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Author: search.filters.author.Chongthammakun, Sukumal

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    17β-estradiol mitigates the inhibition of SH-SY5Y cell differentiation through WNT1 expression
    (2023-12-01)
    Shakya, Rubina
    ;
    Amonruttanapun, Prateep
    ;
    Limboonreung, Tanapol
    ;
    Chongthammakun, Sukumal
    17β-estradiol (E2) and canonical WNT-signaling represent crucial regulatory pathways for microtubule dynamics and synaptic formation. However, it is unclear yet whether E2-induced canonical WNT ligands have significant impact on neurogenic repair under inflammatory condition. In this study, first, we prepared the chronic activated-microglial-conditioned media, known to be comprised of neuro-inflammatory components. Long term exposure of microglial conditioned media to SH-SY5Y cells showed a negative impact on differentiation markers, microtubule associated protein-2 (MAP2) and synaptophysin (SYP), which was successfully rescued by pre and co-treatment of 10 nM 17β-estradiol. The inhibition of estrogen receptors, ERα and ERβ significantly blocked the E2-mediated recovery in the expression of differentiation marker, SYP. Furthermore, the inflammatory inhibition of canonical signaling ligand, WNT1 was also found to be rescued by E2. To our surprise, E2 was unable to replicate this success with β-catenin, which is considered to be the intracellular transducer of canonical WNT signaling. However, WNT antagonist - Dkk1 blocked the E2-mediated recovery in the expression of the differentiation marker, MAP2. Therefore, our data suggests that E2-mediated recovery in SH-SY5Y differentiation follows a divergent pathway from the conventional canonical WNT signaling pathway, which seems to regulate microtubule stability without the involvement of β-catenin. This mechanism provides fresh insight into how estradiol contributes to the restoration of differentiation marker proteins in the context of chronic neuroinflammation.
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    Suppression of PI3K/Akt/mTOR pathway in chrysoeriol-induced apoptosis of rat C6 glioma cells
    (2022-01-01)
    Wongkularb, Suppanut
    ;
    Limboonreung, Tanapol
    ;
    Tuchinda, Patoomratana
    ;
    Chongthammakun, Sukumal
    Chrysoeriol, a dietary methoxyflavonoid which is found in tropical medicinal plants, has been shown to have antioxidant, anti-inflammatory, and antineoplastic properties. The present study aimed to investigate the effects of chrysoeriol and its related mechanisms in rat C6 glioma cells. Cell viability in rat C6 glioma cells were measured by MTT assay. The protein expression levels of cleaved caspase-3, caspase-3, pro-apoptotic (Bax), anti-apoptotic protein (Bcl-2), and Annexin V were detected by Western blot analysis and immunocytochemical staining. Results showed that chrysoeriol significantly decreased cell viability and induced apoptosis in rat C6 glioma cells. Chrysoeriol significantly increased the levels of Bax/Bcl-2 ratio and cleaved caspase-3/caspase-3 ratio. Moreover, treatment with chrysoeriol significantly reduced the phosphorylation of PI3K, Akt, and mTOR expression in ratios. These results suggest that chrysoeriol promote apoptosis in rat C6 glioma cells via suppression of the PI3K/Akt/mTOR signaling pathway, thereby demonstrating the potential antineoplastic effects of chrysoeriol on glioma cells.