Gastric Histopathological Changes Research Articles

The protective effect of quinoa on the gastric mucosal injury induced by absolute ethanol.

Gastric mucosal injury caused by ethanol is a common gastrointestinal disease. Quinoa (Chenopodium quinoa Willd.), as a nutrient-rich grain, plays a significant role in preventing and treating gastric mucosal damage. The present study aimed to explore the protective effect of quinoa on alcohol-induced gastric mucosal damage and its possible mechanism. The ethanol-induced gastric mucosal injury rat model was used for in vivo experiments and H2 O2 -induced GES-1 cells for in vitro experiments to elucidate the protective effect of quinoa. The results show that quinoa water extract can increase the superoxide dismutase level and decrease the malondialdehyde level in vitro and in vivo. Furthermore, quinoa also reduced the bleeding point and bleeding area in rats with ethanol-induced gastric mucosal injury and improved gastric histopathological changes. H2 O2 significantly increased the levels of inflammatory factors in GES-1 cells, which were markedly ameliorated by quinoa water extract. Likewise, quinoa water extract regulated the protein expression levels of Nrf2, Keap1, HO-1, p-IKK, and p-NF-κB through Nrf2 and nuclear factor-κB signaling pathways, reducing the production of oxidative stress and inflammation, thereby repairing the damaged gastric mucosa. The findings of this study demonstrated that quinoa shows protective effect against ethanol-induced gastric mucosal injury through its anti-inflammatory and anti-oxidant effects. We propose that our research will provide a reference for quinoa as a functional food. © 2022 Society of Chemical Industry.

Xiangsha Liujunzi Decoction improves gastrointestinal motility in functional dyspepsia with spleen deficiency syndrome by restoring mitochondrial quality control homeostasis

BackgroundXiang Sha Liu Junzi decoction (XSLJZD) is a famous traditional Chinese medicinal prescription for the treatment of functional dyspepsia (FD) in spleen deficiency. However, its therapeutic mechanism has not been fully clarified. PurposeThe present study aimed to determine the role of mitochondrial quality control (MQC)-mediated gastrointestinal motility disorder in FD treated with XSLJZD by using spleen-deficient FD rats and gastrointestinal smooth muscle cells (GSMCs). MethodsIn vivo, an FD with spleen deficiency syndrome model was established by gastric perfusion with iodoacetamide solution combined with the modified multiple platform method (MMPM), followed by intragastric gavage with XSLJZD for 4 weeks. Improvement of pathological symptoms was evaluated based on food intake, water intake, grip strength, gastric histopathological changes, gastric emptying rate, small intestinal propulsion rate, and average amplitude and frequency of smooth muscle strips. The mitochondrial ultrastructure was observed by transmission electron microscopy. The colocalization of LC3 and Parkin with mitochondria was detected by immunofluorescence. The expression and localization of Drp1 proteins were detected by immunohistochemistry. In vitro, GSMCs were treated with different concentrations of XSLJZD-CS for 24 h, followed by treatment with 20 μM carbon cyanide 3-chlorophenylhydrazone (CCCP) for 4 h. Cell viability, mitochondrial membrane potential (MMP), mitochondrial reactive oxygen species (mtROS), cellular ATP generation and mitochondrial Keima (mtKeima) expression were examined. Both in vivo and in vitro, gene expression was assessed by Western blotting. All experiments were performed in duplicate. ResultsDisorders of the mitochondrial quality control system existed in gastric smooth muscle in FD spleen deficiency syndrome. XSLJZD administration promoted the contraction of gastric smooth muscle and restored mitochondrial function by downregulating the colocalization of LC3 or Parkin with mitochondria, reducing the ratio of LC3II/LC3I, decreasing the expression of PINK1, Parkin and Drp1 and increasing the expression of p62 to restore mitochondrial morphology and function. In vitro studies showed that the improvement in mitochondrial function by XSLJZD was related to PINK1-parkin-mediated mitochondrial quality control. ConclusionWe demonstrated that XSLJZD can improve gastrointestinal motility disorder in functional dyspepsia with spleen deficiency syndrome, which was related to reconstruction of the mitochondrial quality control system by restraining PINK1/Parkin-mediated mitophagy and division. This study illustrates a novel clinical significance of herbal medicine in the treatment of FD and clarifies the important role of MQC in treating gastrointestinal motility disorder.

