Abstract
Amyloid-β (Aβ) is commonly recognized as the most important factor that results in neuronal cell death and accelerates the progression of Alzheimer’s disease (AD). Increasing evidence suggests that microglia activated by Aβ release an amount of neurotoxic inflammatory cytokines that contribute to neuron death and aggravate AD pathology. In our previous studies, we found that lychee seed fraction (LSF), an active fraction derived from the lychee seed, could significantly improve the cognitive function of AD rats and inhibit Aβ-induced neuroinflammation in vitro, and decrease neuronal injuries in vivo and in vitro. In the current study, we aimed to isolate and identify the specific components in LSF that were responsible for the anti-neuroinflammation effect using preparative high performance liquid chromatography (pre-HPLC), liquid chromatography-mass spectrometry (LC-MS), and nuclear magnetic resonance (NMR) methods. To this end, we confirmed two polyphenols including catechin and procyanidin A2 that could improve the morphological status of BV-2 cells and suppress the release, mRNA levels, and protein expression of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) through downregulating the nuclear factor-κB (NF-κB) signaling pathway using ELISA, RT-PCR, and Western blotting methods. Furthermore, catechin and procyanidin A2 could inhibit Aβ-induced apoptosis in BV-2 cells by upregulating Bcl-2 and downregulating Bax protein expression. Therefore, the current study illustrated the active substances in lychee seed, and first reported that catechin and procyanidin A2 could suppress neuroinflammation in Aβ-induced BV-2 cells, which provides detailed insights into the molecular mechanism of catechin and procyanidin A2 in the neuroprotective effect, and their further validations of anti-neuroinflammation in vivo is also essential in future research.
Highlights
Alzheimer’s disease (AD) is the most common type of late-onset dementia, which is characterized by dysfunction in cognition and behavior
Aggregated proteins such as Aβ, α-synuclein, and mHtt associated with AD, Parkinson’s disease (PD), and Huntington’s disease (HD) respectively, can activate microglia and release amounts of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), nitric oxide (NO), and reactive oxygen species (ROS)
We found that lychee seed fraction (LSF), a bioactive fraction derived from lychee seed, could improve cognitive function of AD rats, suppress apoptosis in Aβ-induced PC-12 cells, and reduce Aβ and tau proteins in T2DM rats [19,20]
Summary
Alzheimer’s disease (AD) is the most common type of late-onset dementia, which is characterized by dysfunction in cognition and behavior. Aggregated proteins such as Aβ, α-synuclein, and mHtt associated with AD, Parkinson’s disease (PD), and Huntington’s disease (HD) respectively, can activate microglia and release amounts of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), nitric oxide (NO), and reactive oxygen species (ROS). These toxic inflammatory cytokines induce microglial activation and neuronal death, which in turn further aggravate the inflammatory response. In AD patients, the morphology of microglia has been found to be abnormal and over-activated by oligomeric Aβ [9,10]
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