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Start Over Author "El-Shitany NA" Topic antineoplastic agents
2 results on '"El-Shitany NA"'

1. Honey protects against cisplatin-induced hepatic and renal toxicity through inhibition of NF-κB-mediated COX-2 expression and the oxidative stress dependent BAX/Bcl-2/caspase-3 apoptotic pathway.

Author

Neamatallah T, El-Shitany NA, Abbas AT, Ali SS, and Eid BG

Subjects
Animals, Antioxidants administration & dosage, Apoptosis drug effects, Caspase 3 genetics, Caspase 3 metabolism, Cyclooxygenase 2 genetics, Cyclooxygenase 2 metabolism, Humans, Kidney metabolism, Liver metabolism, Male, NF-kappa B genetics, NF-kappa B metabolism, Proto-Oncogene Proteins c-bcl-2 genetics, Proto-Oncogene Proteins c-bcl-2 metabolism, Rats, Rats, Sprague-Dawley, Signal Transduction drug effects, Tumor Necrosis Factor-alpha genetics, Tumor Necrosis Factor-alpha metabolism, bcl-2-Associated X Protein genetics, Antineoplastic Agents adverse effects, Cisplatin toxicity, Honey analysis, Kidney drug effects, Liver drug effects, Oxidative Stress drug effects, Protective Agents administration & dosage, bcl-2-Associated X Protein metabolism
Abstract

The protective effects of both manuka and talh honeys were assessed using a rat model of cisplatin (CISP)-induced hepatotoxicity and nephrotoxicity. The results revealed that both honeys exerted a protective effect against CISP-induced hepatotoxicity and nephrotoxicity as demonstrated by decreasing liver and kidney function. Manuka honey also prevented CISP-induced histopathological changes observed in the liver and decreased the changes seen in the kidneys. Talh honey decreased CISP-induced liver histopathological changes but had no effect on CISP-induced kidney histopathological changes. Both honeys reduced the oxidative stress in the liver. Conversely, they have no effect on kidney oxidative stress, except that manuka honey increased CAT activity. GC-MS analysis showed the presence of the antioxidant octadecanoic acid in talh honey while heneicosane and hydrocinnamic acid were present at a higher content in manuka honey. The molecular mechanism was to limit the expression of inflammatory signals, including COX-2 and NF-κB, and the expression of the apoptotic signal, BAX and caspase-3 while inducing Bcl-2 expression.

Published
2018
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2. Proanthocyanidin protects against cisplatin-induced oxidative liver damage through inhibition of inflammation and NF-κβ/TLR-4 pathway.

Author

El-Shitany NA and Eid B

Subjects
Animals, Antioxidants metabolism, Apoptosis drug effects, Chemical and Drug Induced Liver Injury etiology, Chemical and Drug Induced Liver Injury metabolism, Cyclooxygenase 2 metabolism, Cytokines blood, Inflammation chemically induced, Inflammation metabolism, Liver drug effects, Liver metabolism, Male, Nitric Oxide metabolism, Oxidation-Reduction, Proanthocyanidins therapeutic use, Rats, Sprague-Dawley, Reactive Oxygen Species metabolism, Signal Transduction, Antineoplastic Agents toxicity, Chemical and Drug Induced Liver Injury drug therapy, Cisplatin toxicity, NF-kappa B metabolism, Oxidative Stress drug effects, Proanthocyanidins pharmacology, Toll-Like Receptor 4 metabolism
Abstract

Although cisplatin (CIS) is a highly effective anticancer drug, hepatotoxicity is one of the most common adverse effects associated with its use. Recently, reactive oxygen species (ROS) and inflammation are suggested to be key factors in the pathophysiology of CIS-induced acute liver damage. The aim of this study is to investigate the possible protective effect of proanthocyanidin (PRO) against CIS-induced acute hepatotoxicity. Rats were divided into four groups: 1, Control; 2, PRO; 3, CIS; and 4, PRO + CIS. Biochemical studies and histopathology were used to assess liver damage. ROS, inflammatory cytokines, nuclear factor kappa beta (NF-κβ), inducible cyclooxygenase enzyme (COX-2), inducible nitric oxide synthase (iNOS), toll-like receptor-4 (TLR-4) gene expression, and apoptotic markers were also assessed. PRO pretreatment protected the liver against CIS-induced toxicity as indicated by decreased plasma levels of liver function enzymes and the normal liver histopathology observed in the PRO + CIS group. PRO pretreatment also diminished indicators of oxidative stress in the liver, including nitric oxide (NO) and malondialdehyde (MDA). It also increased the antioxidants, reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) in the liver. Plasma interleukin-1 beta (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α) were all reduced. Liver gene expression of NF-κβ, COX-2, iNOS, and TLR-4 were all downregulated. Furthermore, PRO administration downregulated the liver expression of the apoptotic marker, Bax, while upregulated the antiapoptotic marker, Bcl2. In conclusion, our results revealed that PRO may protect against CIS-induced acute liver damage mainly through inhibition of ROS, inflammation, and apoptosis., (© 2017 Wiley Periodicals, Inc.)

Published
2017
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