About the school

The School of Pharmacy at the Hebrew University, one of the world leaders in pharmacist training and basic research in the pharmaceutical sciences, was established in 1953.
The school prepares its graduates to practice the pharmacy profession, provides them with a scientific and professional foundation, and offers higher studies in pharmacology, medicinal chemistry and pharmacy sciences (M.Sc. and Ph.D.), as well as doctoral studies in clinical pharmacy (Pharm.D.).
Graduates of the school are integrated in community pharmacy (community pharmacies, private and institutional), clinical pharmacy (hospitals and health funds), the pharmaceutical industry, the biological, chemical and biotechnology industries, the pharmacy administration and science and research institutions in Israel and abroad.
The school conducts extensive scientific research in the fields of pharmaceutical sciences and life sciences, and dozens of articles are published each year in the leading press in the world of science.
The School of Pharmacy is part of the Faculty of Medicine, located on the Ein Kerem campus of the Hebrew University and works closely with physicians and researchers from Hadassah Hospital.


Recent Publications

Bruno V.S. Valiate, Celso M. Queiroz-Junior, Francesca Levi-Schaffer, Izabela Galvão, and Mauro M. Teixeira. 2021. “CD300a contributes to the resolution of articular inflammation triggered by MSU crystals by controlling neutrophil apoptosis.” Immunology. Abstract
Gout is an inflammatory disease triggered by deposition of monosodium urate (MSU) crystals in the joints, resulting in high neutrophil influx and pain. Here, we studied the role of the inhibitory receptor CD300a in the resolution process in a murine model of gout. We found increased CD300a expression on neutrophils emigrated to the joint. When compared to WT mice, CD300a−/− mice had persistent neutrophil influx till 24 hr after MSU injection. This was associated with increased concentration of IL-1$\beta$ and greater tissue damage in the joints of CD300a−/− mice. There was an increase in the percentage of apoptotic neutrophils in the synovial lavage of WT mice, as compared to CD300a−/− mice. This difference was reflected in the decline of efferocytic events in the synovial cavity of CD300a−/− mice 24 hr after MSU injection. A CD300a agonistic antibody was shown, for the first time, to increase apoptosis of human neutrophils, and this was associated with cleavage of caspase-8. In conclusion, our results reveal an important role of CD300a in the control of leucocyte infiltration, IL-1$\beta$ production and caspase-8 cleavage in neutrophils, contributing to the resolution of inflammation triggered by MSU injection.
Igor Khaliulin, Raimondo Ascione, Leonid N. Maslov, Haitham Amal, and M. Saadeh Suleiman. 2021. “Preconditioning or Postconditioning with 8-Br-cAMP-AM Protects the Heart against Regional Ischemia and Reperfusion: A Role for Mitochondrial Permeability Transition.” Cells, 10, 5. Abstract
The cAMP analogue 8-Br-cAMP-AM (8-Br) confers marked protection against global ischaemia/reperfusion of isolated perfused heart. We tested the hypothesis that 8-Br is also protective under clinically relevant conditions (regional ischaemia) when applied either before ischemia or at the beginning of reperfusion, and this effect is associated with the mitochondrial permeability transition pore (MPTP). 8-Br (10 $μ$M) was administered to Langendorff-perfused rat hearts for 5 min either before or at the end of 30 min regional ischaemia. Ca2+-induced mitochondria swelling (a measure of MPTP opening) and binding of hexokinase II (HKII) to mitochondria were assessed following the drug treatment at preischaemia. Haemodynamic function and ventricular arrhythmias were monitored during ischaemia and 2 h reperfusion. Infarct size was evaluated at the end of reperfusion. 8-Br administered before ischaemia attenuated ventricular arrhythmias, improved haemodynamic function, and reduced infarct size during ischaemia/reperfusion. Application of 8-Br at the end of ischaemia protected the heart during reperfusion. 8-Br promoted binding of HKII to the mitochondria and reduced Ca2+-induced mitochondria swelling. Thus, 8-Br protects the heart when administered before regional ischaemia or at the beginning of reperfusion. This effect is associated with inhibition of MPTP via binding of HKII to mitochondria, which may underlie the protective mechanism.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder manifested in repetitive behavior, abnormalities in social interactions, and communication. The pathogenesis of this disorder is not clear, and no effective treatment is currently available. Protein S-nitrosylation (SNO), the nitric oxide (NO)-mediated posttranslational modification, targets key proteins implicated in synaptic and neuronal functions. Previously, we have shown that NO and SNO are involved in the ASD mouse model based on the Shank3 mutation. The energy supply to the brain mostly relies on oxidative phosphorylation in the mitochondria. Recent studies show that mitochondrial dysfunction and oxidative stress are involved in ASD pathology. In this work, we performed SNO prote-omics analysis of cortical tissues of the Shank3 mouse model of ASD with the focus on mitochondrial proteins and processes. The study was based on the SNOTRAP technology followed by systems biology analysis. This work revealed that 63 mitochondrial proteins were S-nitrosylated and that several mitochondria-related processes, including those associated with oxidative phosphorylation, oxidative stress, and apoptosis, were enriched. This study implies that aberrant SNO signaling induced by the Shank3 mutation can target a wide range of mitochondria-related proteins and processes that may contribute to the ASD pathology. It is the first study to investigate the role of NO-dependent mitochondrial functions in ASD.
Nethanel Friedman, Arie Dagan, Jhonathan Elia, Sharon Merims, and Ofra Benny. 2021. “Physical properties of gold nanoparticles affect skin penetration via hair follicles.” Nanomedicine: Nanotechnology, Biology, and Medicine, 36. Abstract
Drug penetration through the skin is significant for both transdermal and dermal delivery. One mechanism that has attracted attention over the last two decades is the transport pathway of nanoparticles via hair follicle, through the epidermis, directly to the pilosebaceous unit and blood vessels. Studies demonstrate that particle size is an important factor for drug penetration. However, in order to gain more information for the purpose of improving this mode of drug delivery, a thorough understanding of the optimal physical particle properties is needed. In this study, we fabricated fluorescently labeled gold nanoparticles (GNP) with a tight control over the size and shape. The effect of the particles' physical parameters on follicular penetration was evaluated histologically. We used horizontal human skin sections and found that the optimal size for polymeric particles is 0.25 $μ$m. In addition, shape penetration experiments revealed gold nanostars' superiority over spherical particles. Our findings suggest the importance of the particles' physical properties in the design of nanocarriers delivered to the pilosebaceous unit.
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