الفهرس 
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Abstract
Peptic ulcer disease is a leading cause of death (PU). The significant risk of complications, including bleeding, pyloric stenosis, and life-threatening perforations, makes peptic ulcer diseases very risky (10-20 percent of patients). Environmental factors including smoking, alcohol usage, meals high in salt, steroids and non-steroidal anti-inflammatory drugs, infection with Helicobacter pylori, and stress may all have a part in the development of peptic ulcer, but patient genetics may also play a role. This has to do with changes in gene expression that defend the stomach lining physiologically.
Peptic ulcer disease may have a genetic component, and changes in the ABCG2 gene may be one such cause. It encodes a member of the ABCG2 transporter family, a half-transporter with 655 amino acids named ABCG2 (previously known as BCRP, breast cancer resistance protein). Intestinal cells localise ABCG2, suggesting it has a protective role by reducing the accumulation of harmful xenobiotics in cells and organs. A single incidence of its dysfunction may hasten the development of peptic ulcers.
Mucosal injury causes gastric lesions, which are linked to cellular infiltration, free radical production, cytokines, and growth factors. Major contributors to gastric ulceration include the acute inflammatory marker myeloperoxidase (MPO), pro-inflammatory cytokines (tumour necrosis factor-alpha [TNF-α], interleukin-6 [IL-6], and interleukin-1 beta [IL-1β].
Research has linked ethanol drinking to an increased risk of developing a stomach ulcer.
The purpose of this research was to examine the potential protective roles of the ABCG2 and NF- κB genes in peptic ulcers using real-time polymerase chain reaction (PCR) and the TNF-α and IL-1β using an enzyme-linked immunosorbent assay (ELISA).
The main results of the study revealed that:
The mean levels of serum IL-1β were found to be significantly higher in the ulcer groups than in the control group, with a Pvalue < 0.0001. When comparing the protected group to the ulcer group, there was a statistically significant reduction in the protected group. When comparing the omega-3treated group to the ulcer group, the amount dropped considerably greater in the omega-3 treatedgroup (Pvalue <0.0001).
The mean levels of serum TNF-α were significantly higher in the ulcer groups than in the control group, with a Pvalue < 0.0001. The level was found to be considerably lower in the protected group compared to the ulcer group (Pvalue< 0.0001). When comparing the omega-3treated group to the ulcer group, the amount dropped considerably greater in the omega-3treated group (Pvalue< 0.0001).
When comparing the expression of the ABCG 2 gene between the control group and the omega treated group, the omega treated group showed a statistically significant increase (Pvalue< 0.0001). ABCG 2 gene expression was found to be considerably higher in the protected group compared to the omega- treated group (Pvalue< 0.0001). This indicates that omega was successful in increasing ABCG 2 gene expression in stomach tissue.
The expression level of the NF-κB gene was considerably higher in the omega-treated group compared to the ulcer group and the control group (Pvalue< 0.0001). The shielded group showed considerably higher NF-κB gene expression than the omega-treated group (Pvalue< 0.0001). This suggests that omega was able to increase the expression of the NF- κB gene in stomach tissue at the molecular level.