Xiaojianzhong decoction attenuates aspirin-induced gastric mucosal injury via the PI3K/AKT/mTOR/ULK1 and AMPK/ULK1 pathways.

CONTEXT: Xiaojianzhong decoction (XJZD), classically prescribed in Chinese medicine, has protective and healing effects on gastric mucosal injury. However, the exact mechanism behind this effect remains unclear. OBJECTIVE: To investigate the effect of XJZD on gastric mucosal injury and explore its underlying mechanisms. MATERIALS AND METHODS: C57BL/6 mice were randomized into six groups (n = 10): the control group receiving sterile water, the model (aspirin 300 mg/kg), the XJZD high-dose (12 g/kg), XJZD medium-dose (6 g/kg), XJZD low-dose (3 g/kg) and omeprazole (20 mg/kg) groups, by gavage daily for 14 days. The area of gastric mucosal injury, mucosal injury index and degree of histopathological damage were analysed. Gastric mucosal epithelial cell apoptosis was detected. Epithelial cell autophagy was observed. The expression levels of tight junction proteins and proteins related to apoptosis, autophagy and the pentose phosphate pathway were analysed. RESULTS: The results showed that after treatment with XJZD (12, 6 and 3 g/kg), the mucosal injury area was reduced (83.4%, 22.6% and 11.3%), the expression level of ZO-1 and occludin was up-regulated, the apoptosis rate of epithelial cells was reduced (40.8%, 25.4% and 8.7%), the expression of autophagy-related proteins LC3 and Beclin1 was decreased and the expression of p62 was increased, the PI3K/AKT/mTOR/ULK1(ser757) signalling pathway was activated, and the AMPK/ULK1(ser317) signalling pathway was inhibited. In addition, XJZD can antagonize the imbalance of redox homeostasis caused by aspirin and protect the gastric mucosa. DISCUSSION AND CONCLUSIONS: XJZD protects against aspirin-induced gastric mucosal injury, implying it to be a potential therapeutic agent.

Ovotransferrin alleviated acute gastric mucosal injury in BALB/c mice caused by ethanol.

Acute gastric mucosal injury is a common gastrointestinal disorder, which influences patients' life quality. It was found that ovotransferrin (OVT) reduces the abundance of Helicobacter pylori associated with gastric disease in the intestine of immunosuppressed mice. To clarify its gastric protective function, the present study investigated the effect of OVT on BALB/c mice with ethanol-induced gastric mucosal injury. Results showed that OVT attenuated the ethanol-induced gastric mucosal injury. Furthermore, OVT effectively downregulated the expression of inflammatory markers (tumor necrosis factor-α, interleukin (IL)-1ß and IL-6) but enhanced the secretion of IL-4, IL-10 and prostaglandin E2. And OVT pretreatment significantly inhibited the activation of the MAPK/NF-κB pathway. Additionally, OVT improved gastric antioxidant ability by increasing superoxide dismutase and glutathione levels and decreasing malondialdehyde and myeloperoxidase content. Pretreatment with OVT modulated the equilibrium between B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X. The above results indicated that OVT alleviated inflammatory responses, oxidative stress and apoptosis in gastric mucosal injury mice caused by ethanol.

Doxycycline-Induced Gastric Perforation.

Esophageal and gastric mucosal injuries are well-documented adverse effects of doxycycline leading to odynophagia, chest pain, and abdominal pain. There are no clear diagnostic criteria for such adverse effects; hence, the diagnosis depends heavily on thorough history. There is a paucity of literature describing life-threatening complications from doxycycline-induced mucosal injury, such as hemorrhage and perforation. We present the first case report describing a gastric perforation from doxycycline use.

Zinc Acetate Dihydrate Tablet-associated Gastric Lesions.

