Avocado Oil Nanoemulsion Ameliorates STZ-Induced Diabetic Brain Dysfunction through PI3K/AKT/mTOR-Related Gene Modulation and Attenuation of Apoptosis
4 affiliations
- 1Department of Pathology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211 Egypt
- 2Medicinal and Aromatic Plants Research Department, Pharmaceutical and Drug Industries Research Institute, National Research Centre, Giza, Dokki 12622 Egypt
- 3Department of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211 Egypt
- 4Phytochemistry and Plant Systematics Department, National Research Centre, Giza, Dokki 12622 Egypt
Abstract
Diabetes mellitus is associated with progressive neurological complications characterized by hyperglycemia-induced oxidative stress, neuronal apoptosis, and disruption of intracellular survival signaling pathways. This study investigated the neuroprotective effects of avocado cold-pressed oil (ACPO) and its nano-formulation against diabetes-induced cerebral alterations in streptozotocin (STZ)-induced diabetic rats. Seventy adult male Wistar rats were randomly allocated to ten groups (n = 7/group): normal control (NC), blank nano-formulation vehicle control (BC), metformin control (RC), ACPO control (OC), ACPO nano-formulation control (FC), diabetic positive control (PC), diabetic blank nano-formulation vehicle control (BT), diabetic + metformin (RT; 500 mg/kg), diabetic + ACPO (OT; 500 mg/kg), and diabetic + ACPO nano-formulation (FT; 500 mg/kg). The untreated diabetic group served as the reference for diabetes-associated alterations, whereas the diabetic vehicle-control group was included to account for potential effects of the nano-formulation vehicle. Diabetes was induced by a single intraperitoneal injection of STZ (40 mg/kg). Plasma glucose levels, cerebral gene expression of phosphatidylinositol-3-kinase (PI3K), protein kinase B (AKT1), mechanistic target of rapamycin (mTOR), glycogen synthase kinase-3β (GSK3β), pannexin-1 (PANX1), and acetylcholinesterase (AChE) were evaluated. Histopathological examination and caspase-3 immunohistochemistry were performed to assess neuronal injury and apoptosis. Treatment with ACPO and its nano-formulation significantly reduced plasma glucose levels and modulated key molecular pathways involved in neuronal survival. Both treatments upregulated PI3K, AKT1, and mTOR expression while downregulating GSK3β, PANX1, and AChE compared with untreated diabetic rats. Histopathological examination demonstrated marked preservation of cerebral cortical architecture, accompanied by reduced caspase-3 immunoexpression, indicating attenuation of neuronal apoptosis. The nano-formulation exerted greater effects on the investigated molecular biomarkers than conventional ACPO and produced histopathological and immunohistochemical improvements comparable to those observed with metformin.
Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s12035-026-06238-4.
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BibTeX
@article{ahmed2026avocado,
title = {{Avocado Oil Nanoemulsion Ameliorates STZ-Induced Diabetic Brain Dysfunction through PI3K/AKT/mTOR-Related Gene Modulation and Attenuation of Apoptosis}},
author = {Fatma A. Ahmed and Marwa S. Khattab and Faten M. Ibrahim and Aya M. Yassin and Mahmoud Emam and Kawkab A. Ahmed},
journal = {Molecular Neurobiology},
year = {2026},
month = nov,
doi = {10.1007/s12035-026-06238-4},
url = {https://doi.org/10.1007/s12035-026-06238-4},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Avocado Oil Nanoemulsion Ameliorates STZ-Induced Diabetic Brain Dysfunction through PI3K/AKT/mTOR-Related Gene Modulation and Attenuation of Apoptosis
AU - Fatma A. Ahmed
AU - Marwa S. Khattab
AU - Faten M. Ibrahim
AU - Aya M. Yassin
AU - Mahmoud Emam
AU - Kawkab A. Ahmed
PY - 2026
DA - 2026/11/04
JO - Molecular Neurobiology
DO - 10.1007/s12035-026-06238-4
UR - https://doi.org/10.1007/s12035-026-06238-4
AB - Diabetes mellitus is associated with progressive neurological complications characterized by hyperglycemia-induced oxidative stress, neuronal apoptosis, and disruption of intracellular survival signaling pathways. This study investigated the neuroprotective effects of avocado cold-pressed oil (ACPO) and its nano-formulation against diabetes-induced cerebral alterations in streptozotocin (STZ)-induced diabetic rats. Seventy adult male Wistar rats were randomly allocated to ten groups (n = 7/group): normal control (NC), blank nano-formulation vehicle control (BC), metformin control (RC), ACPO control (OC), ACPO nano-formulation control (FC), diabetic positive control (PC), diabetic blank nano-formulation vehicle control (BT), diabetic + metformin (RT; 500 mg/kg), diabetic + ACPO (OT; 500 mg/kg), and diabetic + ACPO nano-formulation (FT; 500 mg/kg). The untreated diabetic group served as the reference for diabetes-associated alterations, whereas the diabetic vehicle-control group was included to account for potential effects of the nano-formulation vehicle. Diabetes was induced by a single intraperitoneal injection of STZ (40 mg/kg). Plasma glucose levels, cerebral gene expression of phosphatidylinositol-3-kinase (PI3K), protein kinase B (AKT1), mechanistic target of rapamycin (mTOR), glycogen synthase kinase-3β (GSK3β), pannexin-1 (PANX1), and acetylcholinesterase (AChE) were evaluated. Histopathological examination and caspase-3 immunohistochemistry were performed to assess neuronal injury and apoptosis. Treatment with ACPO and its nano-formulation significantly reduced plasma glucose levels and modulated key molecular pathways involved in neuronal survival. Both treatments upregulated PI3K, AKT1, and mTOR expression while downregulating GSK3β, PANX1, and AChE compared with untreated diabetic rats. Histopathological examination demonstrated marked preservation of cerebral cortical architecture, accompanied by reduced caspase-3 immunoexpression, indicating attenuation of neuronal apoptosis. The nano-formulation exerted greater effects on the investigated molecular biomarkers than conventional ACPO and produced histopathological and immunohistochemical improvements comparable to those observed with metformin. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s12035-026-06238-4.
SN - 0893-7648
SN - 1559-1182
ER -