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Article: Astragaloside IV attenuates neuroinflammation and ameliorates cognitive impairment in Alzheimer's disease via inhibiting NF-κB signaling pathway.

He, Li / Sun, Jinxia / Miao, Zhulei / Chen, Shengmin / Yang, Guizhen

2023 Volume 9, Issue 2, Page(s) e13411

Abstract: The inflammatory process plays a significant role in the pathophysiology of Alzheimer's disease (AD). Anti-neuroinflammatory cascade is now considered an important measure for AD treatment. Astragaloside IV (AS-IV), a saponin of Astragali radix, has ... ...

Abstract	The inflammatory process plays a significant role in the pathophysiology of Alzheimer's disease (AD). Anti-neuroinflammatory cascade is now considered an important measure for AD treatment. Astragaloside IV (AS-IV), a saponin of Astragali radix, has shown significant anti-inflammatory properties and protective effects against neurodegenerative diseases. However, the mechanisms of AS-IV in treating Alzheimer's disease (AD) have not been fully determined. The experiment research was carried out to comprehensively confirm the beneficial effects and underlying molecular mechanisms of AS-IV to AD. In this research, BV-2 cells were cultured
Language	English
Publishing date	2023-02-03
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e13411
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Astragaloside IV attenuates neuroinflammation and ameliorates cognitive impairment in Alzheimer’s disease via inhibiting NF-κB signaling pathway

Li He / Jinxia Sun / Zhulei Miao / Shengmin Chen / Guizhen Yang

Heliyon, Vol 9, Iss 2, Pp e13411- (2023)

2023

Abstract: The inflammatory process plays a significant role in the pathophysiology of Alzheimer’s disease (AD). Anti-neuroinflammatory cascade is now considered an important measure for AD treatment. Astragaloside IV (AS-IV), a saponin of Astragali radix, has ... ...

Abstract	The inflammatory process plays a significant role in the pathophysiology of Alzheimer’s disease (AD). Anti-neuroinflammatory cascade is now considered an important measure for AD treatment. Astragaloside IV (AS-IV), a saponin of Astragali radix, has shown significant anti-inflammatory properties and protective effects against neurodegenerative diseases. However, the mechanisms of AS-IV in treating Alzheimer’s disease (AD) have not been fully determined. The experiment research was carried out to comprehensively confirm the beneficial effects and underlying molecular mechanisms of AS-IV to AD. In this research, BV-2 cells were cultured in vitro and treated by AS-IV under the stimulation of LPS, qRT-PCR was adopted to analyze the mRNA expression level of inflammatory factors. Western-blot was carried out to analyze the phosphorylation level of NF-κB signaling pathway. 5xFAD mice were administrated AS-IV mixed in the diet for 3 months. Behavioral experiments were adopted to analyze learning and memory abilities. Immunohistochemical staining was adopted to observe the proliferation of microglias and the accumulation of Aβ plaques. AS-IV cut down the mRNA expression of IL-1β, COX-2, iNOS and TNF-α in LPS-stimulated BV-2 cells by suppressing the phosphorylation of IκB and p65, and inhibited the phosphorylated p65 from entering the nucleus. AS-IV increased the frequency of recognizing new objects in the novel object recognition test, shortened the escape latency, raised the number of crossing platform in the Morris water maze, inhibited the hyperplasia of microglias, and reduced the production of senile plaques in 5xFAD mice. In brief, AS-IV ameliorates learning and memory impairment by relieving the intensity of neuroinflammatory response in AD. Therefore, AS-IV is very promising to be a herbal medicine for AD treatment.
Keywords	Alzheimer’s disease ; Astragaloside IV ; Neuroinflammation ; NF-κB ; Science (General) ; Q1-390 ; Social sciences (General) ; H1-99
Subject code	630
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Micheliolide attenuates neuroinflammation to improve cognitive impairment of Alzheimer's disease by inhibiting NF-κB and PI3K/Akt signaling pathways.

Yang, Guizhen / Hu, You / Qin, Xiangyang / Sun, Jinxia / Miao, Zhulei / Wang, Lixin / Ke, Zunji / Zheng, Yuejuan

Heliyon

2023 Volume 9, Issue 7, Page(s) e17848

Abstract: Inflammatory reaction in the brain activates glial cells, and over-activated glial cells secrete inflammatory mediators, which aggravates the inflammatory response in the brain and accelerates the development of Alzheimer's disease (AD) in turn. Numerous ...