Objective This study aimed to determine the prevalence and endoscopic features of zinc acetate dihydrate tablet-associated gastric lesions. Methods We retrospectively examined the endoscopic features of 47 patients taking zinc acetate dihydrate tablets who underwent esophagogastroduodenoscopy. Results Gastric mucosal alterations, including redness, erosions, ulcers, and adhesion of the white coat, were observed in 29 of 47 patients (61.7%). Among patients with gastric lesions (group A), there was a significantly higher percentage of symptomatic patients in comparison to patients without lesions (group B) (65.5% vs. 22.2%; p<0.01). The background characteristics of the two groups did not differ to a statistically significant extent. On esophagogastroduodenoscopy, mucosal redness (n=27, 93.1%), erosions (n=26, 90.0%), adhesion of the white coat (n=25, 86.2%), and ulcers (n=9, 31.0%) were observed. None of the 19 patients who previously underwent esophagogastroduodenoscopy had gastric lesions before starting zinc acetate dihydrate. Esophagogastroduodenoscopy was performed after the cessation of zinc acetate dihydrate intake in six patients, and revealed the resolution of gastric lesions. Conclusion Gastric lesions were observed in 29 of 47 patients who were taking zinc acetate dihydrate tablets. The most common endoscopic findings were mucosal redness (93.1%), erosions (90.0%), adhesion of the white coat (86.2%), and ulcers (31.0%). Although the exact pathogenesis is uncertain, we believe that understanding the unique manifestations of this gastric lesion will help physicians manage adverse events in patients taking zinc acetate dihydrate tablets.

Prophylactic effects of Glycyrrhiza glabra root extract on phenylbutazone-induced Equine Glandular Gastric Disease (EGGD).

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), like phenylbutazone (PBZ), are prescribed to treat pain and inflammation in the equine. However, experimentally their use has been associated with the development of Equine Glandular Gastric Disease (EGGD). To evaluate the prophylactic effects of Glycyrrhiza glabra root extracts (GGRE) on EGGD induction following oral administration of PBZ, 12 donkeys were used. Animals were divided into three equal groups (A, B and C) in a randomized block design. A: placebo, B: PBZ (4.4 mg/kg PO q 12 h) and C: PBZ plus GGRE (17.6 mg/kg PO q 24h). Gastroscopy and blood sampling for CBC, biochemical tests and antioxidant status were performed days 0 and 7. All but 1 animal had no EGGD lesions on day 0, but on day 7, severe EGGD lesions were seen in group B animals (grade 1/4 (× 1), grade 2/4 (× 2), and grade 3/4 (× 1)). Only mild changes were seen in group C animals, the most severe lesions being grade 1/4 lesions in 2 animals. No change was observed in Group A. Hematology and serum antioxidant status did not change significantly in any group. In group B glucose decreased and ALT and ALP increased, while in group C only ALP increased. In conclusion, GGRE reduced the severity of EGGD caused by PBZ. Further, GGRE prevented PBZ induced hypoglycemia and might reduce the possible hepatic injury of PBZ.

Effects of real-ambient PM2.5 exposure plus lipopolysaccharide on multiple organ damage in mice.

Background: The toxicological effects of fine particulate matter (PM2.5) on the cardiopulmonary and nervous systems have been studied widely, whereas the study of PM2.5 on systemic toxicity is not in-depth enough. Lipopolysaccharide (LPS) can cause multiple organ damage. The combined effects of co-exposure of PM2.5 plus LPS on the stomach, spleen, intestine, and kidney are still unclear. Purpose: This study was aimed to explore the toxicological effects of co-exposure of PM2.5 and LPS on the different organs of mice. Research Design and Study Sample Using a real-ambient PM2.5 exposure system and an intraperitoneal LPS injection mouse model, we investigated multiple organ damage effects on male BALB/c mice after co-exposure of PM2.5 plus LPS for 23 weeks in Linfen, a city with a high PM2.5 concentration in China. Data Collection: Eosin-hematoxylin staining, ELISA and the biochemical assay analysed the toxicological effects. Results: The pathological tissue injury on the four organs above appeared in mice co-exposed to PM2.5 plus LPS, accompanied by the body weight and stomach organ coefficient abnormality, and significant elevation of pro-inflammatory cytokines levels, oxidative stress in the spleen and kidney, and levels of kidney injury molecule (KIM-1) increase in the kidney. There were tissue differences in the pathological damage and toxicological effects on mice after co-exposure, in which the spleen and kidney were more sensitive to pollutants. In the PM2.5 + LPS group, the superoxide dismutase inhibition and catalase (CAT) activity promotion in the kidney or spleen of mice were significant relative to the PM2.5 group; the CAT and interleukin-6 (IL-6) levels in the spleen were raised considerably compared with the LPS group. Conclusions: These findings suggested the severity and sensitivity of multiple organ injuries in mice in response to PM2.5 plus LPS.