Helicobacter spp. in the Stomach of Cats: Successful Colonization and Absence of Relevant Histopathological Alterations Reveals High Adaptation to the Host Gastric Niche.

In addition to Helicobacter pylori, many non-Helicobacter pylori Helicobacters (NHPH) are able to cause gastric disease in humans. Cats are a natural reservoir for many of these species. Accordingly, living in close and intimate contact with animals has been identified as a risk factor, and an important zoonotic significance has therefore been attributed to NHPH. To determine the prevalence and associated gastric histopathological changes of Helicobacter species, the gastric mucosa of 71 cats were evaluated. Only four presented normal histopathological mucosa with the absence of spiral-shaped organisms. Normal gastric mucosa and the presence of spiral-shaped bacteria were observed in 13 cats. The remaining animals presented histopathological changes representative of gastritis. Helicobacter species were detected in 53 cats (74.6%) by at least one detection method. None of the animals were positive for H. pylori or for H. ailurogastricus. Helicobacter heilmannii organisms were identified in 20 animals, predominantly in the body gastric region. Helicobacter salomonis was the second most prevalent species (57.1%), although it was mainly found in association with other NHPH. Helicobacter felis and H. bizzozeronii were less frequently detected. The great majority of the Helicobacter spp. PCR-positive animals presented normal features regarding fibrosis/mucosal atrophy, neutrophils, eosinophils, or other inflammatory cells and lymphofollicular hyperplasia. Given the controversy and the strong evidence of absence of significant histopathological alterations associated with the presence of Helicobacter spp. in cats, it is possible to hypothesize that these bacteria may be able to adapt to the feline gastric microenvironment or even to comprise part of the gastric microbiome of this animal species. Thus, prudency must be taken when prescribing an antibiotic therapy based solely on the presence of these bacteria in the feline stomach.

Gastroprotective Effects of Spirulina platensis, Golden Kiwifruit Flesh, and Golden Kiwifruit Peel Extracts Individually or in Combination against Indomethacin-Induced Gastric Ulcer in Rats.

This study was conducted to investigate the therapeutic effect of hydro-alcoholic extract of Spirulina platensis (SP), golden kiwifruit (Actinidia chinensis) flesh (KF), and golden kiwifruit peel (KP) individually or in combination (SFP) on indomethacin-induced gastric ulcer in rats. Negative control rats (GI) were orally administered distilled water in parallel with other treatments. The positive control rat group (GII) was administered 30 mg kg−1 indomethacin to induce gastric ulcers. The KF and KF extracts were used individually or together with SP in treating indomethacin-induced gastric ulcerated rat groups. Gastric ulcerated rat’s groups GIII, GIV, GV, GVI, and GVII were orally administered at 30 mg kg−1 rat body weight as total phenolic content (TPC) equivalent from SP, KF, KP, SPF extracts, and Lansoprazole (30 mg kg−1, as reference drug) daily up to 14 days, respectively. The relevant biochemical parameters, antioxidant biomarkers, and histopathological examination were examined. Remarkably, treating rats with SP, KF, KP, and SFP extracts markedly reduced gastric juice and stomach volume expansion induced by indomethacin. The SP significantly retrieved the pH of gastric juice to a regular rate compared to GI. The ulcer index (UI) was significantly attenuated by SP, KF, KP, and SFP administration. The protection index percentage (PI %) was 80.79, 54.51, 66.08, 75.74, and 74.86% in GIII, GIV, GV, GVI, and GVII, respectively. The gastric mucin content was significantly better attenuated by 95.7 in GIII compared to its content in GI. Lansoprazole increased mucin content by 80.3%, which was considerably lower than SP and SFP. SP, KF, KP, SFP, and Lansoprazole improved the reform of gastric mucosal-increased secreted mucus by 95.6, 61.3, 64.8, 103.1, and 80.2% in GIII, GIV, GV, GVI, and GVII, respectively. Interestingly, SFP efficiently increased vit. B12 level by 46.0% compared to other treatments. While Lansoprazole administrating did not significantly attenuate vit. B12 level. The SP and SFP improved iron and Hemoglobin (HB) levels depending on treatment. SP, KF, KP, and SFP significantly decreased the malondialdehyde (MDA) and increased reduced glutathione (GSH) as well as superoxide dismutase (SOD) levels in blood and stomach tissues. The most potent effect was observed with SP, and SFP was even better than Lansoprazole. Histopathologically, treating rats with SP extract showed a marked reduction of gastric damage and severity changes induced by indomethacin. KP was much better than KF in lessening gastric histopathological damages caused by indomethacin. SFP significantly alleviates gastric histopathological alterations. The lansoprazole-treated group (GVII) greatly relieved the gastric histopathological changes and recorded mild focal necrosis and desquamation of the mucosa in addition to mild oedema in the serosal layer. In conclusion, the presented results proved the antiulcer potential of SP and A. chinensis extracts against an indomethacin-induced gastric ulcer in rats, which may be due to their antioxidant and anti-inflammation efficiency. Thus, these data suggested that SP, KF, KP, and SFP extracts as natural and safe alternatives have a gastroprotective potential against indomethacin-induced gastric ulceration. The antioxidative and anti-inflammatory properties are probable mechanisms.

