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005			20231211140427.0
008			211026s2021 ua a|||| bm|| 00| 0 eng d
040			_aEG-NcFUE _erda
041	0		_aeng _bara
082	0	4	_222 _a616.99 _bE.E.P
100	1		_933889 _aEl Sawaf, Engie Samir, _eauthor.
245	1	4	_aThe possible impact of vitamin D3 on peripheral neuropathy induced by diabetes in a rat model / _cby Engie Samir El Sawaf (Teaching Assistant Pharmacology & Toxicology & Biochemistry department, Faculty of Pharmaceutical Sciences and Pharmaceutical Industries, Future University in Egypt)
246	1	5	_aالتأثير المحتمل لفتيامين د 3 في التهاب الأعصاب الطرفية المصاحب لمرض السكري المحدث في الجزان
264		1	_c2021
300			_a1 online resource (156 pages, 4 pages) : _billustrations (some color)
336			_2rdacontent _atext
337			_2rdamedia _acomputer
338			_2rdacarrier _aonline resource
500			_aSupervision of Dr. Dalaal Moustafa Abdallah (Professor of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University), Dr. Samira Saleh Mostafa (Professor of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University), Dr. Hanan Salah El-Din El-Abhar (Professor & Head of Pharmacology, Toxicology & Biochemistry department, Faculty of Pharmaceutical Sciences & Pharmaceutical Industries, Future University in Egypt (FUE)
502			_aThesis (M.Sc.)-Cairo university, Faculty of pharmacy, Department of Pharmacology and Toxicology, 2021.
504			_aIncludes bibliographical references.
520	3		_aVitamin D and rosuvastatin are two well-known drugs that mediate beneficial effects in type 2 diabetes (T2D) complications, however, their anti-neuropathic potential is still debatable. Hence, we studied the possible neurotherapeutic effect & the possible underling mechanisms. Additionally, evaluating the merit of their combination using a high fat fructose diet/streptozotocin (HFFD/STZ) T2D model. In addition to the control group, rats with T2D-associated neuropathy (6 weeks post STZ) were allocated into untreated and treated with vitamin D (cholecalciferol, 3500 IU/kg/week), rosuvastatin (10 mg/kg/day), or both. After 2 months of treatment, the therapeutic effect on small/large nerves was investigated using tail flick test, electrophysiological examination and histological evaluation, which documented that long-term use of vitamin D and/or rosuvastatin regenerated neuronal function and architecture of the sciatic nerve. These treatment regimens also decreased neuronal inflammation and apoptosis verified by inhibiting neuron content of TNF- and IL-18, as well as caspase-3 activity, while augmenting Bcl-2 content. On the molecular level, vitamin D and rosuvastatin abated the protein expression of NICD1, Wnt-10, β-catenin and TGF-β, while augmented the sciatic nerve content of SMAD7. These effects were associated with an upturn in the neuronal mitochondrial function (NRF-1, TFAM, mtDNA, and ATP). In conclusion, vitamin D and/or rosuvastatin abridged diabetes-induced neuropathy via turning off Notch1, Wnt-10/β-catenin and modulating TGF-β/SMAD7 signaling along with enhancing mitochondrial function, effects that lessened neuronal degeneration, demyelination and fibrosis.
546			_aText in English, abstracts in English and Arabic.
650		0	_aRats _xDiseases
650		0	_aDiabetes
650		0	_aVitamin D _xTherapeutic use
856	4	0	_3DSpace electronic resource _uhttp://repository.fue.edu.eg/xmlui/handle/123456789/5795
942			_cTHESIS _2ddc
999			_c12996 _d12996