Abstract	Inflammatory reaction in the brain activates glial cells, and over-activated glial cells secrete inflammatory mediators, which aggravates the inflammatory response in the brain and accelerates the development of Alzheimer's disease (AD) in turn. Numerous natural compounds from herbs can alleviate inflammation, and it is very promising to find
Language	English
Publishing date	2023-07-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e17848
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Article: Transcription factor

Sun, Zhulei / Huang, Gui / Cheng, Hepeng

Cancer management and research

2019 Volume 11, Page(s) 6079–6090

Abstract: Background: Taurine-upregulated gene 1: Methods: Nuclear factor-erythroid 2: Results: Nrf2: Conclusions: ... ...

Abstract	Background: Taurine-upregulated gene 1 Methods: Nuclear factor-erythroid 2 Results: Nrf2 Conclusions: Nrf2
Language	English
Publishing date	2019-07-04
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2508013-1
ISSN	1179-1322
ISSN	1179-1322
DOI	10.2147/CMAR.S200998
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Article ; Online: Astragaloside IV attenuates neuroinflammation and ameliorates cognitive impairment in Alzheimer's disease via inhibiting NF-κB signaling pathway

He, Li / Sun, Jinxia / Miao, Zhulei / Chen, Shengmin / Yang, Guizhen

Heliyon. 2023 Feb., v. 9, no. 2 p.e13411-

2023

Abstract	The inflammatory process plays a significant role in the pathophysiology of Alzheimer's disease (AD). Anti-neuroinflammatory cascade is now considered an important measure for AD treatment. Astragaloside IV (AS-IV), a saponin of Astragali radix, has shown significant anti-inflammatory properties and protective effects against neurodegenerative diseases. However, the mechanisms of AS-IV in treating Alzheimer's disease (AD) have not been fully determined. The experiment research was carried out to comprehensively confirm the beneficial effects and underlying molecular mechanisms of AS-IV to AD. In this research, BV-2 cells were cultured in vitro and treated by AS-IV under the stimulation of LPS, qRT-PCR was adopted to analyze the mRNA expression level of inflammatory factors. Western-blot was carried out to analyze the phosphorylation level of NF-κB signaling pathway. 5xFAD mice were administrated AS-IV mixed in the diet for 3 months. Behavioral experiments were adopted to analyze learning and memory abilities. Immunohistochemical staining was adopted to observe the proliferation of microglias and the accumulation of Aβ plaques. AS-IV cut down the mRNA expression of IL-1β, COX-2, iNOS and TNF-α in LPS-stimulated BV-2 cells by suppressing the phosphorylation of IκB and p65, and inhibited the phosphorylated p65 from entering the nucleus. AS-IV increased the frequency of recognizing new objects in the novel object recognition test, shortened the escape latency, raised the number of crossing platform in the Morris water maze, inhibited the hyperplasia of microglias, and reduced the production of senile plaques in 5xFAD mice. In brief, AS-IV ameliorates learning and memory impairment by relieving the intensity of neuroinflammatory response in AD. Therefore, AS-IV is very promising to be a herbal medicine for AD treatment.
Keywords	astragalosides ; cognitive disorders ; diet ; gene expression ; herbal medicines ; hyperplasia ; immunohistochemistry ; memory ; memory disorders ; pathophysiology ; phosphorylation ; Alzheimer's disease ; Astragaloside IV ; Neuroinflammation ; NF-κB
Language	English
Dates of publication	2023-02
Publishing place	Elsevier Ltd
Document type	Article ; Online
Note	Use and reproduction
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e13411
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Micheliolide attenuates neuroinflammation to improve cognitive impairment of Alzheimer's disease by inhibiting NF-κB and PI3K/Akt signaling pathways

Guizhen Yang / You Hu / Xiangyang Qin / Jinxia Sun / Zhulei Miao / Lixin Wang / Zunji Ke / Yuejuan Zheng

Heliyon, Vol 9, Iss 7, Pp e17848- (2023)