Analysis of long-term results of pathogenetic treatment of Helicobacter pylori-associated gastroduodenopathies induced by nonsteroidal anti-inflammatory drugs in patients with osteoarthritis.

The study of the pathogenetic treatment and prevention of Helicobacter pylori (Hp)-associated gastroduodenopathies (GDP) induced by nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with osteoarthritis (OA) is one of the most serious problems in modern clinical medicine. Sixty patients with OA and concomitant Hp-associated GDP induced by NSAIDs were examined. The levels of epidermal growth factor (EDF), sAPO-1/Fas and tumor necrosis factor-α (TNF-α) were determined. Group I included 30 patients who received triple anti-Helicobacter (AHT) therapy, and group II included 30 patients who received rebamipide. Long-term effects were assessed 6 months and 1 year after treatment. All subjects showed a significant increase in TNF-α (4.7 times), EDF (2.2 times) and a decrease in sAPO-1/Fas (3.6 times) levels compared to healthy individuals. After 1 month of treatment, a significantly more significant decrease in TNF-α and an increase in sAPO-1/Fas and EDF was found in group II. In the long-term treatment, a further decrease in TNF-α and an increase in the content of sAPO-1/Fas levels were observed in all groups. However, these changes were significantly more significant in group I compared to group I. The long-term follow-up showed a declining trend of EDF in all groups. The data obtained indicate the effectiveness of rebamipide in the complex pathogenetic treatment and prevention of Hp-associated GDP induced by NSAIDs in patients with OA.

Activation of AMPK/mTOR-driven autophagy and inhibition of NLRP3 inflammasome by saxagliptin ameliorate ethanol-induced gastric mucosal damage.

AIMS: Saxagliptin, a selective/potent dipeptidyl peptidase-4 inhibitor, has revealed remarkable anti-inflammatory features in murine models of nephrotoxicity, hepatic injury, and neuroinflammation. However, its potential effect on ethanol-induced gastric mucosal injury has not been examined. Hence, the present work investigated the prospect of saxagliptin to attenuate ethanol-evoked gastric injury, with emphasis on the AMPK/mTOR-driven autophagy and NLRP3/ASC/caspase-1 pathway. MATERIALS AND METHODS: In ethanol-induced gastropathy, the gastric tissues were examined by immunohistochemistry, immunoblotting, histopathology, and ELISA. KEY FINDINGS: The results demonstrated that saxagliptin (10 mg/kg; by gavage) suppressed the gastric pathological signs (area of gastric ulcer and ulcer index scores), histopathologic aberrations/damage scores, without provoking hypoglycemia in rats. These protective features were attributed to the enhancement of gastric mucosal autophagy flux, as proven with increased expression of LC3-II and Beclin 1, decreased accumulation of p62 SQSTM1, and activation of the autophagy-linked AMPK/mTOR pathway by increasing the expression of p-AMPK/AMPK and decreasing the expression of the autophagy suppressor p-mTOR/mTOR signal. In tandem, saxagliptin counteracted the ethanol-induced pro-apoptotic events by downregulating Bax, upregulating Bcl2 protein, and lowering the Bax/Bcl2 ratio. Equally important, saxagliptin suppressed the NLRP3 inflammasome in the gastric tissue by lowering the expression of NLRP3, ASC, and nuclear NF-κBp65, decreasing the activity of caspase-1, and diminishing the IL-1ß levels. In the same regard, saxagliptin suppressed the mucosal oxidative stress by lowering lipid peroxide levels, increasing GSH and GPx antioxidants, and activating Nrf2/HO-1 pathway. SIGNIFICANCE: Saxagliptin may be a promising intervention against ethanol-evoked gastropathy by activating AMPK/mTOR-driven autophagy and inhibiting NLRP3 inflammasome.