Antibiotic Resistance Among Helicobacter pylori Strains Isolated from Patients with Gastric Pathologies Towards Metronidazole, Clarithromycin, and Ciprofloxacin

Background: The extent of antibiotic resistance among Helicobacter pylori strains influences current clinical therapeutic regimens in each region. Objectives: This cross-sectional study aimed to determine the resistance property and minimum inhibitory concentration (MIC50-90) of Helicobacter pylori strains toward metronidazole, clarithromycin, and ciprofloxacin in patients with distinct gastric histopathological changes in Tehran, Iran. Methods: This study was conducted on 170 patients suffering from gastric complications in three hospitals in Tehran from October 2014 until March 2015. Two separate biopsy samples were collected from each patient and used for pathological and microbiological examinations. Antimicrobial susceptibility tests were performed by agar dilution method according to the CLSI guidelines. The MIC values and susceptibility to varying concentrations of metronidazole (4 to 64 µg/mL), ciprofloxacin (0.5 to 16 µg/mL), and clarithromycin (0.25 to 16 µg/mL) were determined based on EUCAST recommendations. Results: Our results indicated the infection with H. pylori in a frequency of 32% (55/170) among the study patients (female, 51% and male, 49%). Endoscopic findings indicated that 42% of the patients suffered from peptic ulcers, 33% from duodenal ulcers, and 25% with a non-ulcer disease. Pathological findings indicated 58% of the patients had chronic gastritis, 33% had active chronic gastritis, and 9% suffered from intestinal metaplasia. In terms of antibiotic susceptibility, nearly 76.3%, 49%, and 45.5% of the strains were resistant to metronidazole, clarithromycin, and ciprofloxacin, respectively. The MIC values at which the growth of 50% and 90% of the strains was inhibited (MIC50-90) were 32 - 64 µg/mL for metronidazole, 0.5 - 16 µg/mL for clarithromycin, and 2 - 16 µg/mL for ciprofloxacin. Conclusions: The overall resistance levels were relatively high among the study patients. Accordingly, the administration of other anti-Helicobacter drugs, as well as more appropriate therapeutic regimens based on laboratory results, is recommended in patients with a history of treatment failure.

GASTRIC AND JEJUNAL HISTOPATHOLOGICAL CHANGES IN PATIENTS UNDERGOING BARIATRIC SURGERY.

ABSTRACTBackground:Morbid obesity is a multifactorial disease that increasingly is being treated by surgery. Aim: To evaluate gastric histopathological changes in obese, and to compare with patients who underwent gastrojejunal bypass and the jejunal mucosa after the surgery. Methods:This is an observational study performed at a tertiary public hospital, evaluating endoscopic biopsies from 36 preoperative patients and 35 postoperative. Results:In the preoperative group, 80.6% had chronic gastritis, which was active in 38.9% (77.1% and 20.1%, respectively, in the postoperative). The postoperative group had a significant reduction in H. pylori infection (p=0.0001). A longer length of the gastric stump and a time since surgery of more than two years were associated with Helicobacter pylori infection. The jejunal mucosa was normal in 91.4% and showed slight nonspecific chronic inflammation in 8.6%. Conclusion:There was a reduction in the incidence of Helicobacter pylori infection in the postoperative group. A longer length of the gastric stump and longer time elapsed since surgery were associated with Helicobacter pylori infection. The jejunal mucosa was considered normal in an absolute majority of patients.