2023

Abstract	Inflammatory reaction in the brain activates glial cells, and over-activated glial cells secrete inflammatory mediators, which aggravates the inflammatory response in the brain and accelerates the development of Alzheimer's disease (AD) in turn. Numerous natural compounds from herbs can alleviate inflammation, and it is very promising to find anti-neuroinflammatory natural compounds. Micheliolide (MCL) is an asesquiterpene lactone. Studies have proved that MCL showed an obvious anti-inflammatory property. Nevertheless, whether MCL can treat AD has not been determined. In this research, AD model mice were fed with a diet supplemented MCL for 3 months, the cognitive ability and inflammatory state of mice were detected. We found that MCL raised the frequency of touching novel objects, cut down the escape latency, raised the number of crossing platform, inhibited the infiltration of inflammatory cells and the secretion of interleukin-1α (IL-1α), IL-12p40, IL-13, IL-17A, tumor necrosis factor-α (TNF-α), granulocyte colony stimulating factor (G-CSF), macrophage inflammatory protein-1α (MIP-1α) and monocyte chemotactic protein-1 (MCP-1) in peripheral blood samples, inhibited the hyperplasia of glial cells and the production of IL-1α, IL-4, G-CSF, granulocyte-macrophage colony stimulating factor (GM-CSF), MIP-1α and MIP-1β, and reduced the deposition of Aβ peptides in the brain of AD mice. We also concluded that MCL dropped the expression of IL-1β, TNF-α, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and the phosphorylation of IκB, p65 and Akt in BV-2 cells. In conclusion, MCL alleviates the intensity of systemic inflammatory reaction via inhibiting nuclear transcription factor κ gene binding (NF-κB) and phosphoinositide-3-kinase/serine/threonine kinase (PI3K/Akt) pathways in glial cells, and improves the cognitive impairment of AD mice. Therefore, MCL could be a therapeutic candidate for AD.
Keywords	Alzheimer's disease ; Micheliolide ; Neuro-inflammation ; NF-κB ; PI3K/Akt ; Glial cells ; Science (General) ; Q1-390 ; Social sciences (General) ; H1-99
Subject code	616
Language	English
Publishing date	2023-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Quercitrin improved cognitive impairment through inhibiting inflammation induced by microglia in Alzheimer's disease mice.

Wang, Lixin / Sun, Jinxia / Miao, Zhulei / Jiang, Xin / Zheng, Yuejuan / Yang, Guizhen

Neuroreport

2022 Volume 33, Issue 8, Page(s) 327–335

Abstract: Objective: Diets rich in quercitrin show a neuroprotective effect, but the mechanism is not very clear at present. The objective of this study is to explore the effect and mechanism of quercitrin in the treatment of alzheimer's disease (AD).: Methods!# ...

Abstract	Objective: Diets rich in quercitrin show a neuroprotective effect, but the mechanism is not very clear at present. The objective of this study is to explore the effect and mechanism of quercitrin in the treatment of alzheimer's disease (AD). Methods: 5XFAD transgenic mice were fed with a diet supplemented with quercitrin for three consecutive months. Behavioral experiments were conducted to assess the cognitive ability, luminex liquid chip technology was used to assess the production of proinflammatory cytokines and immunohistochemistry was used to elucidate the activation of microglia. Results: Quercitrin increased the frequency in exploring new objects, shortened the escape latency and increased the frequency crossing the platform in AD model mice. Quercitrin inhibited the activation and proliferation of microglia, inhibited the secretion of inflammatory cytokines and chemokines and reduced the accumulation of amyloid-β plaques in AD model mice. Conclusion: Quercitrin improved mice cognitive impairment through alleviating the intensity of inflammatory response and is a promising medicinal plant extract in the treatment of AD.
MeSH term(s)	Alzheimer Disease/drug therapy ; Amyloid beta-Peptides/pharmacology ; Animals ; Cognitive Dysfunction/drug therapy ; Cytokines ; Disease Models, Animal ; Inflammation/drug therapy ; Mice ; Mice, Transgenic ; Microglia/metabolism ; Quercetin/analogs & derivatives ; Quercetin/therapeutic use
Chemical Substances	Amyloid beta-Peptides ; Cytokines ; quercitrin (2Y8906LC5P) ; Quercetin (9IKM0I5T1E)
Language	English
Publishing date	2022-04-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1049746-8
ISSN	1473-558X ; 0959-4965
ISSN (online)	1473-558X
ISSN	0959-4965
DOI	10.1097/WNR.0000000000001783
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Article ; Online: The diagnostic and prognostic value of

Sun, Zhulei / Liu, Juncai / Jing, Hong / Dong, Shu-Xiao / Wu, Jiang

Oncotarget

2017 Volume 8, Issue 51, Page(s) 89142–89148

Abstract: The Checkpoint with Forkhead-associated and Ring finger domains ( ...

