Protective effects of genistein on Aβ₂₅₋₃₅-induced PC12 cell injury via regulating CaM-CaMKIV signaling pathway

Copyright© by the Chinese Pharmaceutical Association..

Genistein is a kind of isoflavone compounds, also called phytoestrogens, with clinical effects on cardiovascular disease, cancer and postmenopausal-related gynecological diseases, and also has the potentiality in the prevention and treatment of Alzheimer's disease(AD). In this study, the protective effect of genistein on Aβ₂₅₋₃₅-induced PC12 cell injury and effect on CaM-CaMKIV signaling pathway were observed to investigate its mechanism for AD. PC12 cells were cultured in vitro and then the safe concentration of genistein and the modeling concentration and optimal time point of administration of Aβ₂₅₋₃₅ were screened by MTT assay. After being pretreated with different concentrations of genistein(25, 50, 100 μmol·L⁻¹) on PC12 cells, the AD model of PC12 cells was induced by Aβ₂₅₋₃₅. Then the survival rate of cells was detected by MTT assay; morphological change of cells was observed under the inverted microscope, and apoptosis of cells was assessed by AO/EB fluorescence staining; the neuroprotective effects of genistein on AD cell model were observed and the optimal concentration of genistein was determined. Expressions of mRNA and protein levels of CaM, CaMKK, CaMKIV and tau were detected by qRT-PCR and Western blot assay, respectively. The results showed that as compared with the blank group, the cell survival rate was decreased; the cell damage and apoptosis were increased; and the expressions of mRNA and protein levels of CaM, CaMKK, CaMKIV and tau were increased in AD model group. Genistein could significantly improve the cell survival rate, reduce the cell damage and apoptosis of AD cell model, and significantly down-regulate the expressions of mRNA and protein levels of CaM, CaMKK, CaMKIV and tau of AD cell model. These results indicated that genistein has obviously neuroprotective effect on the AD cell model induced by Aβ₂₅₋₃₅, and the mechanism may be related to the down-regulation of CaM-CaMKIV signaling pathway and Tau protein expression.

Medienart:

E-Artikel

Erscheinungsjahr:

2018

Erschienen:

2018

Enthalten in:

Zur Gesamtaufnahme - volume:43

Enthalten in:

Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica - 43(2018), 3 vom: 02. Feb., Seite 571-576

Sprache:

Chinesisch

Beteiligte Personen:

Cai, Biao [VerfasserIn]
Ye, Shu [VerfasserIn]
Wang, Yan [VerfasserIn]
Hua, Ru-Peng [VerfasserIn]
Wang, Ting-Ting [VerfasserIn]
Lix, Li Jing [VerfasserIn]
Jiang, Ai-Juan [VerfasserIn]
Shen, Guo-Ming [VerfasserIn]

Links:

Volltext

Themen:

Alzheimer's disease
Amyloid beta-Peptides
Amyloid beta-protein (25-35)
CaM-CaMKIV signaling pathway
Calcium-Calmodulin-Dependent Protein Kinase Type 4
Calmodulin
Camk4 protein, rat
DH2M523P0H
EC 2.7.11.17
Genistein
Journal Article
PC12 cell
Peptide Fragments
Protective Agents
Tau protein

Anmerkungen:

Date Completed 10.07.2019

Date Revised 10.07.2019

published: Print

Citation Status MEDLINE

doi:

10.19540/j.cnki.cjcmm.2018.0012

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM282501584