Presence and significance of Helicobacter spp. in the gastric mucosa of Portuguese dogs.

BackgroundNon-Helicobacter pylori Helicobacters (NHPH) are also able to cause disease in humans. Dogs are a natural reservoir for many of these species. Close and intense human contact with animals has been identified as a risk factor and therefore, an important zoonotic significance has been attributed to NHPH.MethodsTo determine the prevalence of Helicobacter species and the gastric histopathological changes associated, gastric mucosa samples of 69 dogs were evaluated.ResultsOnly one dog presented a normal histopathological mucosa with absence of spiral-shaped organisms. A normal gastric mucosa and the presence of spiral-shaped bacteria was observed in two dogs. All remaining animals presented histopathological changes representative of gastritis. Helicobacter species were detected in 60 dogs (87.0%) by at least one detection method. Histological, histochemical and immunohistochemical evaluations revealed that Helicobacter spp. were present in 45 (65.2%), 52 (75.4%) and 57 (82.6%) dogs, respectively. Spiral-shaped bacteria were detected by qPCR analysis in 33 (47.8%) dogs. H. heilmannii-like organisms were identified in 22 animals (66.7%) and predominantly in the antral gastric region. H. salomonis was the second most prevalent species (51.5%) although it was mainly found in association with other Helicobacter spp. and in the body gastric region. H. bizzozeronii and H. felis were less frequently detected.ConclusionsIt was concluded that, despite the high incidence and worldwide distribution of gastric NHPH in dogs, the presence of specific Helicobacter species may vary between geographic regions. NHPH infections were significantly accompanied by mild to moderate intraepithelial lymphocyte infiltration and mild to moderate gastric epithelial injury, but a clear relationship between gastritis and Helicobacter infection could not be established.

DupA as a risk determinant in Helicobacter pylori infection

The Helicobacter pylori duodenal ulcer promoting (dupA) gene has been previously described as a risk marker for duodenal ulcer (DU) development and a protective factor against gastric cancer (GC). Recent studies which have assessed the application of dupA in the prediction of clinical outcomes have been controversial. In the current study, the association of dupA with the clinical outcomes and histopathological changes following H. pylori infection was evaluated in Iranian patients. A total of 157 H. pylori-infected patients with DU (n=30), gastric ulcer (n=23), gastritis (n=68) or GC (n=36) were assessed. The presence of jhp0917 and jhp0918 genes was determined by gene specific PCR. Gastric histopathological changes were recorded according to the updated Sydney system. Seventy-eight (49.7 %) and 71 (45.2 %) of the 157 tested strains, respectively, were positive and negative for both genes. The remaining 8 (5.09 %) of the 157 strains were jhp0917-positive/jhp0918-negative. Univariate analysis showed inverse associations between dupA and histological features including dysplasia as the penultimate stage of GC and lymphoid follicles as a consequence of relatively long-standing H. pylori-associated gastritis. The degrees of nucleotide sequence identity of Iranian strains to Colombian, Brazilian and Indian strains ranged from 86.1 to 100 % for the aligned regions of jhp0917, from 88 to 98.8 % for jhp0918 and from 93.4 to 99.5 % for the partial sequences of the dupA gene. Despite the fact that possession of the dupA gene showed no association with any disease category in our population as reported in several other countries, association of dupA-negative strains of H. pylori with pre-malignant lesions calls for additional studies to evaluate the role of this gene as a protective marker against GC.

