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Fucoidan
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Ellya Sinurat, Dina Fransiska, Nurhayati, Hari Eko Irianto
The ulcer is a frequent gastrointestinal illness that gives patients great pain, disrupts their daily routines, and creates mental anguish. It is more common among those who are always in a rush, worry a lot, and eat curries. Inflammation of the mucosa and tissue that protects the gastrointestinal system characterizes peptic ulcer disease. Peptic ulcers cause damage to the mucus membrane that typically shields the esophagus, stomach, and duodenum from gastric acid and pepsin (Maury et al., 2012).
Blood lead level and Helicobacter pylori infection in a healthy population: A cross-sectional study
Published in Archives of Environmental & Occupational Health, 2020
Won-Ju Park, Soo-Hyeon Kim, WonYang Kang, Ji-Sung Ahn, Seunghyeon Cho, Dae-Young Lim, Suwhan Kim, Jai-Dong Moon
In South Korea, H. pylori seroprevalence rate as determined by serum IgG testing was 51.0% and tended to be lower compared to the past.8 The causes of decreased H. pylori infection rate include the generalization of eradication, improved sanitation, and better living conditions.9 The IARC has classified H. pylori as a carcinogen to humans (Group 1A).10H. pylori is an important cause of gastric cancer, mucosal-associated lymphoid tissue lymphoma, and peptic ulcer disease.11 As such, an association between blood lead level (BLL) and stomach cancer and between H. pylori infection and stomach cancer has been found. This cross-sectional study aimed to investigate the relationship between BLL and H. pylori infection rate.
Bacteria-targeting chitosan/carbon dots nanocomposite with membrane disruptive properties improve eradication rate of Helicobacter pylori
Published in Journal of Biomaterials Science, Polymer Edition, 2021
Muhammad Arif, Mohamed Sharaf, Quanjiang Dong, Lili Wang, Zhe Chi, Chen-Guang Liu
In order to effectively eliminate H. pylori infection, it is essential to extend antibiotic residence time in the stomach. This may be done by obtaining a concentration that is high enough to permeate the stomach mucosa. The antibiotic may reach the point of contact between the mucus gel layer and the epithelial cells, where H. pylori thrive [45]. H. pylori exist mainly in the intact mucus layer near the epithelial surface [44]. UCPM-NPs permeation through the mucus layer and retention on the stomach wall is essential for successful antibacterial treatment. Mice were administered orally with UCPM-NPs to study the retention and distribution of UCPM-NPs in the mouse stomach. After administering the UCPM-NPs, the mouse's whole stomach was removed and opened at 4 and 24 h. The luminal lining was then rinsed with PBS and flattened for fluorescence imaging. The gastric tissue collected from untreated mice as a control group exhibited no detectable fluorescence emissions, as shown in Figure 7A. On the other hand, high fluorescence was detected in the gastric tissue collected at 4 h after oral gavage, which was longer than the gastric emptying times recorded for mice, as shown in Figure 7B [46]. Therefore, the evident presence of the UCPM-NPs detected here suggested successful retention of the UCPM-NPs in the stomach lining. The image obtained after 24 h of oral gavage also showed signs of fluorescence in the entire stomach, although the fluorescence intensity decreased slightly, as shown in Figure 7C. Further quantification of the gastric retention of UCPM-NPs showed that ∼73 μg of UCPM-NPs remained 4 h after treatment in the stomach; this number decreased to ∼31 μg at 24 h after treatment as depicted in Figure 7D. The in vivo therapeutic effectiveness of AMX-UCPM-NPs against bacterial infection in H. pylori-infected BALB/c mice models was also investigated. Before treatment, rod-shaped H. pylori were widely distributed over the gastric tissue surface of the infected mouse, as shown in Figure 8 control, indicating successful H. pylori colonization of the gastric mucosa. When the stomach mucosa of untreated mice infected with H. pylori was stained with H&E (hematoxylin and eosin), it exhibited mucosal damage. Neutrophil infiltration was found to be a common component of inflammation. Infected mice treated with AMX-UCPM-NPs, on the other hand, exhibited standard gastric folds that were indistinguishable from uninfected mice administered with NS in control groups. In the H&E-stained slice of stomach tissue, there were almost no intact H. pylori, but well-defined heterochromatin and nucleoli in epithelial cells were clearly visible. As seen in the H&E stained slice, the stomach ulcer was delayed mainly, which is likely due to the inflammatory response produced by H. pylori infection [44]. The current study also demonstrates a helpful approach for effectively suppressing H. pylori infection and accelerating stomach ulcer healing since H. pylori infection is responsible for most cases of peptic ulcer disease in humans.