Mona Kamal El-Awam
Asst. Professor
Ellagic Acid Alleviates Imidacloprid-Induced Thyroid Dysfunction via PI3K/Akt/mTOR-Mediated Autophagy
• 2025
Publication Information
Authors
Amina A. Farag 1 , Mahmoud Mostafa 2,3,* , Reham M. Abdelfatah 4 , Alshimaa Ezzat ELdahshan 5,
Samar Fawzy Gad 6, Shimaa K. Mohamed 7, Mona K. Alawam
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publication.type
International
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Abstract
Imidacloprid (IMI) is a widely used insecticide known for its high selectivity
toward insects. Ellagic acid (EA) is a plant-derived polyphenolic compound recognized for
its therapeutic potential and favorable safety profile in the treatment of various diseases.
This study aimed to evaluate the therapeutic effects of EA, formulated as novasomes (NOV),
against IMI-induced thyroid dysfunction and to investigate the underlying mechanisms.
Rats were divided into four equal groups: control, EA-NOV, IMI, and IMI + EA-NOV.
Thyroid function was assessed by measuring free triiodothyronine (T3), free thyroxine (T4),
and thyroid-stimulating hormone (TSH) levels. Thyroid tissues were examined to evaluate
histopathological alterations, as well as to assess the oxidative/antioxidant pathway (Nrf2,
SOD, TAC, MDA), inflammatory pathway (IL-1β, TNF-α, NF-κB), apoptotic pathway (Bcl,
BAX), and autophagy pathway (PI3K/Akt/mTOR, P53, Beclin-1). Exposure to IMI resulted
in impaired thyroid function, the upregulated gene expression of the PI3K/Akt/mTOR pathway,
and downregulated P53 expression. Additionally, immunohistochemical staining
revealed Beclin-1-mediated autophagy, alongside increased apoptosis, oxidative stress, and
elevated levels of inflammatory cytokines
toward insects. Ellagic acid (EA) is a plant-derived polyphenolic compound recognized for
its therapeutic potential and favorable safety profile in the treatment of various diseases.
This study aimed to evaluate the therapeutic effects of EA, formulated as novasomes (NOV),
against IMI-induced thyroid dysfunction and to investigate the underlying mechanisms.
Rats were divided into four equal groups: control, EA-NOV, IMI, and IMI + EA-NOV.
Thyroid function was assessed by measuring free triiodothyronine (T3), free thyroxine (T4),
and thyroid-stimulating hormone (TSH) levels. Thyroid tissues were examined to evaluate
histopathological alterations, as well as to assess the oxidative/antioxidant pathway (Nrf2,
SOD, TAC, MDA), inflammatory pathway (IL-1β, TNF-α, NF-κB), apoptotic pathway (Bcl,
BAX), and autophagy pathway (PI3K/Akt/mTOR, P53, Beclin-1). Exposure to IMI resulted
in impaired thyroid function, the upregulated gene expression of the PI3K/Akt/mTOR pathway,
and downregulated P53 expression. Additionally, immunohistochemical staining
revealed Beclin-1-mediated autophagy, alongside increased apoptosis, oxidative stress, and
elevated levels of inflammatory cytokines