Application of a new hyperbaric oxygen therapy protocol in patients with arterial and venous gas embolism due to hydrogen peroxide poisoning.

Hydrogen peroxide (H2O2) ingestion can cause vascular gas embolism (GE). Hyperbaric oxygen therapy (HBO2) is known to improve neurological abnormalities in patients with arterial gas embolism (AGE). Previously, HBO2 based on the U.S. Navy Table 6 diving protocol has been adopted for treating AGE and preventing the progression of portal venous GE, caused by H2O2 ingestion, to AGE. However, the indication and protocol for HBO2 have not been established for GE related to H2O2 ingestion. Herein, we describe a case in which GE caused by H2O2 ingestion was treated using HBO2 with a short protocol. A 69-year-old female patient presented with abdominal pain, vomiting, and transient loss of consciousness after ingesting 35% H2O2. Computed tomography revealed gastric wall and portal venous gas. She was administered an HBO2 protocol with 2.8-atmosphere absolute (ATA) compression for 45 minutes. This was followed by a 2.0-ATA treatment for 60 minutes with a five-minute air break, after which all gas bubbles disappeared. After HBO2 treatment, brain magnetic resonance imaging revealed focal cytotoxic edema lesions; however, the patient was discharged without additional symptoms.

Zuojin Pill ameliorates inflammation in indomethacin-induced gastric injury via inhibition of MAPK pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Zuojin Pill (ZJP) has been a classic prescription for the treatment of gastrointestinal diseases in China since ancient times. But its effect on non-steroidal anti-inflammatory drugs (NSAIDs) induced gastric injury (GI) is still uncharted. AIM OF THE STUDY: This study aims to investigate the therapeutic effect and molecular mechanism of ZJP on indomethacin (IDO) induced gastric injury. MATERIALS AND METHODS: GI was induced in rat by oral administration of 5 mg/kg IDO. Then the rats were treated with ZJP (1.26, 2.52, 5.04 g/kg, ig). The changes of food intake, body weight, gastric pH and general state observation were carried out to determine the improvement of ZJP in IDO-induced GI: HE staining and AB-PAS staining was analyzed to characterize the thickness of gastric mucosa and micro mucosal injury; in order to elucidate the effect of ZJP on IDO-induced inflammatory injury, the inflammatory infiltration of gastric tissue was observed by MPO immunohistochemical method, and the contents of TNF-α, IL-6 and IL-10 were measured. Furthermore, the regulatory mechanism of ZJP in treating IDO-induced GI was predicted with the help of network pharmacology, and the expression levels of key proteins ERK, p-ERK, P38, p-P38, JNK, p-JNK were determined to elucidate the molecular mechanism of ZJP. RESULTS: Current data strongly demonstrated that ZJP alleviated food intake reduction, weight loss and gastric injury caused by IDO and made gastric pH and mucosal thickness return to normal. In addition, ZJP could reduce the level of MPO to alleviate the inflammatory infiltration of gastric tissue. Simultaneously, ZJP could down regulate the expression of TNF-α and IL-6 and up regulate the expression of IL-10 to reduce the damage caused by inflammatory, and create a healing environment. Furthermore, ZJP could significantly inhibit the phosphorylation of ERK, p38 and JNK, which leaded to the increase of inflammatory factors and the damage of gastric mucosa. CONCLUSION: ZJP improved local inflammation by inhibiting MAPK signaling pathway, and had a good therapeutic effect on IDO-induced GI. This study has reference significance for the study of ZJP in the prevention and treatment of NSAID induced gastric injury. In addition, ZJP may be a new treatment option for the prevention and treatment of NSAID induced gastric disease.

