Protective Effects of Ginkgolide on a Cellular Model of Alzheimer’s Disease via Suppression of the NF-κB Signaling Pathway

NF-κB signaling has been reported to play a key regulatory role in the pathogenesis of Alzheimer’s disease (AD). The purpose of this study is to investigate the effects of ginkgolide on cell viability in an AD cellular model involving an APP/PS1 double gene-transfected HEK293 cell line (APP/PS1-HEK2...

Descripción completa

Detalles Bibliográficos
Autores principales: Niu, Tian-Tong, Yin, He, Xu, Bao-Lei, Yang, Ting-Ting, Li, Hui-Qin, Sun, Yi, Liu, Guang-Zhi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9117391/
https://www.ncbi.nlm.nih.gov/pubmed/35129804
http://dx.doi.org/10.1007/s12010-022-03828-5
_version_ 1784710324476182528
author Niu, Tian-Tong
Yin, He
Xu, Bao-Lei
Yang, Ting-Ting
Li, Hui-Qin
Sun, Yi
Liu, Guang-Zhi
author_facet Niu, Tian-Tong
Yin, He
Xu, Bao-Lei
Yang, Ting-Ting
Li, Hui-Qin
Sun, Yi
Liu, Guang-Zhi
author_sort Niu, Tian-Tong
collection PubMed
description NF-κB signaling has been reported to play a key regulatory role in the pathogenesis of Alzheimer’s disease (AD). The purpose of this study is to investigate the effects of ginkgolide on cell viability in an AD cellular model involving an APP/PS1 double gene-transfected HEK293 cell line (APP/PS1-HEK293) and further explore the mechanisms of action related to NF-κB signaling. The optimal time point and concentration of ginkgolide for cell proliferation were screened using a cell counting kit-8 assay. Based on the results, an in vitro study was performed by co-culture of APP/PS1-HEK293 with different dosages of ginkgolide, followed by an enzyme-linked immunosorbent assay to measure the levels of supernatant tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, as well as western blotting and real-time polymerase chain reaction to detect intracellular protein and mRNA expression of NF-κB p65, IκBa, Bcl-2, and Bax. APP/PS1-HEK293 cells exhibited the highest cell viability at a concentration of 100 µg/ml after 48 h of treatment with ginkgolide. The supernatant levels of TNF-α, IL-1β, and IL-6 in the high-dosage ginkgolide-treated groups were lower than those in the control group. Compared with the control group, there were decreased intracellular protein and mRNA expression of NF-κB p65 and Bax, but increased protein and mRNA expression of IκBa in both high-dosage and low-dosage groups. Ginkgolide may enhance cell viability, indicative of its neuroprotective effects on AD, at least partially via suppression of the NF-κB signaling pathway involving anti-apoptosis and anti-inflammation mechanisms. Therefore, ginkgolide might be a promising therapeutic agent against AD. GRAPHICAL ABSTRACT: [Image: see text] SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12010-022-03828-5.
format Online
Article
Text
id pubmed-9117391
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Springer US
record_format MEDLINE/PubMed
spelling pubmed-91173912022-05-20 Protective Effects of Ginkgolide on a Cellular Model of Alzheimer’s Disease via Suppression of the NF-κB Signaling Pathway Niu, Tian-Tong Yin, He Xu, Bao-Lei Yang, Ting-Ting Li, Hui-Qin Sun, Yi Liu, Guang-Zhi Appl Biochem Biotechnol Original Article NF-κB signaling has been reported to play a key regulatory role in the pathogenesis of Alzheimer’s disease (AD). The purpose of this study is to investigate the effects of ginkgolide on cell viability in an AD cellular model involving an APP/PS1 double gene-transfected HEK293 cell line (APP/PS1-HEK293) and further explore the mechanisms of action related to NF-κB signaling. The optimal time point and concentration of ginkgolide for cell proliferation were screened using a cell counting kit-8 assay. Based on the results, an in vitro study was performed by co-culture of APP/PS1-HEK293 with different dosages of ginkgolide, followed by an enzyme-linked immunosorbent assay to measure the levels of supernatant tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, as well as western blotting and real-time polymerase chain reaction to detect intracellular protein and mRNA expression of NF-κB p65, IκBa, Bcl-2, and Bax. APP/PS1-HEK293 cells exhibited the highest cell viability at a concentration of 100 µg/ml after 48 h of treatment with ginkgolide. The supernatant levels of TNF-α, IL-1β, and IL-6 in the high-dosage ginkgolide-treated groups were lower than those in the control group. Compared with the control group, there were decreased intracellular protein and mRNA expression of NF-κB p65 and Bax, but increased protein and mRNA expression of IκBa in both high-dosage and low-dosage groups. Ginkgolide may enhance cell viability, indicative of its neuroprotective effects on AD, at least partially via suppression of the NF-κB signaling pathway involving anti-apoptosis and anti-inflammation mechanisms. Therefore, ginkgolide might be a promising therapeutic agent against AD. GRAPHICAL ABSTRACT: [Image: see text] SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12010-022-03828-5. Springer US 2022-02-07 2022 /pmc/articles/PMC9117391/ /pubmed/35129804 http://dx.doi.org/10.1007/s12010-022-03828-5 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Original Article
Niu, Tian-Tong
Yin, He
Xu, Bao-Lei
Yang, Ting-Ting
Li, Hui-Qin
Sun, Yi
Liu, Guang-Zhi
Protective Effects of Ginkgolide on a Cellular Model of Alzheimer’s Disease via Suppression of the NF-κB Signaling Pathway
title Protective Effects of Ginkgolide on a Cellular Model of Alzheimer’s Disease via Suppression of the NF-κB Signaling Pathway
title_full Protective Effects of Ginkgolide on a Cellular Model of Alzheimer’s Disease via Suppression of the NF-κB Signaling Pathway
title_fullStr Protective Effects of Ginkgolide on a Cellular Model of Alzheimer’s Disease via Suppression of the NF-κB Signaling Pathway
title_full_unstemmed Protective Effects of Ginkgolide on a Cellular Model of Alzheimer’s Disease via Suppression of the NF-κB Signaling Pathway
title_short Protective Effects of Ginkgolide on a Cellular Model of Alzheimer’s Disease via Suppression of the NF-κB Signaling Pathway
title_sort protective effects of ginkgolide on a cellular model of alzheimer’s disease via suppression of the nf-κb signaling pathway
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9117391/
https://www.ncbi.nlm.nih.gov/pubmed/35129804
http://dx.doi.org/10.1007/s12010-022-03828-5
work_keys_str_mv AT niutiantong protectiveeffectsofginkgolideonacellularmodelofalzheimersdiseaseviasuppressionofthenfkbsignalingpathway
AT yinhe protectiveeffectsofginkgolideonacellularmodelofalzheimersdiseaseviasuppressionofthenfkbsignalingpathway
AT xubaolei protectiveeffectsofginkgolideonacellularmodelofalzheimersdiseaseviasuppressionofthenfkbsignalingpathway
AT yangtingting protectiveeffectsofginkgolideonacellularmodelofalzheimersdiseaseviasuppressionofthenfkbsignalingpathway
AT lihuiqin protectiveeffectsofginkgolideonacellularmodelofalzheimersdiseaseviasuppressionofthenfkbsignalingpathway
AT sunyi protectiveeffectsofginkgolideonacellularmodelofalzheimersdiseaseviasuppressionofthenfkbsignalingpathway
AT liuguangzhi protectiveeffectsofginkgolideonacellularmodelofalzheimersdiseaseviasuppressionofthenfkbsignalingpathway