S. Sirirattanakul, R. Santiyanont
Published: March 14, 2023
Genet. Mol. Res. 22(1): GMR19080
DOI: https://doi.org/10.4238/gmr19080
Cite this Article:
S. Sirirattanakul, R. Santiyanont (2023). Fimbristylis ovata (Cyperaceae) extract alleviates neuronal degeneration and death through AGEs/RAGE/JNK regulation in human neuroblastoma cell line, SH-SY5Y. Genet. Mol. Res. 22(1): GMR19080. https://doi.org/10.4238/gmr19080
About the Authors
S. Sirirattanakul, R. Santiyanont
Corresponding Author
Email: rachana.s@chula.ac.th
ABSTRACT
Clinical evidence has implicated advanced glycation end products (AGEs) as one of the risk factors for neurological dysfunction and death. However, the neurodegeneration regulation initiated by external AGEs has not yet been fully identified. We investigated the neuroprotective effect of Fimbristylis ovata extract, a medicinal plant utilized in Thai traditional medicine, against neuronal cell death in response to AGEs-induced cellular stress stimuli. SH-SY5Y, a human neuroblastoma cell, was used to investigate the relationship between AGEs induction and neuronal cell damage. The herbal extract derived from F. ovata, a member of the Cyperaceae family, was tested for its properties against AGEs-induced neuronal stress through changes in RAGE, Mn-SOD, p38 MAPK, and JNK protein expression. APP-related genes, including APP, ADAM10, BACE1, PSEN1, and TACE, were also tested. We found that F. ovata extract exerted its antioxidant activity by normalized AGEs-mediated RAGE elevation and increased Mn-SOD levels. Total apoptotic cells were also decreased by F. ovata extract treatment; this perhaps was due to its ability to suppress JNK activation. Additionally, reduction of expression of APP-related genes including APP, PSEN1, and TACE (or ADAM17) was observed in the F. ovata extract-treated groups. These results provide evidence that F. ovata extract has potential as a neuroprotective agent through its antioxidant and anti-apoptotic properties.
Key words: AGEs, Fimbristylis ovata, JNK, Mn-SOD, Neuronal death.