CHRONIC USE OF PROTON PUMP INHIBITORS AND THE QUANTITY OF G, D, AND ECL CELLS IN THE STOMACH.

BACKGROUND: Acid inhibition from chronic proton pump inhibitor use and a possible increase in gastrin can lead to changes in the regulation of hydrochloric acid production. However, it has not known whether such chronic use changes the presence of gastrin, delta, and enterochromaffin-like cells in the stomach or the relationship between gastrin and delta cells. AIM: To analyze the number of gastrin-producing gastrin cells, somatostatin-producing cells, and histamine-producing cells in patients who were chronic users of proton pump inhibitor, with or without related Helicobacter pylori infection. METHODS: Biopsies from 105 patients, including 81 chronic proton pump inhibitor users (experimental group) and 24 controls, were processed immunohistochemically and subjected to counting of gastrin, delta, and enterochromaffin-like cells in high-magnification microscopic fields and in 10 glands. RESULTS: Gastrin cell, delta cell, and enterochromaffin-like cells counts were similar across the groups and appeared to be unaffected by Helicobacter pylori infection. The ratio between gastrin cells and delta cells was higher in the chronic users of proton pump inhibitor group than in controls. CONCLUSION: Chronic users of proton pump inhibitor does not affect gastrin cell, delta cell, and enterochromaffin-like cell counts significantly, but may alter the ratio between gastrin cells and delta cells.

The Efficacy of Processing Strategies on the Gastroprotective Potentiality of Chenopodium quinoa Seeds.

The current study has been conducted to evaluate the effect of different processing techniques on the 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging capacity and the gastroprotective potential of Chenopodium quinoa red seeds in acute gastric injury induced by absolute ethanol in rats. Seven groups of female Sprague Dawley rats were assigned to normal and absolute ethanol (absolute EtOH) groups, given distilled water, reference control omeprazole (OMP, 20 mg/kg), pressure-cooked quinoa seeds (QP, 200 mg/kg), first stage-germinated quinoa seeds (QG, 200 mg/kg), Lactobacillus plantarum bacteria-fermented quinoa seeds (QB, 200 mg/kg), and Rhizopus oligosporus fungus-fermented quinoa seeds (QF, 200 mg/kg). One hour after treatment, all groups were given absolute ethanol, except for the normal control rats. All animals were sacrificed after an additional hour, and the stomach tissues were examined for histopathology of hematoxylin and eosin staining, immunohistochemistry of cyclooxygenase 2 (COX-2), and nitric oxide synthase (iNOS). Stomach homogenates were evaluated for oxidative stress parameters and prostaglandin E2 (PGE2). Gene expression was performed for gastric tumor necrosis factor alpha (TNF-α) and nuclear factor kappa of B cells (NF-kB). QB and QG recorded the highest DPPH scavengers compared to QF and QP. The gastroprotective potential of QB was comparable to that of OMP, followed by QF, then QG, and QP as confirmed by the histopathology, immunohistochemistry, and gene expression assessments. In conclusion, differently processed red quinoa seeds revealed variable antioxidant capacity and gastroprotective potential, while the bacterial fermented seeds (QB) showed the highest potential compared to the other processing techniques. These results might offer promising new therapy in the treatment of acute gastric injury.

Bombax Costatum extract abrogates piroxicam-mediated hepatic and gastric toxicities in rats.

OBJECTIVE: Concurrent administration of orthodox drugs and herbs is common in tropical Africa. This study investigates the effect of co-administration of piroxicam and Bombax costatum on hepatic and gastric toxicities and levels of oxidative stress markers. MATERIALS AND METHODS: Twenty male wistar rats were grouped into four. Rats in group one were administered 1mL/kg distilled water as normal control; group two were treated with 400mg/kg of extract; group three were treated with 20mg/kg of piroxicam; while those in group four were treated with both extract and piroxicam at 400mg/kg and 20mg/kg, respectively. All treatments were given orally for 14 days. At the end of the treatment period, the rats were euthanised; blood samples and stomach were collected for determination of hepatic and gastro-toxicity alongside with oxidative stress markers. RESULTS: Treatment with piroxicam alone shows the presence of oxidative stress with marked hepatic and gastric toxicities. Oxidative stress markers, hepatic and gastric toxicity indices after treatment with extract alone and in combination with piroxicam appear like that of the control group. CONCLUSION: Concurrent administration of piroxicam and Bombax costatum prevents piroxicam-induced hepatic and gastric toxicities with a positive effect on antioxidant levels. This may indicate important health benefits of this drug-herb combination.

