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    Neuroprotective Potential of Thunbergia laurifolia Lindl. Leaf Extracts against Beta Amyloid-induced Neurotoxicity: An in vitro Model of Alzheimer’s Disease

    Kritsana Homwuttiwong1, Benjaporn Buranrat1, Supataechasit Yannasithinon1, Parinya Noisa2, Nootchanat Mairuae1★★ Corresponding author

    1. 1Faculty of Medicine, Mahasarakham University, Talad Subdistrict Muang District, Maha Sarakham, THAILAND.
    2. 2School of Biotechnology, Institute of Agricultural Technology, Suranaree University of Technology, Nakhon Ratchasima, Thailand.

    CORRESPONDENCE

    Nootchanat Mairuae

    Faculty of Medicine, Mahasarakham University, Talad Subdistrict Muang District, Maha Sarakham, THAILAND.

    nootchanat.m@msu.ac.th

    Received: 11-09-2023; Accepted: 18-12-2023.

    Volume 20, Issue 3 · pp. 773–783 · PUBLISHED 2024 · DOI: 10.1177/09731296241226769

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Background: Beta-amyloid peptide (Aβ) induces oxidative stress, contributing to Alzheimer’s disease (AD) initiation and progression. This study aims to explore Thunbergia laurifolia (T. laurifolia) leaf extract’s protective effects on Aβ25–35-induced oxidative stress and cell injury in SH-SY5Y cells and investigate underlying mechanisms. Materials and Methods: SH-SY5Y cells were treated with T. laurifolia leaf extract in the presence or absence of Aβ25–35. After 24 h, neuroprotective effects were assessed using cell viability and lactate dehydrogenase (LDH) assays. Caspase-3/7 activity, intracellular reactive oxygen species (ROS) levels, catalase (CAT), and superoxide dismutase (SOD) activities were measured to examine mechanisms. Total flavonoid and phenolic content assays were performed. Results: The findings showed that exposure to Aβ25–35 led to a notable rise in oxidative stress in SH-SY5Y cells, as evidenced by increased levels of ROS. Additionally, Aβ25–35 treatment increased caspase-3/7 activity and LDH release and decreased cell viability. However, T. laurifolia extract effectively suppressed ROS production, attenuated caspase-3/7 activity, and concentration-dependently reduced Aβ25–35-induced neurotoxicity. LDH release decreased, and cell viability increased. SOD and CAT activities also increased after T. laurifolia treatment. The extract had total phenolic and flavonoid contents of 178.5 ± 6.86 and 32.51 ± 1.26 mg/g, respectively. Conclusion: T. laurifolia extract demonstrated neuroprotective effects against Aβ25–35-induced injury in SH-SY5Y cells. These effects were attributed to reduced oxidative stress, elevated SOD and CAT activity, and suppressed caspase-3/7 activity. T. laurifolia extract shows potential as an alternative or therapeutic approach to AD mediated by Aβ. Nevertheless, further research is needed to elucidate the mechanism by which T. laurifolia ameliorates neuronal cell death induced by Aβ25–35.

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      Homwuttiwong, K., Buranrat, B., Yannasithinon, S., Noisa, P., & Mairuae, N. (2024). Neuroprotective Potential of Thunbergia laurifolia Lindl. Leaf Extracts against Beta Amyloid-induced Neurotoxicity: An in vitro Model of Alzheimer’s Disease. Pharmacognosy Magazine, 20(3), 773–783. https://doi.org/10.1177/09731296241226769