000			04093ntm a2200313 i 4500
001			12102116
005			20240922101356.0
008			150118s2021 ua a f bm 000 0 eng |
040			_aEG-EULC _cEG-EULC _erda
041	0		_aeng _bara
082	0	4	_a615.19 _bE.N.P _222
100	1		_aSalem, Mohamed Ahmed Mahmoud _933910 _eauthor
245	1	0	_aPossible modulatory effect of tadalafil and bergapten on experimentally induced cognitive impairment in mice / _cMohamed Ahmed Mahmoud Salem (B. Pharm. 2016), Teaching Assistant of Pharmacology, Toxicology, and Biochemistry, Faculty of Pharmacy, Future University in Egypt (FUE), Supervision of Dr. Nesrine Salah El Dine El Sayed, Professor and Head of Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Dr. Suzan Mohamed Mansour, Associate Professor of Pharmacology, Toxicology and Biochemistry, Faculty of Pharmacy, Future University in Egypt (FUE)
246	1	5	_aتأثير فاعلية التطبيع المحتمل لعقاري التادالافيل والبيرجابتين لاعتلال الادراك المستحدث تجريبيا في الفئران
264		1	_c2021
300			_a139 pages, 4 pages : _billustrations (some color) ; _c21 cm
336			_2rdacontent _atext
337			_2rdamedia _aunmediated
338			_2rdacarrier _avolume
500			_aSupervision of Dr. Nesrine Salah El Dine El Sayed, Professor and Head of Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Dr. Suzan Mohamed Mansour, Associate Professor of Pharmacology, Toxicology and Biochemistry, Faculty of Pharmacy, Future University in Egypt (FUE)
502			_aThesis (M.Sc.)-Cairo University, Faculty of Pharmacy, Department of Pharmacology & Toxicology, 2021.
504			_aIncludes bibliographical references.
520	3		_aSporadic Alzheimer’s disease (SAD) is a slowly progressive neurodegenerative disorder characterized by deposition of amyloid beta (Aβ) plaques, tau protein aggregation, impaired insulin signaling, and neuroinflammation. This study aimed to investigate the neuroprotective potential of tadalafil (TAD) and bergapten (BG) in SAD-induced cognitive impairment in mice. SAD was induced by a single intracerebroventricular injection of streptozotocin (STZ) (3 mg/kg). TAD or BG was administered intraperitoneally at doses of 20 and 25 mg/kg, respectively, 5 hours after STZ injection for 21 consecutive days. TAD and BG conceivably attenuated STZinduced hippocampal insult, preserved neuronal integrity, and improved cognitive function in the Morris water maze and object recognition tests paralleled by reduced Aβ expression and phosphorylation of tau. Moreover, TAD and BG enhanced the protein expression of pAkt, pGSK-3β, beclin-1, and methylated protein phosphatase 2A (PP2A) and cyclin D1 gene expression and raised brain-derived neurotrophic factor immunoreactivity. In addition, both drugs boosted the hippocampal levels of cyclic guanosine monophosphate (cGMP), protein kinase G (PKG), WNT3A, and adenosine monophosphate-activated protein kinase coupled by reduced protein expression of β-catenin and mammalian target of rapamycin (mTOR). TAD and BG also halted neuroinflammation as evidenced by reduced IL-23 and IL27 levels and NF-κB protein expression. However, the effects of BG were superior than that of TAD on the restoration of the brain histological profile. In conclusion, this study offers novel insights on the neuroprotective effects of TAD or BG in the management of AD as evidenced by the improved cognitive function and histopathological architecture. This could be attributed to modulation of the crosstalk among Akt/GSK-3β, PP2A, mTOR/autophagy, cGMP/PKG, and Wnt/β-catenin signaling cascades and mitigation of neuroinflammation.
546			_aText in English, abstracts in English and Arabic.
650		0	_apharmacology
856	4	0	_3DSpace electronic resources _uhttp://repository.fue.edu.eg/handle/123456789/6045
942			_cTHESIS _2ddc
999			_c13025 _d13025