Scutellarin Mitigates Aβ-Induced Neurotoxicity and Improves Behavior Impairments in AD Mice

Zeng, Yaqiong; Cui, Yin-Bo; Gu, Juan-Hua; Chen, Liang; Zhou, Xin‐Fu

doi:10.3390/molecules23040869

Cited by 25 publications

(10 citation statements)

References 27 publications

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“…Therefore, the PC12 cell line was used for the therapeutic evaluation of Scue. Similar to previous studies, 2 µg/ml Aβ induced ~32% cell death, whereas, pretreatment with Scue inhibited Aβ-induced apoptosis (9,38), thus, demonstrating that Scue may protect against the pro-apoptotic cellular effects of Aβ in vitro .…”

Section: Discussionsupporting

confidence: 88%

“…The flavonoid compound scutellarin (Scu) is ubiquitous in nature, particularly in the genus Erigeron (Asteraceae) and Scutellaria (Lamiaceae), and has been widely used in traditional Chinese medicine for a number of millennia (9–11). Recently, studies have made significant progress assessing the benefits of Scu, which exhibited neuroprotective effects, including anti-oxidant, anti-inflammatory and anti-apoptotic activities in numerous diseases (12–14).…”

Section: Introductionmentioning

confidence: 99%

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Scutellarein suppresses Aβ‑induced memory impairment via inhibition of the NF‑κB pathway in�vivo and in�vitro

Huang

Sui

et al. 2019

Oncol Lett

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The flavonoid compound scutellarin (Scu) is a traditional Chinese medicine used to treat a variety of diseases; however, the use of scutellarein (Scue), the hydrolysate of Scu, and its mechanisms of action in Alzheimer's disease (AD) have not been fully elucidated. In the present study, the effects of Scue on amyloid β (Aβ)-induced AD-like pathology were investigated. An in vitro model of inflammation and an aged rat model were used to confirm the effects of Scue. In vitro MTT assays and flow cytometry were used to assess the effects of Scue on cell viability and apoptosis, respectively. A Morris water maze was used to evaluate spatial learning and memory, and the levels of Aβ deposition, superoxide dismutase, malondialdehyde, apoptosis, neuro-inflammatory factors and nuclear factor-κB (NF-κB) activation in hippocampal tissues in vivo were measured to determine the effect of Scue in AD. Scue may be protective, as it decreased the apoptosis of hippocampal cells in vitro , inhibited Aβ-induced cognitive impairment, suppressed hippocampal neuro-inflammation and suppressed activation of NF-κB in vivo . Therefore, Scue may be a useful agent for the treatment of Aβ-associated pathology in the central nervous system through inhibition of the protein kinase B/NF-κB signaling pathway and thus, future studies are required to investigate the efficacy of Scue in patients with AD.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Scutellarein suppresses Aβ‑induced memory impairment via inhibition of the NF‑κB pathway in�vivo and in�vitro

Huang

Sui

et al. 2019

Oncol Lett

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“…Alzheimer's is the most common cause of dementia, accounts for 80% of cases, which leads to the progressive loss of cognitive skills, mental abilities, and learning capability (Anand et al, 2014;Zeng et al, 2018). Altering APP proteolysis is the most obvious feature of Alzheimer's, which produces abnormal Ab to induce neurotoxic effects; soluble Ab oligomerization is strongly correlated with cognitive decline in AD patients (Kim et al, 2013).…”

Section: Figmentioning

confidence: 99%

Curcumin Promotes Proliferation of Adult Neural Stem Cells and the Birth of Neurons in Alzheimer's Disease Mice via Notch Signaling Pathway

Li¹,

Han²,

et al. 2019

Cellular Reprogramming

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The abnormal deposition of amyloid-b peptide, a major component of senile plaques, has been reported to be the major cause of neuronal cell death and cognitive impairment in Alzheimer's disease (AD). Adult neurogenesis is related to the amelioration of impaired neurons and cognitive impairment. In the research, we investigated the function of curcumin on endogenous neural stem cells (NSCs) and hippocampal neurogenesis in mice. APP/PS1 transgenic mice as animal models were treated with curcumin, and a significant improvement in learning and memory function was observed. The improvement was associated with a significant increase in the number of new neural stem cells (BrdU + /Nestin +) and newborn neurons (NeuN/kI67 +) in the hippocampal region and decreased the number of apoptotic neurons (TUNEL + and Caspase-3/NeuN +). These results suggested that curcumin activated NSCs proliferation, improved neurogenesis, and ameliorated cognitive impairment of AD mice. Then, we identified that curcumin upregulated the expression of self-renewal genes, Notch1 and Hes1, and augmentation of CDK4, Cyclin D1, NICD, and Hes1 protein. As Notch activity was blocked by the DAPT, the related proteins were downregulated, and the initiating cell proliferation of curcumin was abolished. These results might suggest that the function of curcumin was dependent on Notch signaling pathway.

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“…Inflammation in the brain is one of the hallmarks of AD and is initiated in the central nervous system (Zeng et al, 2018). Numerous studies have reported that Aβ can trigger oxidative stress in the brain, and also activate microglia leading to neuroinflammation and cognitive dysfunction (Kobayashi et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Treatment with Bifidobacteria can suppress Aβ accumulation and neuroinflammation in APP/PS1 mice

Zhang

et al. 2020

PeerJ

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Background Alzheimer’s disease (AD), being a complex disorder, is affected either by genetic or environmental factors or both. It is observed that there is an excessive accumulation of amyloid β (Aβ) in the extracellular space of the brain. AD is the first neurodegenerative disease in the elderly, and so far there is no effective treatment. In recent years, many studies have reported that Alzheimer’s disease has a relationship with gut microflora, indicating that regulating gut microbiota could offer therapeutic intervention for AD. This study explored the effect Bifidobacteria has in averting AD. Methods WT and APP/PS1 mice were used for the experiments. The mice were randomly assigned to four groups: WT group, WT + Bi group, AD group (APP/PS1 mouse) and AD + Bi group (Bifidobacteria-treated APP/PS1 mouse). Treatment with Bifidobacteria lasted for 6 months and mice were prepared for immunohistochemistry, immunofluorescence, Thioflavin S staining, Western blotting, PCR and Elisa quantitative assay. Results The results show that after 6 months of treatment with Bifidobacteria signiis to be lesficantly reduces Aβ deposition in cortex and hippocampus of AD mice. The level of insoluble Aβ in the hippocampus and cortex of AD+Bi mice was decreased compared with AD mice. Meanwhile, a significant decrease in the level of soluble Aβ in the cortex of AD+Bi mice but not in the hippocampus was observed. The activation of microglia and the release of inflammatory factors were also determined in this study. From the results, Bifidobacteria inhibited microglial activation and reduced IL-1β, TNF-α, IL-4, IL-6 and INF-γ release. Altogether, these results implied that Bifidobacteria can alleviate the pathological changes of AD through various effects.

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Scutellarin Mitigates Aβ-Induced Neurotoxicity and Improves Behavior Impairments in AD Mice

Cited by 25 publications

References 27 publications

Scutellarein suppresses Aβ‑induced memory impairment via inhibition of the NF‑κB pathway in�vivo and in�vitro

Scutellarein suppresses Aβ‑induced memory impairment via inhibition of the NF‑κB pathway in�vivo and in�vitro

Curcumin Promotes Proliferation of Adult Neural Stem Cells and the Birth of Neurons in Alzheimer's Disease Mice via Notch Signaling Pathway

Treatment with Bifidobacteria can suppress Aβ accumulation and neuroinflammation in APP/PS1 mice

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