Effects of electroacupuncture on stress-induced gastric dysrhythmia and mechanisms involving autonomic and central nervous systems in functional dyspepsia.

Electroacupuncture (EA) is widely used as an effective method to treat stress-related disorders. However, its mechanisms remain largely unknown. The aim of this study was to investigate the effects and mechanisms of EA on gastric slow wave (GSW) dysrhythmia and c-Fos expression in the nucleus of the solitary tract (NTS) induced by stress in a rodent model of functional dyspepsia (FD). Rats in the neonatal stage were treated using intragastric iodoacetamide. Eight weeks later, the rats were implanted with electrodes in the stomach for the measurement of GSW and electrodes into accupoints ST36 for EA. Autonomic functions were assessed by spectral analysis of heart rate variability. Rats were placed for 30 min in a cylindrical plastic tube for acute restraint stress. The involvement of a central afferent pathway was assessed by measuring c-Fos-immunoreactive cells in the NTS. 1) EA normalized restraint stress-induced impairment of GSW in FD rats. 2) EA significantly increased vagal activity (P = 0.002) and improved sympathovagal balance (P = 0.004) under stress in FD rats. 3) In FD rats under restraint stress, plasma norepinephrine concentration was increased substantially (P < 0.01), which was suppressed with EA. 4) The EA group showed increased c-Fos-positive cell counts in the NTS compared with the sham EA group (P < 0.05) in FD rats. Acute restraint stress induces gastric dysrhythmia in a rodent model of FD. EA at ST36 improves GSW under stress in FD rats mediated via the central and autonomic pathways, involving the NTS and vagal efferent pathway.

Self-Emulsifying Drug Delivery System of Celecoxib for Avoiding Delayed Oral Absorption in Rats with Impaired Gastric Motility.

This study aimed to develop a self-emulsifying drug delivery system (SEDDS) of celecoxib (CEL) for suppressed delay in oral absorption under impaired gastric motility. A pseudo-ternary phase diagram was constructed for the determination of the optimal component ratio in SEDDS of CEL (SEDDS/CEL), and the SEDDS/CEL was physicochemically characterized. A pharmacokinetic study on orally dosed CEL samples (5-mg CEL/kg) was carried out in normal and propantheline (PPT)-treated rats to mimic impaired gastric motility. SEDDS/CEL rapidly formed a fine emulsion with a mean size of 147 nm in distilled water and significantly improved the dissolution behavior of CEL under pH 1.2 condition with a 20-fold higher dissolved amount than crystalline CEL. In normal rats, orally dosed SEDDS/CEL provided a 4.6-fold higher systemic exposure than that of crystalline CEL, due to the improved dissolution properties of CEL. Crystalline CEL showed delayed and decreased oral absorption of CEL in PPT-treated rats as evidenced by a 6.9-h-delayed mean absorption time and only 12% of the systemic exposure of CEL compared with those in normal rats. In contrast, SEDDS/CEL enhanced the oral absorption of CEL with a 14.6-fold higher systemic exposure with significant suppression of delay in absorption than crystalline CEL even in PPT-treated rats. SEDDS/CEL could be an efficacious option for suppressing delay in CEL absorption even under impairment of gastric motility, possibly leading to rapid and reproducible management of severe acute pain.

Inferior prognosis of gastric involvement in patients with gastrointestinal Burkitt Lymphoma.

