Browsing by Author "Saleh, Dalia O"

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Progression of hepatic encephalopathy induced by bile duct ligation versus thioacetamide in rats: Regulatory role of apigenin
(Open Science Publishers LLP Inc., 2021-12) Fayez, Ahmed M; Mansour, Dina F; Saleh, Dalia O
Hepatic encephalopathy (HE) is the decline in brain functions due to liver insufficiency. A high mortality rate was reported due to the rapid progression of HE from covert to overt, leading to detrimental consequences. This study aims to assess the progression of HE and the potential hepatoprotective and neuroprotective effect of apigenin (APG) in bile duct ligation (BDL) versus thioacetamide (TAA)-induced HE models in rats. Wistar albino rats were divided into eight groups; four groups for the BDL model and the other four groups for the TAA model (100 mg/kg, i.p., thrice weekly for five consecutive weeks). APG (20 mg/kg/day) or lactulose (LAC) (8 ml/kg/day), as the standard, was administered orally for three consecutive weeks starting from day 14 of the experiment. Liver enzymes, total bilirubin, serum ammonia, brain and liver glutathione and malondialdehyde, brain dopamine, hepatic interleukin-6, and nuclear factor kappa B were assessed, as well as the beam walking test and histopathological examinations were carried out. APG showed significant anti-hyperammonemic, anti-oxidant, and anti-inflammatory effects in HE groups. Additionally, improvement in behavioral test and histological image of livers and brains of HE rats treated with APG was observed. In conclusion, APG exerted a significant regulatory role compared to LAC in progression of HE in BDL and TAA models. © 2021. Ahmed M. Fayez et al. All Rights Reserved.
Thioacetamide-induced acute hepatic encephalopathy: central vs peripheral effect of Allicin
(Springer, 3/25/2021) Saleh, Dalia O; Mansour, Dina F; Fayez, Ahmed M
Hepatic encephalopathy (HE) is a debilitating and life-threatening disease. Results from acute or chronic liver failure and is characterized by abnormal cerebral and neurological alterations. This study aimed at investigating the effect of allicin, the major functional component in freshly crushed garlic extract, on thioacetamide (TAA)-induced HE in rats. Induction of HE by a single dose of TAA (300 mg/kg; I.P.) was associated with a marked elevation in the serum levels of alanine amino- transferase, aspartate aminotransferase, bilirubin, albumin, total protein, blood urea nitrogen and serum ammonia besides reduction in the serum level of albumin. Moreover, it was accompanied with an increase in the hepatic and brain levels of inflammatory mediators; TNF-α and IL-1β as well as elevation of the hepatic and brain levels of oxidative stress biomarkers; reduced glutathione and lipid peroxidation evidenced by malondialdeyde. Oral administration of allicin (50, 100 and 200 mg/kg; P.O.) for 6 days prior to TAA injection restored the serum liver function, hepatic and brain levels of inflamma- tory mediators as well as oxidative stress biomarkers in a dose-dependent manner. From our results, it can be concluded that allicin has a protective effect on TAA-induced HE in rats in a dose-dependent manner due to its powerful antioxidant and anti-inflammatory properties.
Uro-protective role of chrysin against cyclophosphamide-induced hemorrhagic cystitis in rats involving the turning-off NF-κB/P38-MAPK, NO/PARP-1 and STAT-3 signaling cascades
(Elsevier Ireland Ltd, 2023-05) Saleh, Dalia O; Abo El Nasr, Nesma M.E; Fayez, Ahmed M; Ahmed, Kawkab A; Mohamed, Reem A
Chemico-Biological Interactions Available online 30 May 2023, 110585 In Press, Journal Pre-proofWhat’s this? Research paper Uro-protective role of chrysin against cyclophosphamide-induced hemorrhagic cystitis in rats involving the turning-off NF-κB/P38-MAPK, NO/PARP-1 and STAT-3 signaling cascades Author links open overlay panelDalia O. Saleh a, Nesma M.E. Abo El Nasr a, Ahmed M. Fayez b, Kawkab A. Ahmed c, Reem A. Mohamed d a Pharmacology Department, Medical Research and Clinical Studies Institute, National Research Centre, Giza, Egypt b Pharmacology and Toxicology Department, School of Life and Medical Sciences, University of Hertfordshire Hosted by Global Academic Foundation, New Administrative Capital, Cairo, Egypt c Pathology Department, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt d Department of Pharmacology, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA), Giza, Egypt Received 2 March 2023, Revised 6 May 2023, Accepted 29 May 2023, Available online 30 May 2023. Show less Outline Share Cite https://doi.org/ Background Chemotherapeutic agents are used to treat a wide range of cancer types, but they cause serious side effects which must be managed after treatment. Cyclophosphamide (CYP) is one of chemotherapeutic drugs that causes hemorrhagic cystitis (HC) induced by acrolein. Objective The current investigation intended to uncover the role of chrysin (CHR) in CYP-induced HC in rats and explore the signaling pathway beyond this effect. Analysis process: A single dose of CYP (200 mg/kg/IP) was injected, meanwhile CHR (25, 50 and 100 mg/kg, P.O) was administered respectively for 7 days prior to CYP administration and resume for 7 days afterwards. Urinary bladder tissue was then isolated from all rats to assess oxidative stress and inflammatory biomarkers. Moreover, histopathological examinations were performed. Results Treatment with CHR showed a marked alleviation in oxidative stress biomarkers induced by CYP. Furthermore, CHR treatment presented a dose-dependent boost in the anti-inflammatory; IL-10 levels and a drop in the pro-inflammatory biomarkers; IL-1β, IL-6, and TNF–α. Additionally, stabilization of the PARP-1 protein expression was also detected thus preventing DNA damage. Similarly, CHR restored the urinary bladder cGMP levels. Notably, CHR treatment was accompanied with inhibition in NF-κB/p38-MAPK, NO/PARP-1 and STAT-3 signaling pathways inflammatory cascades. All these findings conformed with the histopathological examinations as well as iNOS immunostaining in the urinary bladder tissue. Conclusion Co-administration of CHR and CYP attained uro-protective therapeutic potential to guard against HC as well as spot the tangled mechanism of CHR in attenuating the HC induced by CYP.