Lobna Khedr

Dr. Lobna Khedr

orcid

Research Focus & Metrics

Academic Career Length

8Years (2019-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 December 2019 in Life Sciences
Verified
Journal Article
Closed access
LKLobna Khedr
Lobna Khedr
NNN.N. Nassar
N.N. Nassar
LRLaila Rashed
Laila Rashed
EEE.D. El-Denshary
E.D. El-Denshary
AAA.M. Abdel-Tawab
A.M. Abdel-Tawab

1 June 2020 in Food and Chemical Toxicology
Verified
Journal Article
Closed access
LKLobna Khedr
Lobna Khedr
RRRania M. Rahmo
Rania M. Rahmo
DFDoaa Boshra Farag
Doaa Boshra Farag
MSMona F. Schaalan
Mona F. Schaalan
HMHekmat M. El Magdoub
Hekmat M. El Magdoub

1 October 2020 in Toxicology and Applied Pharmacology
Verified
Journal Article
Closed access
HMHekmat Mohamed El Magdoub
Hekmat Mohamed El Magdoub
MSMona Schaalan
Mona Schaalan
RRRania M. Rahmo
Rania M. Rahmo
DFDoaa B. Farag
Doaa B. Farag
LKLobna Khedr
Lobna Khedr

2 November 2026 in Pharmaceuticals
Verified
Journal Article
Open access
PDF file
SASawsan Aboul-Fotouh
Sawsan Aboul-Fotouh
MHMohamed Z. Habib
Mohamed Z. Habib
EEEsraa M. Elnahas
Esraa M. Elnahas
YAYasmin M. Aboul-Ela
Yasmin M. Aboul-Ela
GAGhada A. Abdel-Latif
Ghada A. Abdel-Latif
LKLobna Khedr
Lobna Khedr
Background: Disrupted iron homeostasis is increasingly perceived as a key driver of major depressive disorder pathogenesis; hence, targeting ferroptotic cascades may reveal novel therapeutic targets. This study evaluated the neuroprotective potential of the oral iron chelator deferasirox (DEF) against chronic unpredictable mild stress (CUMS)-induced depressive-like behaviors and cognitive deficits in Wistar rats. Methods: We specifically explored whether DEF could provide neuroprotection by targeting ferroptotic and oxidative stress pathways. Male Wistar rats were exposed to a 6-week CUMS protocol and treated with DEF (10, 20, or 40 mg/kg). Results: CUMS-exposed rats exhibited significant anhedonia, behavioral despair, and impaired spatial and recognition memory. Further analyses revealed a reduction in colonic and choroid plexus occludin, reflecting compromised structural integrity of both the intestinal and blood-CSF barriers, accompanied by enhanced hippocampal iron accumulation with increased Acyl-CoA synthetase long-chain family member 4 (ACSL4), Acyl-CoA synthetase family member 2 (ACSF2), and citrate synthase expression, alongside exaggerated oxidative stress and deficient neuroprotective mediators, specifically BDNF and synaptophysin, and increased neurofibrillary tangle (NFT) deposition, collectively exacerbating neurodegenerative pathology. DEF treatment ameliorated most of these effects, significantly reducing iron deposition, attenuating ferroptosis-related signaling, reducing oxidative stress, diminishing the ongoing neurodegeneration, and replenishing the depleted pool of BDNF and synaptophysin, which was accompanied by a reduction in depressive-like symptoms and improved cognitive functions. Conclusions: These findings support a link between ferroptosis-related signaling and depression-like phenotypes, reinforcing the concept of a metal-driven component in depression pathophysiology and offering a mechanistic rationale for further exploring targeting ferroptotic pathways and central iron regulation as potential targeted strategies in depression management.