Browsing by Author "Attia Y.M."
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Item Anticancer potentiality of lignan rich fraction of six Flaxseed cultivars(Nature Publishing Group, 2018) Ezzat, Shahira M; Shouman S.A.; Elkhoely A.; Attia Y.M.; Elsesy M.S.; El Senousy A.S.; Choucry M.A.; El Gayed S.H.; El Sayed A.A.; Sattar E.A.; El Tanbouly N.; Pharmacognosy Department; Faculty of Pharmacy; Cairo University; Kasr El-Einy Street; Cairo; 11562; Egypt; Department of Pharmacognosy; Faculty of Pharmacy; October University for Modern Science and Arts (MSA); 6th October; 12566; Egypt; Cancer Biology Department; National Cancer Institute; Cairo University; Cairo; Egypt; Pharmacology and Toxicology Department; Faculty of Pharmacy; Helwan University; Helwan; EgyptThe objective of our study is to highlight the therapeutic effect and mechanism of action by which purified Flaxseed hydrolysate (PFH) which is a lignan rich fraction exerts its anticancer activity on a human breast cancer cell line (T47D) and in mice bearing tumor. HPLC analysis of PFH of six flaxseed cultivars had shown that PFH of the cultivar Giza 9 (PFH-G9) contains the highest concentration of SDG (81.64 mg/g). The in vitro cytotoxic potentiality of PFH's of six flaxseed cultivars was screened against a panel of human cancer cell lines. PFH -G9 showed the most significant cytotoxic activity against ER-receptor positive breast cell lines MCF7 and T47D with IC50 13.8 and 15.8 ?g/ml, respectively. Moreover, PFH-G9 reduced the expression of the metastasis marker, 1-?, metalloproteinases and vascular endothelial growth factor (VEGF), one of the most potent stimulators of angiogenesis, while it increased the caspase-3 dependent apoptosis. Our study also showed that dietary intake of 10% of Giza 9 Flaxseeds (FS), fixed oil (FSO) or Flax meal (FSM) twice daily for 3 weeks in mice-bearing solid Ehrlich ascites carcinoma (EAC) resulted in reducing the tumor volume, the expression of estrogen, insulin growth factor, progesterone, VEGF and MMP-2, but enhanced expression of caspase-3. � 2018 The Author(s).Item Modification of Hippocampal Markers of Synaptic Plasticity by Memantine in Animal Models of Acute and Repeated Restraint Stress: Implications for Memory and Behavior(Humana Press Inc., 2015) Amin S.N.; El-Aidi A.A.; Ali M.M.; Attia Y.M.; Rashed L.A.; Department of Medical Physiology; Kasr Al Ainy Faculty of Medicine; Cairo University; Al Manyal; Cairo; 11451; Egypt; Faculty of Pharmacy; MSA University; Cairo; Egypt; Department of Biochemistry; Faculty of Medicine; Cairo University; Cairo; EgyptStress is any condition that impairs the balance of the organism physiologically or psychologically. The response to stress involves several neurohormonal consequences. Glutamate is the primary excitatory neurotransmitter in the central nervous system, and its release is increased by stress that predisposes to excitotoxicity in the brain. Memantine is an uncompetitive N-methyl D-aspartate glutamatergic receptors antagonist and has shown beneficial effect on cognitive function especially in Alzheimer�s disease. The aim of the work was to investigate memantine effect on memory and behavior in animal models of acute and repeated restraint stress with the evaluation of serum markers of stress and the expression of hippocampal markers of synaptic plasticity. Forty-two male rats were divided into seven groups (six rats/group): control, acute restraint stress, acute restraint stress with Memantine, repeated restraint stress, repeated restraint stress with Memantine and Memantine groups (two subgroups as positive control). Spatial working memory and behavior were assessed by performance in Y-maze. We evaluated serum cortisol, tumor necrotic factor, interleukin-6 and hippocampal expression of brain-derived neurotrophic factor, synaptophysin and calcium-/calmodulin-dependent protein kinase II. Our results revealed that Memantine improved spatial working memory in repeated stress, decreased serum level of stress markers and modified the hippocampal synaptic plasticity markers in both patterns of stress exposure; in ARS, Memantine upregulated the expression of synaptophysin and brain-derived neurotrophic factor and downregulated the expression of calcium-/calmodulin-dependent protein kinase II, and in repeated restraint stress, it upregulated the expression of synaptophysin and downregulated calcium-/calmodulin-dependent protein kinase II expression. � 2015, Springer Science+Business Media New York.