Transcriptomic Response of Caenorhabditis Elegans Expressing Human Aß42Gene Treated with Salvianolic Acid A

• Main Authors: Chee, Wah Yuen, Mardani Abdul Halim, Nazalan Najimudin, Ghows Azzam
• Format: Article
• Language: English; English
• Published: Indian Academy of Sciences 2021
• Subjects: RC321-571 Neurosciences. Biological psychiatry. Neuropsychiatry
• Online Access: https://eprints.ums.edu.my/id/eprint/32678/1/Transcriptomic%20Response%20of%20Caenorhabditis%20Elegans%20Expressing%20Human%20A%C3%9F42Gene%20Treated%20with%20Salvianolic%20Acid%20A.pdf; https://eprints.ums.edu.my/id/eprint/32678/3/Transcriptomic%20Response%20of%20Caenorhabditis%20Elegans%20Expressing%20Human%20A%C3%9F42Gene%20Treated%20with%20Salvianolic%20Acid%20A%20_ABSTRACT.pdf; https://eprints.ums.edu.my/id/eprint/32678/; https://www.currentscience.ac.in/Volumes/120/12/1882.pdf

Alzheimer’s disease is associated with the deposition of ß-amyloid peptide in the brain. A genome-wide transcriptomic study was performed to determine the response of transgenic Caenorhabditis elegans expressing full-length human Aß42 gene towards salvianolic acid A (Sal A). The genes associated with antioxidant response, gst-4, gst-10, spr-1 and trxr-2, were upregulated. Aß42 caused oxidative stress and the antioxidant response genes possibly provide some sort of protection to the nematode. trxr-2 gene product was also associated with the defence system and probably has a role in the lifespan of the nematode. Other genes involved in DNA replication, reproduction, immune response and antimicrobial activities were also found to be upregulated. Treatment of Sal A also increased the rate of reproduction in the nematode, and elevated its immunological protection system towards microorganisms. On the other hand, the genes responsible for ligand-gated cation channel, embryonic and postembryonic development, locomotion and neuromodulation of chemosensory neurons were found to be downregulated. As an effector, Sal A might conceivably reduce the movement of the nematode by interfering with neuronal transmission, and embryonic and postembryonic development.