Browsing by Author "Maher A."

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Comparative lyophilized platelet-rich plasma wafer and powder for wound-healing enhancement: formulation, in vitro and in vivo studies
(Taylor and Francis Ltd., 2019) Yassin G.E.; Dawoud M.H.S.; Wasfi R.; Maher A.; Fayez A.M.; Department of Pharmaceutics and Industrial Pharmacy; Faculty of Pharmacy; Al Azhar University; Cairo; Egypt; Department of Pharmaceutics; Faculty of Pharmacy; October University for Modern Sciences and Arts (MSA University); Giza; Egypt; Department of Microbiology; Faculty of Pharmacy; October University for Modern Sciences and Arts (MSA University); Giza; Egypt; Department of Biochemistry; Faculty of Pharmacy; October University for Modern Sciences and Arts (MSA University); Giza; Egypt; Department of Pharmacology; Faculty of Pharmacy; October University for Modern Sciences and Arts (MSA University); Giza; Egypt
Platelet-rich plasma (PRP) accelerates wound healing, as it is an excellent source of growth factors. PRP was separated from whole human blood by centrifugation. PRP powder and wafers were prepared by lyophilization, with the wafers prepared using sodium carboxymethylcellulose (Na CMC). The PRP wafers showed porous structures, as indicated by scanning electron microscopy (SEM) images, and the ability of the wafer to absorb exudates and thus promote wound healing was tested with the hydration capacity test. The platelet count was tested and indicated that the presence of PRP in the wafers had no effect on the platelet count. An antimicrobial activity test was carried out, showing that PRP had antibacterial activity against Gram-negative bacteria. Compared with lyophilized PRP powder and PRP-free wafers, PRP wafers showed the highest percent of wound size reduction on induced wounds in rats. Histopathological examination of rat skin showed that the PRP wafers achieved the shortest healing time, followed by the lyophilized PRP powder and finally the PRP-free wafers. The present study revealed that PRP can be formulated as a wafer, which is a promising pharmaceutical delivery system that can be used for enhanced wound-healing activity and improved the ease of application compared to lyophilized PRP powder. 2019, 2019 Informa UK Limited, trading as Taylor & Francis Group.
The role of nitric oxide from neurological disease to cancer
(Springer New York LLC, 2017) Maher A.; Abdel Rahman M.F.; Gad M.Z.; Biochemistry Department; Faculty of Pharmacy; October University for Modern Sciences and Arts (MSA); Cairo; Egypt; Clinical Biochemistry Unit; Faculty of Pharmacy & Biotechnology; German University in Cairo (GUC); Cairo; Egypt
Until the beginning of the 1980s, nitric oxide (NO) was just a toxic molecule of a lengthy list of environmental pollutants such as cigarette smoke and smog. In fact, NO had a very bad reputation of being destroyer of ozone, suspected carcinogen and precursor of acid rain. However, by the early 1990s it was well recognized by the medical research community. Over the last two decades, the picture has been totally changed. Diverse lines of evidence have converged to show that this sometime poison is a fundamental player in the everyday business of the human body. NO activity was probed in the brain, arteries, immune system, liver, pancreas, uterus, peripheral nerves, lungs, and almost every system in the human body. NO is a major player in the cardiovascular system as it is involved in regulating blood pressure. In the CNS, it is involved in memory formation and the regulation of cerebral blood flow to ensure adequate supply of blood to the brain. Because NO is involved in many pathways, it has a role in several diseases related to modern life as hypertension, coronary heart diseases, Alzheimer�s Disease, stroke and cancer. This chapter focuses on the discussion of the role of NO in neurological diseases and cancer and how can this Janus-faced molecule play a role in the pathology and personalized treatment of these diseases. � American Association of Pharmaceutical Scientists 2017.
Trans-cinnamaldehyde Modulates Hippocampal Nrf2 Factor and Inhibits Amyloid Beta Aggregation in LPS-Induced Neuroinflammation Mouse Model
(Taylor and Francis Ltd, 2018) Abou El-ezz D.; Maher A.; Sallam N.; El-brairy A.; Kenawy S.; Department of Pharmacology and Toxicology; Faculty of Pharmacy; MSA University; Cairo; Egypt; Department of Biochemistry; Faculty of Pharmacy; MSA University; Cairo; Egypt; Department of Pharmacology and Toxicology; Faculty of Pharmacy; Cairo University; Cairo; Egypt; Department of Physiology and Pharmacology; Cumming School of Medicine; University of Calgary; Calgary; Canada
Trans-cinnamaldehyde (CNM) has recently drawn attention due to its potent anti-inflammatory and antioxidant properties. The current study explored the memory enhancing effects of CNM against lipopolysaccharide (LPS)-induced neuroinflammation in mice. CNM and curcumin (a reference antioxidant) were administered at a dose of 50�mg/kg i.p.�3�h after a single LPS injection (0.8�mg/kg, i.p.) and continued daily for 7�days. Our results displayed that CNM and curcumin significantly ameliorated the LPS-induced impairment of learning and memory, neuroinflammation, oxidative stress and neuronal apoptosis. Memory functions and locomotor activity were assessed by Morris water maze, object recognition test and open field test. Both CNM and curcumin activated the nuclear factor erythroid 2 related factor 2 (Nrf2) and restored levels of downstream antioxidant enzymes superoxide dismutase and glutathione-S-transferase (GST) in the hippocampus. They also attenuated LPS-induced increase in hippocampal contents of interleukin-1? (IL-1?), malondialdehyde and caspase-3. Immunohistochemistry results showed that both CNM and curcumin reduced A?1�42 protein accumulation in brain of mice. Remarkably CNM�s effect on IL-1? was less pronounced than curcumin; however it showed higher GST activity and more potent anti-apoptotic and anti-amylodogenic effect. We conclude that, CNM produces its memory enhancing effects through modulation of Nrf2 antioxidant defense in hippocampus, inhibition of neuroinflammation, apoptosis and amyloid protein burden. � 2018, Springer Science+Business Media, LLC, part of Springer Nature.