Effects of dietary zinc deficiency on esophageal squamous cell proliferation and the mechanisms involved.

BACKGROUND: Dietary zinc deficiency has been shown to be associated with the development of esophageal cancer in humans, but the exact mechanism of action is not known. AIM: To observe the effects of dietary zinc deficiency on esophageal squamous cell proliferation. METHODS: Thirty C57BL/6 mice were randomly divided into three groups: A zinc-sufficient (ZS) group, zinc-deficient (ZD) group, and zinc-replenished (ZR) group. For weeks 1-10, zinc levels in the mice diets were 30.66-30.89 mg/kg in the ZS group and 0.66-0.89 mg/kg in the ZD and ZR groups. During weeks 10-12, the ZR group was switched to the ZS diet; the other two groups had no changes in their diets. Changes in body weight, serum, and esophageal tissue zinc concentrations were assessed as well as differences in the expression of proliferating cell nuclear antigen (PCNA), mitogen-activated protein kinase p38 (p38MAPK), nuclear factor kappa B (NF-κB) p105, NF-κB p65, and cyclooxygenase (COX)-2 proteins in the esophageal mucosa. RESULTS: The body weight and zinc concentration in the serum and esophageal mucosa were significantly lower in the ZD and ZR groups than in the ZS group (P < 0.05). In ZD mice, there was a marked proliferation of basal cells in the esophageal mucosa, resulting in a disturbance in the arrangement of basal cells in layers 2-4, a thickening of the squamous layer, and a significant increase in the expression of the above-mentioned five proteins involved in proliferation and inflammation in the esophageal mucosa. Two weeks after switching to the ZS diet, the serum zinc concentration in the ZR group increased, and the expression of PCNA, NF-κB p105, and COX-2 decreased, but the concentration of zinc in the esophageal mucosa and the structure of the esophageal mucosa did not display any significant changes. CONCLUSION: The ZD diet decreased the growth rate and promoted the proliferation of esophageal squamous cells in mice. The mechanism of proliferation was related to the induced overexpression of COX-2, P38, PCNA, and NF-κB (p105 and p65), and the ZR diet reduced the expression of PCNA, NF-κB p105, and COX-2, thereby reversing this process.

Cleansing efficacy and safety of bowel preparation protocol using sodium picosulfate/magnesium citrate considering subjective experiences: An observational study.

BACKGROUND: Research data from patient reports indicate that the least bearable part of colonoscopy is the administration of laxatives for bowel preparation. AIM: To observe the intestinal cleansing efficacy and safety of sodium picosulfate/magnesium citrate and to discuss the patients' experiences due to the procedure. METHODS: Subjects hospitalized in the International Medical Center Ward of Peking University International Hospital, Beijing, China, from April 29 to October 29, 2020, for whom the colonoscopy was planned, were enrolled. Bowel preparation was performed using sodium picosulfate/magnesium citrate. The effect of bowel cleansing was evaluated according to the Ottawa Bowel Preparation Scale, defecation conditions and adverse reactions were recorded, and the comfort level and subjective satisfaction concerning medication were evaluated by the visual analogue scale/score (VAS). RESULTS: The bowel preparation procedure was planned for all patients enrolled, which included 42 males and 22 females. The results showed an average liquid rehydration volume of 3000 mL, an average onset of action for the first dose at 89.04 min, an average number of bowel movements of 4.3 following the first dose, an average onset of action for the second dose at 38.90 min and an average number of bowel movements of 5.0 after the second dose. The total average Ottawa Bowel Preparation Scale score was 3.6, with 93.55% of bowel preparations in the "qualified" and 67.74% in the "excellent" grade. The average VAS score of effect on sleep was 0, and the average VAS score of perianal pain was also 0. The average VAS score for ease of taking and taste perception of the bowel cleanser was 10. Side effects included mild to moderate nausea (15.63%), mild vomiting (4.69%), mild to moderate abdominal pain (7.81%), mild to moderate abdominal distension (20.31%), mild palpitation (7.81%) and mild dizziness (4.69%). CONCLUSION: Sodium picosulfate/magnesium citrate is effective and safe for bowel preparation before colonoscopy with high subjective patient acceptance, thus improving overall patient compliance.

Effect of Helicobacter pylori infection on Barrett's esophagus and esophageal adenocarcinoma formation in a rat model of chronic gastroesophageal reflux.

OBJECTIVES: To investigate the relationship between Helicobacter pylori infection and Barrett's esophagus (BE), a rat model of chronic gastroesophageal reflux with H. pylori infection was established and the degree of inflammation, incidence of BE and esophageal adenocarcinoma (EA) were evaluated. METHODS: Eight-week-old male specific-pathogen-free SD rats were divided into five groups randomly: pseudo-operation group; esophagojejunum anastomosis (EJA) group; EJA with H. pylori infection group; EJA with H. pylori infection and celecoxib-treated group; EJA with celecoxib-treated group. Rats were kept for 30 weeks after surgery. Esophageal lesion was evaluated grossly and microscopically. The expression of COX-2 and CDX2 was determined by RT-PCR and immunohistochemistry staining. The level of PGE2 was assessed by enzyme-linked immunosorbent assay. RESULTS: Esophageal mucosal injury in the group of EJA with H. pylori infection was decreased than that in EJA group (p < .05). The incidence of BE and EA in rats undergoing EJA with H. pylori infection was increased than in rats undergoing EJA with no statistical difference. Celecoxib treatment decreased the incidence of EA in rats undergoing EJA with H. pylori infection (p < .05). The expression of CDX2 mRNA was decreased in rats with H. pylori infection or treated with celecoxib than in the rats of pseudo-operation group (p < .05). When compared with those in rats of pseudo-operation group, the expression of COX-2 mRNA and the level of PGE2 were upregulated in rats undergoing EJA irrespective of H. pylori infection (p < .05) and downregulated in rats treated with celecoxib (p < .05). When H. pylori colonized in esophagus, the severity of inflammation and the incidence of BE and EA were increased significantly. Higher levels of COX-2 expression and PGE2 were detected in rats with esophageal H. pylori colonization. CONCLUSIONS: When H. pylori infect in stomach, it may reduce the severity of inflammation. However, when colonizes in esophagus, H. pylori increases the severity of esophageal inflammation and the incidence of BE and EA. Celecoxib administration attenuates the incidence of EA by inhibiting COX-2 expression.

Celecoxib inhibits Helicobacter pylori colonization-related factors.

AIM: To investigate the effect of celecoxib, a selective COX-2 inhibitor, on Helicobacter pylori (H. pylori) colonization-related factors and its mechanism. METHODS: After co-incubation with celecoxib, morphology of H. pylori strain 26695 was observed under a transmission electron microscope. Flagella motility was assessed by stab agar motility test. Adherence of H. pylori to AGS cells was determined by enzyme linked immunosorbent assay. Levels of mRNA expression in flagellar genes (flaA, flaB), urease genes (ureA, ureB) and adhesin genes (babA, sabA, alpA, alpB, hpaA, hopZ) were measured by real-time polymerase chain reaction. RESULTS: Separation and non-integrity of bacterial cell wall, rarefaction and asymmetry of cytoplasm, and even lysis of H. pylori were observed in the presence of celecoxib. When H. pylori strains were incubated in the presence of celecoxib, their flagellar motility and adherence to AGS cells were inhibited. The expression of ureA, ureB, babA, sabA, alpA, alpB, hpaA, hopZ was up-regulated while the expression of flaA, flaB was down-regulated in the presence of celecoxib. CONCLUSION: Celecoxib inhibits flagellar motility and adherence of H. pylori to AGS cells, and destructs their normal structure in vitro.