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  1. Article ; Online: Hydroxysafflor Yellow A Exerts Neuroprotective Effect by Reducing Aβ Toxicity Through Inhibiting Endoplasmic Reticulum Stress in Oxygen-Glucose Deprivation/Reperfusion Cell Model.

    Ma, Hui-Han / Wen, Jun-Ru / Fang, Hao / Su, Shan / Wan, Can / Zhang, Chao / Lu, Fang-Mei / Fan, Ling-Ling / Wu, Guang-Liang / Zhou, Zi-Yi / Qiao, Li-Jun / Zhang, Shi-Jie / Cai, Ye-Feng

    Rejuvenation research

    2023  Volume 26, Issue 2, Page(s) 57–67

    Abstract: Ischemia stroke is thought to be one of the vascular risks associated with neurodegenerative diseases, such as Alzheimer's disease (AD). Hydroxysafflor yellow A (HSYA) has been reported to protect against stroke and AD, while the underlying mechanism ... ...

    Abstract Ischemia stroke is thought to be one of the vascular risks associated with neurodegenerative diseases, such as Alzheimer's disease (AD). Hydroxysafflor yellow A (HSYA) has been reported to protect against stroke and AD, while the underlying mechanism remains unclear. In this study, SH-SY5Y cell model treated with oxygen-glucose deprivation/reperfusion (OGD/R) was used to explore the potential mechanism of HSYA. Results from cell counting kit-8 (CCK-8) showed that 10 μM HSYA restored the cell viability after OGD 2 hours/R 24 hours. HSYA reduced the levels of malondialdehyde and reactive oxygen species, while improved the levels of superoxide dismutase and glutathione peroxidase. Furthermore, apoptosis was inhibited, and the expression of brain-derived neurotrophic factor was improved after HSYA treatment. In addition, the expression levels of amyloid-β peptides (Aβ) and BACE1 were decreased by HSYA, as well as the expression levels of binding immunoglobulin heavy chain protein, PKR-like endoplasmic reticulum (ER) kinase pathway, and activating transcription factor 6 pathway, whereas the expression level of protein disulfide isomerase was increased. Based on these results, HSYA might reduce Aβ toxicity after OGD/R by interfering with apoptosis, oxidation, and neurotrophic factors, as well as relieving ER stress.
    MeSH term(s) Humans ; Oxygen/metabolism ; Neuroprotective Agents/pharmacology ; Amyloid Precursor Protein Secretases/pharmacology ; Glucose/metabolism ; Aspartic Acid Endopeptidases/pharmacology ; Neuroblastoma ; Quinones/pharmacology ; Apoptosis ; Chalcone/pharmacology ; Reperfusion Injury/metabolism ; Stroke ; Reperfusion ; Endoplasmic Reticulum Stress
    Chemical Substances Oxygen (S88TT14065) ; Neuroprotective Agents ; hydroxysafflor yellow A (146087-19-6) ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Glucose (IY9XDZ35W2) ; Aspartic Acid Endopeptidases (EC 3.4.23.-) ; Quinones ; Chalcone (5S5A2Q39HX)
    Language English
    Publishing date 2023-03-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2150779-X
    ISSN 1557-8577 ; 1549-1684
    ISSN (online) 1557-8577
    ISSN 1549-1684
    DOI 10.1089/rej.2022.0054
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Kai-Xin-San Improves Cognitive Impairment via Wnt/β-Catenin and IRE1/XBP1s Signalings in APP/PS1 Mice.

    Xu, Yu-Min / Lu, Fang-Mei / Xu, Hong-Cai / Zhang, Jie / Hei, Shang-Yan / Qiu, Yu-Hui / Cai, Ye-Feng / Zhang, Shi-Jie / Zhao, Min

    Rejuvenation research

    2023  Volume 26, Issue 3, Page(s) 105–115

    Abstract: Alzheimer's disease (AD) is the most common type of dementia with an insidious onset and slow progression. Kai-Xin-San (KXS) has been reported to be effective in improving cognitive impairment in AD. However, the mechanism is still confused. In this ... ...

    Abstract Alzheimer's disease (AD) is the most common type of dementia with an insidious onset and slow progression. Kai-Xin-San (KXS) has been reported to be effective in improving cognitive impairment in AD. However, the mechanism is still confused. In this study, we employed APP/PS1 mice to explore the neuroprotective mechanism of KXS. Forty-eight male APP/PS1 mice were randomly divided into model group, KXS groups (0.7, 1.4, and 2.8 g/kg/d, p.o.) and the wild-type mice were assigned to the normal control group (
    MeSH term(s) Animals ; Male ; Mice ; Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; beta Catenin ; Cognitive Dysfunction/drug therapy ; Disease Models, Animal ; Glycogen Synthase Kinase 3 beta ; Mice, Transgenic ; Protein Serine-Threonine Kinases ; Wnt Signaling Pathway/drug effects
    Chemical Substances beta Catenin ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Kai-Xin-San ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ern2 protein, mouse (EC 2.7.1.-) ; Xbp1 protein, mouse
    Language English
    Publishing date 2023-05-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2150779-X
    ISSN 1557-8577 ; 1549-1684
    ISSN (online) 1557-8577
    ISSN 1549-1684
    DOI 10.1089/rej.2022.0063
    Database MEDical Literature Analysis and Retrieval System OnLINE

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