Abstract	The Checkpoint with Forkhead-associated and Ring finger domains (
Language	English
Publishing date	2017-10-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.19408
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Article ; Online: Expression of TdT in Myoepithelial Cells: Investigation in Breasts, Sweat Glands, and Salivary Lesions Emphasizing the Never-Documented Immunohistochemical Findings.

Zhou, Jun / Xu, Haimin / Zeng, Hong / Ma, Hongjun / Yu, Jingjing / Liu, Xia / Sun, Zhulei / Zhou, Luting / Zheng, Saifang / Wang, Xue / Wang, Anran / Wang, Chaofu

International journal of surgical pathology

2020 Volume 28, Issue 7, Page(s) 711–720

Abstract: ... ...

Abstract	Background
MeSH term(s)	Biomarkers, Tumor/analysis ; Breast/metabolism ; Breast Neoplasms/diagnosis ; DNA Nucleotidylexotransferase/analysis ; DNA Nucleotidylexotransferase/biosynthesis ; Female ; Humans ; Immunohistochemistry ; Male ; Salivary Gland Neoplasms/diagnosis ; Salivary Glands/metabolism ; Sweat Gland Neoplasms/diagnosis ; Sweat Glands/metabolism
Chemical Substances	Biomarkers, Tumor ; DNA Nucleotidylexotransferase (EC 2.7.7.31)
Language	English
Publishing date	2020-05-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	1336393-1
ISSN	1940-2465 ; 1066-8969
ISSN (online)	1940-2465
ISSN	1066-8969
DOI	10.1177/1066896920916792
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Article ; Online: Long noncoding RNA MEG3 inhibits breast cancer growth via upregulating endoplasmic reticulum stress and activating NF-κB and p53.

Zhang, Yan / Wu, Jiang / Jing, Hong / Huang, Gui / Sun, Zhulei / Xu, Shouming

Journal of cellular biochemistry

2018 Volume 120, Issue 4, Page(s) 6789–6797

Abstract: Long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) has been implicated as a tumor suppressor gene in several human cancer types. However, little is known regarding its involvement and potential mechanism in human breast cancer. In this study, we ... ...

Abstract	Long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) has been implicated as a tumor suppressor gene in several human cancer types. However, little is known regarding its involvement and potential mechanism in human breast cancer. In this study, we explored the effect of MEG3 on the growth of human breast cancer cell line MDA-MB-231 in vitro and in vivo, and sought to elucidate the potential signaling mechanisms. Ectopic overexpression of MEG3 using a lentiviral vector Lv-MEG3 significantly inhibited breast cancer cell growth in vitro and a cancer xenograft growth in vivo. MEG3 overexpression led to marked increase of apoptosis in breast cancer cells as determined using flow cytometry and fragmented DNA labeling. Moreover, ectopic expression of MEG3 increased the expression of endoplasmic reticulum (ER) stress-related proteins required for unfolded protein response, including glucose-regulated protein 78 (GRP78), inositol-requiring enzyme 1 (IRE1), protein kinase RNA (PKR)-like ER kinase (PERK), and activated transcription factor 6 (ATF6), as well as proapoptotic proteins CCAAT/enhancer binding protein homologous protein (CHOP) and caspase-3. Finally, MEG3 overexpression markedly increased nuclear factor κB (NF-κB) expression, NF-κB translocation to the nucleus, and p53 expression, whereas pharmacological inhibition of NF-κB completely abolished MEG3-induced activation of p53. Together, these results suggest that MEG3 inhibits breast cancer growth and induces breast cancer apoptosis, partially via the activation of the ER stress, NF-κB and p53 pathways, and that NF-κB signaling is required for MEG3-induced p53 activation in breast cancer cells. Our results indicate targeting lncRNA MEG3 may represent a novel strategy for breast cancer therapy.
MeSH term(s)	Animals ; Apoptosis ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Proliferation ; Endoplasmic Reticulum Stress ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Neoplasm Invasiveness ; RNA, Long Noncoding/genetics ; Signal Transduction ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Unfolded Protein Response ; Xenograft Model Antitumor Assays
Chemical Substances	Biomarkers, Tumor ; MEG3 non-coding RNA, human ; NF-kappa B ; RNA, Long Noncoding ; TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2018-12-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.27982
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