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    Sinensetin Shows Neuroprotective Effects in Aluminum Chloride-induced Alzheimer’s Disease in Rats by Regulating BDNF/PPAR-γ/p38MAPK/NF-κB Pathways

    Fuhua Gong1, Yujia Su2, Tao Wu3★, Tahani Awad Alahmadi4, Hesham S. Almoallim5★ Corresponding author

    1. 1Department of Neurology, Xi’an People’s Hospital (Xi’an Fourth Hospital), Xi’an, Shaanxi, CHINA.
    2. 2School of Medicine, Yunnan University, Kunming, Yunnan, CHINA.
    3. 3Department of Neurology, Xi’an GaoXin Hospital, Xi’an, Shaanxi, CHINA.
    4. 4Department of Pediatrics, College of Medicine and King Khalid University Hospital, King Saud University, Medical City, Riyadh, SAUDI ARABIA.
    5. 5Department of Oral and Maxillofacial Surgery, College of Dentistry, King Saud University, Riyadh, SAUDI ARABIA.

    CORRESPONDENCE

    Tao Wu

    Department of Neurology, Xi’an GaoXin Hospital, Xi’an, Shaanxi, CHINA.

    wt7508@outlook.com

    Received: 18-04-2025; Accepted: 25-07-2025.

    Volume 22, Issue 1 · pp. 321–333 · PUBLISHED 2026 · DOI: 10.1177/09731296251379601

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Background: Alzheimer’s disease (AD) is a neurological disorder characterized by behavioral and memory deficits, along with cognitive impairments. The majority of AD cases are often present in individuals aged 60 and above. Objectives: The present work was conducted to investigate the neuroprotective properties of sinensetin against aluminum chloride (AlCl3)-induced Alzheimer’s disease (AD) in rats. Materials and Methods: The rats were given AlCl3 (175 mg/kg) orally for 25 days to induce AD. Sinensetin (20 and 40 mg/kg) was orally given to the AD rats from the 25th to the 36th day. After treatments, behavioral changes were evaluated using the open-field and Morris water maze assays. The inflammatory cytokines, oxidative stress markers, acetylcholinesterase (AChE), and Aβ protein were evaluated using assay kits. The histopathology study was conducted on brain tissues. Results: The findings of the behavioral assessments revealed that sinensetin improved the memory and learning capacity of the AD rats. The levels of oxidative and inflammatory markers were decreased, while antioxidant enzyme activities were elevated in the brain tissues of the sinensetin-treated AD rats. The increase in BDNF and PPAR-γ levels and the reduction in p38MAPK and NF-κB levels were noted in the sinensetin-treated AD rats. The results of histopathological analysis revealed the neuroprotective properties of sinensetin. The outcomes of this work exhibited that the sinensetin treatment of the AD rats resulted in improved memory and learning, reduced oxidative stress and inflammation, an increase in BDNF/PPAR-γ levels, and a reduction in p38MAPK/NF-κB levels in the brain tissues. Conclusion: Therefore, it can be concluded that sinensetin shows promise as a therapeutic candidate to treat AD in the future.

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      Gong, F., Su, Y., Wu, T., Alahmadi, T. A., & Almoallim, H. S. (2026). Sinensetin Shows Neuroprotective Effects in Aluminum Chloride-induced Alzheimer’s Disease in Rats by Regulating BDNF/PPAR-γ/p38MAPK/NF-κB Pathways. Pharmacognosy Magazine, 22(1), 321–333. https://doi.org/10.1177/09731296251379601