Abstract
Gastric ulcer (GU) is a main threat to public health. 1-Deoxynojirimycin (DNJ) has antioxidant and anti-inflammatory properties and may prevent GU but related mechanism remains unclear. DNJ was extracted from the supernatants of Bacillus subtilis by using ethanol and purified by using CM-Sepharose chromatography. A GU mouse model was induced by indomethacin. The functional role of DNJ in GU mice was explored by measuring the main molecules in the NF-KappaB pathway. After the model establishment, 40 GU mice were evenly assigned into five categories: IG (received vehicle control), LG (10 μg DNJ daily), MG (20 μg DNJ daily), HG (40 μg DNJ daily), and RG (0.5 mg ranitidine daily). Meanwhile, eight healthy mice were assigned as a control group (CG). After 1-month therapy, weight and gastric volume were investigated. The levels of serum inflammatory cytokines (IL-6 and TNF-α), antioxidant indices [superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH)], and oxidant biomarker malondialdehyde (MDA) were examined via ELISA. Meanwhile, inflammatory cytokine (IL-6 and TNF-α) levels, and key molecules (NF-κB p65), cyclooxygenase 1 (COX-1 and COX2) involved in NF-κB pathway, were analyzed by using Western Blot. COX-1 and COX-2 levels were further measured by immunohistochemistry. The effects of DNJ on gastric functions were explored by measuring the changes of Motilin (MOT), Substance P (SP), Somatostatin (SS), and Vasoactive intestinal peptide (VIP) in GU mouse models with ELISA Kits. The results indicated that DNJ prevented indomethacin-caused increase of gastric volume. DNJ improved histopathology of GU mice when compared with the mice from IG group (P < 0.05). DNJ consumption decreased the levels of IL-6 and TNF-α (P < 0.05). DNJ increased antioxidant indices of GU mice by improving the activities of SOD, CAT and reduced GSH, and reduced MDA levels (P < 0.05). DNJ increased the levels of prostaglandin E2, COX-1, COX2, and reduced the levels of and NF-κB p65 (P < 0.05). DNJ showed protection for gastric functions of GU mice by reducing the levels of MOT and SP, and increasing the levels of SS and VIP. DNJ treatment inactivates NF-κB signaling pathway, and increases anti-ulceration ability of the models.
Highlights
Gastric ulcer (GU) is a digestive disease in stomach lining and its common symptoms are burning, dull ache, and waking at night
The solvent peak appeared at about 5 min and the retention time of the main peak was 16.9 min, which was similar with that of DNJ standard
The results showed that 40-μg DNJ pretreatment caused significant decrease in gastric volume when compared with other GU models (Figure 2, P < 0.05)
Summary
Gastric ulcer (GU) is a digestive disease in stomach lining and its common symptoms are burning, dull ache, and waking at night. Gastric bleeding occurs in many GU patients and is often hard to be treated (Barola et al, 2017; Godina et al, 2017; Pang and Hagen, 2017; Xing et al, 2017). Medicine therapy is still the main choice in GU treatment of but most medicine has remarkable side effects, which inhibit its clinical use. Gastric acid inhibition is often used for preventing GU bleeding. Somatostatin and pantoprazole are effective for inhibiting gastric acid secretion. Work found that hemifacial paralysis might be an adverse effect associated with omeprazole treatment in a lymphoblastic leukemia patient (Bauters et al, 2010). Severe adverse effects, including an allergic shock, rash and diarrhea, could be caused by the accumulation of omeprazole metabolites (Yu et al, 2016)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
