000			03367cam a2200349 a 4500
003			EG-GiCUC
005			20250223031905.0
008			171227s2017 ua dh f m 000 0 eng d
040			_aEG-GiCUC _beng _cEG-GiCUC
041	0		_aeng
049			_aDeposite
097			_aM.Sc
099			_aCai01.08.09.M.Sc.2017.Am.E
100	0		_aAmal Ahmed Ahmed Basaer
245	1	4	_aThe effect of irbesartan in 2,4,6-trinitrobenzene sulfonic acid induced ulcerative colitis in rats / _cAmal Ahmed Ahmed Basaer ; Supervised Dalaal Moustafa Abdallah , Hanan Salah Eldin Elabhar , Mai Ahmed Galal
246	1	5	_aتأث{u٠٦أأ}رالإ{u٠٦أأ}رب{u٠٦أأ}سارتان في إلتھاب القولون التقرحي المحدث بمادة ٦:٤:٢ تري ن{u٠٦أأ}تروبنز{u٠٦أأ}ن سلفون{u٠٦أأ}ك أس{u٠٦أأ}د في الجراذان
260			_aCairo : _bAmal Ahmed Ahmed Basaer , _c2017
300			_a159 P. : _bcharts , facsimiles ; _c25cm
502			_aThesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology
520			_aAngiotensin (Ang) II plays a pivotal role in the pathogenesis of inflammatory bowel disease (IBD). Both ACEI and Ang II type 1 receptor blockers (ARBs) possess anticolitic efficacy; however, irbesartan (Irb) potential anti-ulcerative properties has not been reported previously. Colitis was induced in male Wistar rats by the rectal installation of 2,4,6-trinitrobenzene sulfonic acid (TNBS). Animals were divided into control, TNBS, sulfasalazine (Sulfz; 300 mg/kg), Irb (30 and 100 mg/kg), and combination (Sulfz/Irb30) groups. Irb at both dose levels attenuated the severity of colitis, as evidenced by decrease of ulcerative area, colon/spleen mass index, weight loss, and histopathological findings. It reduced the inflammatory response, via attenuation of nuclear factor (NF)-mB p65, tumor necrosis factor-{uF061}, interleukin-6, intracellular adhesion molecule-1, as well as myeloperoxidase activity. The drug was also able to restore junctional adhesion molecule (JAM)-A and trefoil factor (TFF)-3 to decrease epithelial barrier dysfunction. In association, the ARB was able to halt oxidative stress evidenced by the suppression of lipid peroxidation and capase-3, a marker of apoptosis. Besides, it increased nuclear factor nuclear factor (erythroidderived 2)-like-2 and hemeoxygenase-1. These effects were more prominent with the 100 mg/kg dose that was comparable to Sulfz. Meanwhile, the combination with Irb surpassed the anti-inflammatory, antioxidant and antiapoptotic effects and improved barrier strengthening mediated by Sulfz alone; however it did not modulate the reduction in the ulcer severity produced by Sulfz alone. In conclusion, Irb hampers IBD through the modulation of colonic inflammation, oxidative stress, and apoptosis, as well as enhancement of TFF-3 to preserve the tight junction JAM-A improving gut barrier function.
530			_aIssued also as CD
653		4	_aApoptosis
653		4	_aInflammation
653		4	_aOxidative stress
700	0		_aDalaal Moustafa Abdallah , _eSupervisor
700	0		_aHanan Salah Eldin Elabhar , _eSupervisor
700	0		_aMai Ahmed Galal , _eSupervisor
856			_uhttp://172.23.153.220/th.pdf
905			_aNazla _eRevisor
905			_aShimaa _eCataloger
942			_2ddc _cTH
999			_c64282 _d64282