During treatments, BV2 cells were cultured in medium containing 1% FBS. LRRK2 inhibitor GSK2578215A (GSK, Tocris Bioscience) and forskolin (Sigma Aldrich) were used at 2 μM and 30 μM, respectively, for 90 min. PDE4 inhibitor rolipram (Tocris Bioscience) was used at 10 μM for 30 min. Dimethyl sulfoxide (DMSO) was used as control.
Gsk2578215a gsk
Manufactured by Bio-Techne
GSK2578215A is a small molecule compound developed by Bio-Techne. It functions as a highly selective and potent inhibitor of the enzyme GSK-3 (glycogen synthase kinase-3). This compound can be utilized in various research applications that require the modulation of GSK-3 activity.
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Lab products found in correlation
2 protocols using gsk2578215a gsk
1
BV2 Cell Treatment Protocols
2
Astrocyte response to Alzheimer's amyloid-beta
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LRRK2 inhibitors were dissolved in DMSO. GSK2578215A (GSK, Tocris Bioscience, Bristol, UK) and IN-1 were used at 2 µM and 1 µM, respectively. Specifically, astrocytes were exposed to LRRK2 inhibitors 90 min before treatment with Aβ1-42 fibrils.
Chloroquine (CQ, Merck/Sigma Aldrich), an inhibitor of lysosomal activity, was dissolved in ultrapure distilled water and used on primary astrocytes at 25 µM for 16 h.
For Western blot and ROS detection experiments, astrocytes were treated with unlabeled 10 µM Aβ1-42 fibrils, or 10 mM-DMSO HCl as a control, for 16 h, while, for FACS experiments, astrocytes were treated with FAM-Aβ1-42 fibrils of 10 µM, or 10 mM-DMSO HCl as a control, for 2 h to analyze Aβ1-42 uptake. For the immunofluorescence, astrocytes were treated with 10 µM Aβ1-42 fibrils for 2 h.
During all the treatments, primary astrocytes were cultured in medium containing 1% FBS.
Chloroquine (CQ, Merck/Sigma Aldrich), an inhibitor of lysosomal activity, was dissolved in ultrapure distilled water and used on primary astrocytes at 25 µM for 16 h.
For Western blot and ROS detection experiments, astrocytes were treated with unlabeled 10 µM Aβ1-42 fibrils, or 10 mM-DMSO HCl as a control, for 16 h, while, for FACS experiments, astrocytes were treated with FAM-Aβ1-42 fibrils of 10 µM, or 10 mM-DMSO HCl as a control, for 2 h to analyze Aβ1-42 uptake. For the immunofluorescence, astrocytes were treated with 10 µM Aβ1-42 fibrils for 2 h.
During all the treatments, primary astrocytes were cultured in medium containing 1% FBS.
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