Browsing by Author "Saleh, Samy M"

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Adiponectin (+276 G/T), Tumor Necrosis Factor-alpha (-308 G/A) and Interleukin-6 (-174 C/G) Genes Polymorphisms in Egyptian Type 2 Diabetic Patients
(OMICS INT PVT LTD, 2016-05) Hamid, Amr M. Abdel; Saleh, Samy M; Mesbah, Noha M; Abo-El Matty, Dina M; Abd-Elbaky, Atif E
Type 2 diabetes mellitus (T2DM) is a metabolic pro-inflammatory disorder characterized by chronic hyperglycemia and increased levels of circulating cytokines. Adiponectin, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (Il-6), are important cytokines mediators in the pathogenesis of T2DM. The single nucleotide polymorphisms (SNPs) present in the regulatory regions of cytokine genes often have an impact on their expression levels. Aim: Explore potential associations between SNP+276 G/T of adiponectin, SNP -308 G/A of TNF-alpha and SNP -174 C/G of IL-6 genes with T2DM and to assess its influence on their serum levels. Subjects and Methods: From the Egyptian population, we enrolled 95 T2DM patients and 85 non-diabetic controls. Serum adiponectin, TNF-alpha and IL-6 were measured. Genotyping for three SNPs of the adiponectin, TNF-alpha and IL-6 genes was performed by polymerase chain reaction-restriction fragment length polymorphism. Results: Subjects with the GT/TT genotype of SNP 276 were at increased risk for T2DM (OR=15.88, CI=7.56-33.31, P = 0.01) and associated with hypoadiponectinemia compared with the GG genotype. Furthermore, the allelic frequency of the A allele of SNP 308 was significantly different between T2DM patients compared to controls (X2(=)30.54, P = 0.0001). Moreover, Individuals with T2DM carrying the GA/AA genotypes had significantly higher serum TNF-alpha levels than those carrying GG genotype. In addition, Carriers of G allele of IL-6 were significantly more likely associated with T2DM. Conclusion: Genetics variations in Adiponectin +276 G/T, TNF-alpha 308 G/A and IL-6 -174 C/G may contribute to the disposition for T2DM in Egyptian patients.
Alcohol-Induced Hepatic Fibrosis and the Relation between Hepcidin and Liver Fibrosis
(Suez Canal University, 2024-05) Ali, Al-shimaa A; Aborehab, Nora M; Saleh, Samy M; Mehanna, Eman T
Abstract: Alcoholic liver disease (ALD) is a worldwide health problem that may lead to development of fatty liver steatosis, hepatitis and cirrhosis. Alcohol is known to exert a harmful effect on a variety of human tissues. In particular, the liver is the major site of alcohol-induced damage because it is the direct recipient of the blood that contains elevated levels of alcohol, and it is the major organ responsible for alcohol metabolism. The damage caused by ethanol is mainly attributed to its metabolic process that results in production of acetaldehyde and reactive oxygen species (ROS) such as hydrogen peroxide, superoxide and free hydroxyl radical. These metabolites cause depletion of reduced glutathione (GSH), peroxidation of cellular membranes, oxidation of macro-molecules such as proteins and nucleic acids, and eventually lead to progressive injury of hepatocytes. Additionally, ethanol and its metabolic products enhance the production of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The enhanced production of those inflammation factors; stimulated partially by oxidative stress; results in cytokine imbalance and immune disorders, leading to further hepatic damage. Thus, agents with anti-inflammatory and anti-oxidative properties might be potential candidates for protection against alcohol-induced liver disease. The metabolic functions of the alcoholic liver are seriously affected. Disorders in iron metabolism are characteristic of ALD. Abnormal levels of iron, ferritin, and transferrin were reported in ALD. Hepcidin, the principle hepatic regulator of the metabolism of iron, is decreased in ALD.