Due to limited information reported on the clinical characteristics and outcomes of Burkitt lymphoma (BL) patients with gastrointestinal (GI) involvement, here we used the Surveillance, Epidemiology, and End Results (SEER) database to perform our study in a population-based scale. Extranodal GI involvement was categorized into gastric and intestinal primary sites. A total of 477 BL patients with GI involvement extracted from the SEER database between 2004 and 2015 were included in this study, 112 (23.5%) with the stomach and 365 (76.5%) with the intestine. Our study demonstrated that gastric involvement, older age, male gender, black race, advanced-stage III/IV, no-chemotherapy, and earlier years of diagnosis were associated with a significantly worse overall survival (OS) in GI BL patients after adjustment in multivariate analysis, whereas marital status did not significantly influence OS. Notably, BL Patients with gastric involvement had a significantly inferior 5-year OS in both univariate and multivariate analysis, as compared to those with intestinal involvement (37.8% vs. 70.2%; Univariate: HR = 2.637, P < .001; Multivariate: HR = 1.489, P = .016). In subgroup analysis, we demonstrated that gastric BL patients had a consistently worse OS than intestinal patients regardless of gender, clinical stage and year of diagnosis. Hopefully, with the advances in modern therapy, improved survival has been found in BL patients with GI involvement as a whole, specifically those with gastric involvement (HR = 0.529, P = .011) in recent years of diagnosis. In conclusion, despite the improved survival achieved in recent years, the prognosis of BL patients with gastric involvement is still poor. Novel personalized therapies and better access to intensive care remain to be needed.

Prophylactic effect of Lactobacillus plantarum KSFY06 on HCl/ethanol-induced gastric injury in mice.

The present study was conducted to determine the prophylactic effect of Lactobacillus plantarum KSFY06 (LP-KSFY06) on HCl/ethanol-induced gastric injury in Kunming mice. The experimental mice were allocated into six groups: the normal group, HCl/ethanol treated group, HCl/ethanol + ranitidine treated group, HCl/ethanol + Lactobacillus delbrueckii subsp. Bulgaricus (LB) treated group, HCl/ethanol + low concentration of Lactobacillus plantans KSFY06 (LP-KSFY06-L) treated group, and HCl/ethanol + high concentration of Lactobacillus plantans KSFY06 (LP-KSFY06-H) treated group. The changes in daily body weight and food intake of the mice in the HCl/ethanol + LP-KSFY06-H treated group were the closest to those of the HCl/ethanol + ranitidine treated and normal groups. LP-KSFY06 significantly inhibited the formation of gastric mucosal lesions, reduced the area of gastric lesions, inhibited gastric-juice secretion, and increased pH compared with the HCl/ethanol treated group. After the treatment, the serum interleukin-6 (IL)-6, IL-12, tumor necrosis factor-α (TNF-α), and interferon-γ levels and the gastric-tissue IL-6 and IL-12 levels in the LP-KSFY06 (including LP-KSFY06-L and LP-KSFY06-H) group decreased compared with those in the HCl/ethanol treated group. The level of serum and gastric tissue malondialdehyde was lower and the nitric oxide, total superoxide dismutase, and glutathione activities in the LP-KSFY06 treated mice were higher than those in the HCl/ethanol treated mice. Quantitative polymerase chain reaction analysis and western blot analysis showed that LP-KSFY06 increased the mRNA and protein expression of the epidermal growth factor, epidermal growth factor receptor, vascular endothelial growth factor, inhibitor kappaB-α, neuronal nitric oxide synthase, and endothelial NOS and reduced the mRNA and protein expression of nuclear factor kappaB, inducible NOS, cyclooxygenase-2, TNF-α, and IL-1ß in gastric tissues compared with the HCl/ethanol treated mice. These experimental results showed that a high concentration (1.0 × 109 CFU per kg B.W.) of LP-KSFY06 had a stronger effect on preventing gastric injury than a low concentration (1.0 × 108 CFU per kg B.W.) of LP-KSFY06. These results suggest that LP-KSFY06 has a potential probiotic effect in preventing gastric injury.