MOESM5 of Aldehyde dehydrogenase 2 activity and aldehydic load contribute to neuroinflammation and Alzheimer’s disease related pathology

Autor: Joshi, Amit, Wassenhove, Lauren, Logas, Kelsey, Paras Minhas, Andreasson, Katrin, Weinberg, Kenneth, Che-Hong Chen, Mochly-Rosen, Daria
Rok vydání: 2019
DOI: 10.6084/m9.figshare.11358419.v1
Popis: Additional file 5: Figure S5. ALDH2*2/*2 deficiency increases astrocyte activation in response to ethanol-induced injury. a) C1q levels were measured using mouse Complement C1q ELISA kit in primary astrocytes in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol). b) Interlukin-6 levels were determined cell supernatant of primary astrocytes using ELISA kit in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol). c) TNF-α levels were determined cell supernatant of primary astrocytes using ELISA kit in the presence or absence of Alda-1 (20 μM/24 h; 50 mM Ethanol). d) Levels of cellular COX-2 at 6 h were determined by immunoblotting in primary astrocytes in the presence or absence of Alda-1 (20 μM; 50 mM Ethanol). β-actin was used as loading control. Protein levels were quantified and represented as fold change of WT Veh. e) Levels of Interlukin-1β release at 6 h were determined by immunoblotting in primary astrocytes in the presence or absence of Alda-1 (20 μM; 50 mM Ethanol). β-actin was used as loading control. Protein levels were quantified and represented as fold change of WT Veh. f) Caspase-1 activity was determined in primary astrocytes in the presence or absence of Alda-1 (20 μM; 50 mM Ethanol) using a fluorometric assay based on the cleavage of substrate YVAD-AFC. Data information: Mean, standard deviation, and p-values are shown. Results are presented as percent/ fold of control. n = 3–4 independent biological replicates; probability by one-way ANOVA (with Holm-Sidak post hoc test).
Databáze: OpenAIRE