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Background: Amyloid beta (Aβ) is a protein of 40-42 aminoacids that are crucially involved in Alzheimer’s disease as the main component of amyloid plaques. Rho-kinase is believed to be involved in the regulation of stress fiber formation, smooth muscle contraction, cell migration and proliferation. Rho-kinase inhibition results in reduced inflammatory response. Fasudil is a ROCK inhibitor. In the present study, we aimed to evaluate cell viability in an astrocyte cell line treated with amyloid beta peptide and fasudil.
Methods and results: C8-D1A (a murine astrocyte cell line) was used to construct a neurotoxicity model induced by Aβ peptide. Astrocyte cells were divided into 2 groups including control and amyloid beta groups and incubated with 5 μM amyloid beta for 24 hours. A separate group was treated with 2.5 μM dose of Fasudil, a Rho-kinase inhibitor, and photographs of the resulting cell samples were taken with 40X magnification objective of the inverted microscope.
A marked increase in cell loss was observed in the group exposed to 5 μM Aβ after incubation in comparison to control group (p<0.001). Fasudil was found to prevent cell loss considerably in the group treated with Fasudil 2.5 μM and Aβ compared to the group treated with Aβ alone (p<0.001).
Conclusion: In the present study, we found that Aβ caused abundant cell death in the murine C8-D1A astrocyte cell line and Fasudil effectively prevented cell loss induced by amyloid beta.
