Browsing by Author "Mesbah, Noha 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.
Anti-Oxidant and Anti-Inflammatory Effects of Lipopolysaccharide from Rhodobacter sphaeroides against Ethanol-Induced Liver and Kidney Toxicity in Experimental Rats
(MDPI, 08/12/2021) Mehanna, Eman T; Ali, Al-Shimaa A; El-Shaarawy, Fatma; Mesbah, Noha M; Abo-Elmatty, Dina M; Aborehab, Nora M
This study aimed to investigate the protective effects of lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS) against ethanol-induced hepatotoxicity and nephrotoxicity in experimental rats. The study involved an intact control group, LPS-RS group, two groups were given ethanol (3 and 5 g/kg/day) for 28 days, and two other groups (LPS-RS + 3 g/kg ethanol) and (LPS-RS + 5 g/kg ethanol) received a daily dose of LPS-RS (800 µg/kg) before ethanol. Ethanol significantly increased the expression of nuclear factor kappa B (NF-κB) and levels of malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the liver tissue and decreased anti-oxidant enzymes. Hepcidin expression was downregulated in the liver, with increased serum levels of ferritin and iron. Prior-administration of LPS-RS alleviated the increase in oxidative stress and inflammatory markers, and preserved iron homeostasis markers. In the kidney, administration of ethanol caused significant increase in the expression of NF-κB and the levels of TNF-α and kidney injury markers; whereas LPS-RS + ethanol groups had significantly lower levels of those parameters. In conclusion; this study reports anti-oxidant, anti-inflammatory and iron homeostasis regulatory effects of the toll-like receptor 4 (TLR4) antagonist LPS-RS against ethanol induced toxicity in both the liver and the kidney of experimental rats.
The antitumour efficacy of hesperidin vs. cisplatin against non‑small lung cancer cells A549 and H460 via targeting the miR‑34a/PD-L1/NF-κB signalling pathway
(Termedia Publishing House Ltd, 2024-08) Ibrahim, Sherine M; Sayed, Maryam S; Abo-Elmatty, Dina M; Mesbah, Noha M; Abdel-Hamed, Asmaa R
Introduction: Lung cancer is the most common type of cancer, causing worldwide mortality. Therefore, this study is necessary for continuing research into new effective and safe treatments. Recently, herbal medicines have been used for the treatment of various diseases such as cancer. This study aimed to investigate the potential anti-proliferative activity and investigate the mechanisms of hesperidin extract on the non-small lung cancer cells A549 and H460 vs. cisplatin via targeting the miR 34a/PD-L1/NF-κB signalling pathway. Material and methods: To determine the cytotoxic effects of the hesperidin extract on non-small lung cancer cells, sulphorhdamine B assay was performed. To show the inhibition of migration by hesperidin extract, wound healing assay was conducted. A quantitative polymerase chain reaction test was used to quantify the expressions of miR-34a, programmed cell death ligand-1 (PDL-1), epidermal growth factor receptor (EGFR), and P53 genes, which are involved in apoptosis pathway. Also, cell cycle assay was performed by using a flow cytometer. Results: The hesperidin extract could significantly inhibit proliferation of non-small lung cancer cells A549 and H460. Western blot assay demonstrated that hesperidin induced suppression of nuclear factor κB signalling pathway. The messenger RNA expression levels of MiR-34a and P53 were up-regulated significantly by hesperidin treatment, while the EGFR and P53 genes were down-regulated. The flow cytometer confirmed that cell cycle arrest occurred at the sub-G1 and G2 phases in A549 and H460, respectively. Conclusions: Our study demonstrated that hesperidin extract could significantly inhibit non-small lung cancer cell growth by induction of the apoptosis signalling pathway. Therefore, hesperidin might open novel strategies for effective and safe cancer treatment and reduce the adverse side effects of several chemotherapeutic treatments such as cisplatin.