000			03467cam a2200349 a 4500
003			EG-GiCUC
005			20250223032711.0
008			210306s2021 ua dh f m 000 0 eng d
040			_aEG-GiCUC _beng _cEG-GiCUC
041	0		_aeng
049			_aDeposite
097			_aPh.D
099			_aCai01.08.09.Ph.D.2021.Ha.I
100	0		_aHanaa Mohamed Mahmoud Badawi
245	1	0	_aInvestigation of the effect of bee venom in a model of parkinson{u2032}s disease in mice / _cHanaa Mohamed Mahmoud Badawi ; Supervised Ezz Eldin Said Eldinshery , Rania Mohsen Abdelsalam , Omar Mohamed Abdelsalam
246	1	5	_aالتحق{u٠٦أأ}ق فى تأث{u٠٦أأ}ر سم النحل فى نموذج من مرض الشلل الرعاش فى الفئران
260			_aCairo : _bHanaa Mohamed Mahmoud Badawi , _c2021
300			_a163 P. : _bcharts , facsimiles ; _c25cm
502			_aThesis (Ph.D.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology
520			_aObjective(s): This study aimed to investigate the effect of bee venom, a form of alternative therapy, on rotenone-induced Parkinson{u2032}s disease (PD) in mice. Moreover, the possible modulation by bee venom of the effect of Ldopa/ carbidopa, bromocriptine or rasagiline was examined; also the pharmacological pathways of the effect of bee venom on the nitric oxide pathway using nitric oxide synthase inhibitors and the effect of cholinergic blockade using atropine were tested. Materials and Methods: Rotenone (1.5 mg/kg, subcutaneously; s.c.) was administered every other day for two weeks and at the same time mice received the vehicle (DMSO, s.c.), bee venom (0.065, 0.13 and 0.26 mg/kg; intradermal; i.d.), L-dopa/carbidopa (25 mg/kg, intraperitoneal; i.p.), Ldopa/ carbidopa + bee venom (0.13 mg/kg, i.d.), bromocriptine (1.5mg/kg mice, i.p.), bromocriptine (1.5mg/kg mice, i.p.) + bee venom (0.13 mg/kg, i.d.), rasagiline (1 mg/kg, i.p.), rasagiline + bee venom (0.13 mg/kg, i.d.), LNAME (10mg/kg mice, i.p.) + bee venom (0.13mg/kg, i.d.), 7-nitroindazole (10 mg/kg mice, i.p.) + bee venom (0.13mg/kg, i.d.) and atropine (1mg/kg mice, i.p.) + bee venom (0.13mg/kg, i.d.). Then, wire hanging and staircase tests were performed and mice were euthanized and brains{u2032} striata separated. Oxidative stress biomarkers namely, malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH), paraoxonase-1 (PON-1) and total antioxidant capacity (TAC) were measured. Additionally, butyrylcholinesterase (BuChE), monocyte chemoattractant protein-1 (MCP- 1), tumor necrosis factor-alpha (TNF-Ü) and dopamine (DA) were evaluated. Brain histopathological changes and caspase-3- expression were examined Results: Bee venom significantly enhanced motor performance and inhibited rotenone-induced oxidative/nitrosative stress, observed as a reduction in both MDA and NO along with increasing GSH, PON-1, and TAC. Besides, bee venom decreased MCP-1, TNF-Ü and caspase-3 expression together with an increase in BuChE activity and DA content
530			_aIssued also as CD
653		4	_aBee venom
653		4	_aMice
653		4	_aModel of parkinson{u2032}s disease
700	0		_aEzz Eldin Said Eldinshery , _eSupervisor
700	0		_aOmar Mohamed Abdelsalam , _eSupervisor
700	0		_aRania Mohsen Abdelsalam , _eSupervisor
856			_uhttp://172.23.153.220/th.pdf
905			_aNazla _eRevisor
905			_aShimaa _eCataloger
942			_2ddc _cTH
999			_c80107 _d80107