Gut injury is a severe and unpredictable illness related to the increased cell death of intestinal epithelial cells (IECs). Excessive IEC apoptotic cell death during the pathophysiological state entails chronic inflammatory diseases. This investigation was undertaken to assess the cytoprotective action and underlying mechanisms of polysaccharides from Tunisian red alga, Gelidium spinosum (PSGS), on H2O2-induced toxicity in IEC-6 cells. The cell viability test was initially carried out to screen out convenient concentrations of H2O2 and PSGS. Subsequently, cells were exposed to 40 µM H2O2 over 4 h in the presence or absence of PSGS. Findings revealed that H2O2 caused oxidative stress manifested by over 70% cell mortality, disturbed the antioxidant defense, and increased the apoptotic rate in IEC-6 cells (32% than normal cells). Pretreatment of PSGS restored cell viability, especially when used at 150 µg/mL and normal cell morphology in H2O2-callenged cells. PSGS also equally sustained superoxide dismutase and catalase activities and hindered the apoptosis induced by H2O2. This protection mechanism of PSGS may be associated with its structural composition. The ultraviolet visible spectrum, Fourier-transformed infrared (FT-IR), X-ray diffraction (XRD), and high-performance liquid chromatography (HPLC) demonstrated that PSGS is mainly sulfated polysaccharides. Eventually, this research work provides a deeper insight into the protective functions and enhances the investment of natural resources in handling intestinal diseases.

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Background Lung carcinoma is a foremost cause of cancer-related mortality worldwide. Variable genetic factors are associated with the development of lung malignancy. This study was performed to evaluate the possible association between epidermal growth factor receptor (EGFR) gene polymorphisms and non small cell lung carcinoma (NSCLC) in Iraqi population. Methods DNA samples were extracted from 100 patients and 100 controls. Four PCR fragments were designed to amplify four high-frequency variants within EGFR, namely rs1050171, rs2072454, rs2227984, and rs2227983. The PCR fragments were genotyped by single-strand conformation polymorphism (SSCP) method, and each genotype was exposed to direct sequencing. Results Genotyping experiments confirmed the variability of three targeted variants, and logistic regression analysis showed that two of these variants (rs1050171 and rs2227983) exhibited a significant association with NSCLC. Individuals with rs1050171:GA genotype showed a significant association with the increased risk of NSCLC (P=0.0110; OD 5.2636; Cl95% 1.4630 to 18.9371). Individuals with rs2227983:GG genotype exhibited a highly significant association with NSCLC (P=0.0037; OD 5.2683; Cl95% 1.7141 to 16.1919). Linkage disequilibrium analysis showed that the effects of the investigated variants are independent of each other. Conclusions Our collective data indicated that EGFR-rs1050171G/A and EGFR-rs2227983G/G SNPs exerted significant and independent association with the increased risk of NSCLC. This study suggests employing both rs1050171 and rs2227983 SNPs as informative diagnostic markers for the early detection of NSCLC in the study population.