The Potential Protective Effect of Curcumin on Amyloid-β-42 Induced Cytotoxicity in HT-22 Cells.
Background. We aimed to investigate the effect and mechanism of curcumin (CUR) in Alzheimer’s disease (AD). Methods. Mouse hippocampal neuronal cell line HT-22 was treated with Aβ1–42 and/or CUR, and then cell viability was evaluated by cell counting kit 8, Beclin-l level was detected using western...
| Publicado en: | BioMed Research International Vol. 2018; pp. 1 - 9 |
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| Autores principales: | , , , , , , , |
| Formato: | diagnostic images research tables/charts Journal Article |
| Publicado: |
Wiley-Blackwell
1/15/2018
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=127324135&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 127324135 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 23146133 FT2T jtl: BioMed Research International issn: 23146133 maglogo: N pubinfo: dt: 1/15/2018 vid: 2018 pid: 480 pub: Wiley-Blackwell place: Malden, Massachusetts artinfo: ui: 127324135 127324135 127324135 10.1155/2018/8134902 127324135 ppf: 1 ppct: 8 formats: fmt: – @attributes: type: T – @attributes: type: P tig: atl: The Potential Protective Effect of Curcumin on Amyloid-β-42 Induced Cytotoxicity in HT-22 Cells. aug: au: Zhang, Lu Fang, Yu Cheng, Xuan Lian, Yajun Zeng, Zhaoshu Wu, Chuanjie Zhu, Hongcan Xu, Hongliang affil: Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China sug: subj: Curcumin Therapeutic Use Peptides Cytotoxicity Tests, Immunologic Alzheimer's Disease Prevention and Control Animal Studies Mouse (Computer) Hippocampus Anatomy and Histology Blotting, Western Phagocytosis Microscopy, Electron Cell Physiology Disease Progression Drug Toxicity Diagnosis Autophagy Proteins Physiology ab: Background. We aimed to investigate the effect and mechanism of curcumin (CUR) in Alzheimer’s disease (AD). Methods. Mouse hippocampal neuronal cell line HT-22 was treated with Aβ1–42 and/or CUR, and then cell viability was evaluated by cell counting kit 8, Beclin-l level was detected using western blotting, and the formation of autophagosomes was observed by transmission electron microscopy (TEM). Furthermore, transcriptome sequencing and analysis were performed in cells with Aβ1–42 alone or Aβ1–42 + CUR. Results. Aβ1–42 treatment significantly inhibited cell viability compared with untreated cells (P<0.01). After treatment for 48 h, CUR remarkably promoted cell viability compared with cell treated with Aβ1–42 alone (P<0.01). Compared with cells treated with Aβ1–42 alone, the expression of Beclin-1 was slightly reduced in cells with combined treatment of Aβ1–42 with CUR (P<0.05). Consistently, TEM results showed that CUR inhibited the formation of autophagosomes in cells treated with Aβ1–42. Furthermore, the protein-protein interaction network showed five key genes, including MYC, Cdh1, Acaca, Egr1, and CCnd1, likely involved in CUR effects. Conclusions. CUR might have a potential neuroprotective effect by promoting cell viability in AD, which might be associated with cell autophagy. Furthermore, MYC, Cdh1, and Acaca might be involved in the progression of AD. pubtype: Academic Journal doctype: diagnostic images research tables/charts Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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