Walaa Adel Mohamed Youssef
B.Sc. Clinical Pharmacy, Faculty of Pharmacy, Alexandria University, 2020
2026
Lifetime prevalence of depression, upper estimate
Women estimated to experience a major depressive episode
Standard pharmacotherapy (SSRIs, SNRIs, tricyclic agents and MAO inhibitors) targets monoaminergic transmission.
Clinical response is frequently partial, and prolonged use is associated with adverse effects. This has prompted interest in natural products and non-pharmacological interventions.
The higher burden in women is the reason female mice were used in this study.
Reduced serotonin, dopamine and noradrenaline signalling.
Impaired Nrf2-dependent antioxidant response, glutathione depletion and lipid peroxidation.
Increased pro-inflammatory cytokines, including TNF-α.
Reduced CREB1–BDNF signalling and impaired hippocampal plasticity.
miR-124 and miR-134 upregulated; LINC00473 reduced, specifically in females.
NAD⁺-dependent deacetylase; reduced activity is associated with depressive-like phenotypes and impaired Nrf2 signalling.

Selective serotonin reuptake inhibitor, used as the positive control.

Anxiolytic, anti-inflammatory and antidepressant activity reported in vivo.

Acts on monoamine release, neurotrophic factors, inflammation and miRNA expression.
Swiss albino mice, 18–25 g. Baseline FST did not differ between groups.
0.1 mg/kg/day, i.p.
Day 5 FST confirmed the model. Treatments then ran daily for 4 weeks.
10% formalin, paraffin, 4.5 µm H&E sections; blinded morphometry, ImageJ; n = 5 per group
5-HT, dopamine, noradrenaline by competitive ELISA; total GSH, FRAP, MDA, total protein by colorimetry
Nrf2, TNF-α, CREB1, BDNF, SIRT1, LINC00473 vs 18S rRNA; miR-124a, miR-134 vs U6; ΔΔCt
| Major constituent | RT, min | Area, % |
|---|---|---|
| Phytol | 26.04 | 18.47 |
| Hexadecanoic acid, methyl ester | 26.04 | 14.62 |
| Methyl linoleate | 27.93 | 12.31 |
| Octadecanoic acid, methyl ester | 28.11 | 9.85 |
| β-Caryophyllene | 44.20 | 7.94 |
Immobility relative to vehicle-treated controls after reserpine
Student's t = 11.16 · p < 0.001 · n = 8 per group
TRI · 130 s
+2% vs control; differs from untreated only (b)
G+E · 145 s
+13% vs control; differs from untreated only (b)
GRV 155 s · FLX 152 s
Graviola alone comparable to fluoxetine; single treatments remained above control (a)
Every group stayed below control (a). G+E gave the highest serotonin and dopamine, fluoxetine the highest noradrenaline. TRI dopamine did not differ from untreated mice.
Nrf2 fold change in G+E, significantly higher than control and every other group
Single treatments: no significant change vs untreated
G+E restored GSH to control level and raised FRAP to 2.1-fold of control. TRI gave the lowest MDA (−48%). Fluoxetine did not change GSH.
TNF-α in G+E relative to control, significantly lower than every single treatment
G+E vs control
Untreated vs control
Fluoxetine did not restore BDNF (−65% vs control).
Fluoxetine did not significantly change either gene. TRI CREB1 (1.25) did not differ from control or untreated mice.
LINC00473 fell by 82% and fluoxetine did not restore it. G+E returned it to control level (1.15-fold); TRI exceeded control (1.70-fold).
BDNF, CREB1, Nrf2 and SIRT1 rise together and fall as TNF-α and the two miRNAs rise.




Partial improvement
Shrunken and apoptotic neurons, few normal cells

Partial improvement
Hyperchromatic and apoptotic neurons, few normal cells

Closest to control
Densely packed pyramidal neurons with basophilic cytoplasm, vesicular nuclei and Nissl granules; occasional ghost cells

Marked improvement
Many vesicular nuclei; few pyknotic and ghost cells
Graviola leaf extract alone reduced immobility to a degree comparable with fluoxetine.
G+ECombined with exercise, it produced the largest changes in Nrf2, BDNF, CREB1, TNF-α and both miRNAs, and the best-preserved CA3 morphology.
TRIAdding fluoxetine normalised immobility time but attenuated the effects on dopamine, FRAP and Nrf2.
NextThese findings support further evaluation of graviola with exercise as a multi-target approach to depression.
Prof. Dr. Wafaa Mahmoud Abdel-Rehim
Assist. Prof. Dr. Rasha Abd El-Mottleb EL-Tahan
Assist. Prof. Dr. Shimaa Abdel Raheem Mahmoud
Dr. Rana Hassan Mahmoud Hassan Khafaga
Prof. Dr. Wafaa Mahmoud EL-Sayed Abdel-Rehim
Prof. Dr. Nagwa Mohamed Assem
Prof. Dr. Hussein Khamis Hussein
Assist. Prof. Dr. Shimaa Abdel Raheem Mahmoud
Histopathology: Dr. Noura Matar, Department of Cell Biology and Histochemistry