain normal mitochondrial function [5]
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