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Articles by Eman F. El Azab
Total Records ( 2 ) for Eman F. El Azab
  Eman F. El Azab , Nihal M. Elguindy , Galila A. Yacout and Dalia A. Elgamal
  Background and Objective: Numerous experimental studies have shown various pharmacological activities including geraniol's cancer prevention agent and antioxidant capacity. The goal of this investigation is to mark the prospective defensive role of geraniol in rat’s carbon tetrachloride (CCl4) instigated in liver fibrosis. Materials and Methods: Liver fibrosis was prompted by subcutaneous injections of CCl4, twice week by week and for about a month. Simultaneously, geraniol (200 mg kg1) was orally regulated every day. Post-Hoc-Test were carried out where p<0.05 has been established as a significant value. Results: The biochemical results showed that geraniol reduced liver damage just as manifestations of liver fibrosis. The administration of geraniol diminished the CCl4-initiated the elevation in serum aminotransferase activities and alkaline phosphatase activity. Geraniol diminished the levels of TNF-α, NO and myeloperoxidase activity which were prompted by the CCl4 treatment. The rise of serum hyaluronidase activity and hepatic hydroxyproline content was also curtailed by geraniol treatment. Besides, geraniol fundamentally declined hepatic malondialdehyde (MDA) formation and increased reduced glutathione (GSH) in CCl4-treated rats. Geraniol has also increased the activity of hepatic antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione peroxidase (GPx) in the rats treated with CCl4. Finally, the histological analysis of the liver bolstered the biochemical results. Conclusion: Our study has demonstrated that geraniol has a hepatoprotective upshot on liver fibrosis caused by CCl4, supposedly due to its free radical scavenging, antioxidant and anti-inflammatory characteristics.
  Eman F. El Azab
  Background and Objective: Lead is defined as a severe adverse metal that induces neurological, renal, haematological and hepatic dysfunctions. It stimulates oxidative stress to disrupt the antioxidative enzyme mechanism, organ structure and lipid membranes of the cell. Kiwifruit (Actinidia deliciosa) is amongst the world's most valuable fruits due to its various pharmacological characteristics and health benefits. The present research was intended to observe the antioxidant efficiency of kiwifruit ethanolic extract on lead toxicity in the hepatic, renal, brain and blood tissues in rats. Materials and Methods: Twenty-four adult Wister albino rats were classified into 4 groups with 6 rats within each group. The rats in group I functioned as normal control. Animals within group II, III and IV were given three intraperitoneal doses of lead acetate (25 mg kg–1 b.wt., liquefied in distilled H2O as a vehicle) on the day 7th, 14th and 21st of the experiment. Group III and IV were the treatment groups and were treated with a daily oral dose of kiwifruit extract (250 and 500 mg kg–1 b.wt., respectively) for 28 days. Results: The protective impact of kiwifruit was observed in the improvement in antioxidant enzyme activity [Catalase (CAT), Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx) and Glutathione Reductase (GR)] and decreased level of Lipid Peroxidation (LPO) in the liver, brain and kidney tissues. Additionally, Actinidia deliciosa has a great effect on increasing acetylcholine esterase activity in the brain and also, improved the delta-aminolevulinic acid dehydratase activity in the blood. Conclusion: Kiwifruit emerged as an effective factor for the alleviation of lead-induced oxidative damage in cells.
 
 
 
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