Reply —Helicobacter pylori and gastro‐oesophageal reflux disease

S IRS, Mr Attwood correctly states that the main argument in favour of H. pylori eradication in GERD is the fact that proton pump inhibitor therapy in H. pylori-positive GERD appears to accelerate the development of atrophic corpus gastritis.1 Given the established precancerous nature of atrophic gastritis,2 the recommendation for eradication seems reasonable. Accelerated atrophic corpus gastritis and epithelial cell proliferation is not seen in H. pylori-negative patients treated with proton pump inhibitors.3 More importantly, Moayyedi et al. have recently shown that the shift from antral to corpus predominant gastritis seen with long-term proton pump inhibitor therapy can be prevented by prior H. pylori eradication.4 GERD is a chronic relapsing disorder where patients are often dependent on long-term proton pump inhibitor therapy to relieve symptoms and prevent complications. Although we do not yet know what adverse changes, if any, might occur in the H. pylori-positive stomach after decades of proton pump inhibitor therapy, the possibility that neoplastic change might be prevented by H. pylori eradication is a compelling one. Mr Attwood argues for the preservation of H. pylori on the basis that eradication may accelerate the development of reflux disease, its complications and cancer of the lower oesophagus. The idea that H. pylori eradication is associated with accelerated development of GERD has its origin in studies of peptic ulcer patients, where a proportion of the patients apparently developed oesophagitis in the years following cure of H. pylori.5 It should be remembered, however, that GERD and peptic ulcer disease can coexist6 and some of the cases of ‘new’ post-eradication GERD may, in fact, be unmasking of pre-existent disease. In essence, the ulcer is cured but the reflux persists. In the first reported controlled trial of effective H. pylori therapy in GERD, H. pylori eradication did not have an adverse effect on GERD symptoms.7 There is some evidence that H. pylori-negative GERD tends to be more severe than H. pylori-positive GERD.8910 Preservation of acid secretion in the healthy H. pylori-negative stomach is the putative link between the absence of H. pylori and severity of GERD. Mr Attwood emphasizes the work of Schnell et al.11 who found an association between Cag A seronegativity and severe reflux disease, but this study only included 12 patients with Barrett’s oesophagus and six with oesophageal dysplasia/adenocarcinoma. The decreasing prevalence of H. pylori infection in developed countries is cited as a possible reason for the falling prevalence of gastric cancer and parallel rise in oesophageal cancer.12 This suggestion is unproven and it is certainly premature to suggest that H. pylori eradication might accelerate the development of cancer of the oesophagus. Present arguments for or against H. pylori eradication in GERD should not be a reason for discord, but simply underscore our need for accurate long-term data on crucial issues, such as the natural history of gastric histopathological changes in H. pylori-positive GERD patients treated with proton pump inhibitors, and the behaviour of Barrett’s oesophagus in H. pylori-positive and -negative subjects. With that type of information, it might then be possible to give definitive guidelines on the management of H. pylori infection in GERD.

Review article: Helicobacter pylori and gastro-oesophageal reflux disease-clinical implications and management.

A significant proportion of patients with gastro-oesophageal reflux disease (GERD) have Helicobacter pylori infection, but it is unclear whether or not H. pylori should be treated in this clinical setting. The aim of this review was to critically assess the relationship between H. pylori and GERD and its potential implications for the management of GERD. Data for this review were gathered from the following sources up to April 1998-the biomedical database MEDLINE, a detailed review of medical journals, and a review of abstracts submitted to relevant international meetings. On average, 40% of GERD patients carry H. pylori infection, with a reported infection prevalence ranging from 16% to 88%. To date, there has been no reported controlled trial of effective H. pylori therapy in GERD. GERD has been reported to develop de novo following the cure of H. pylori in peptic ulcer disease. In the presence of H. pylori, proton pump inhibitor therapy appears to accelerate the development of atrophic corpus gastritis, a potentially precancerous condition. Conversely, proton pump inhibitor therapy seems to become less effective after cure of H. pylori. The mechanisms underlying these important contrasting phenomena are poorly understood. The relationship between H. pylori and GERD is complex, and it is difficult to give definitive guidelines on the management of H. pylori infection in GERD. Controlled trials of H. pylori therapy in GERD are urgently needed, as well as further long-term data on both the natural history of gastric histopathological changes in the H. pylori-positive GERD patient treated with proton pump inhibitors, and the impact of H. pylori status on the clinical efficacy of antisecretory therapy. Pending these data, it is perhaps advisable to advocate cure of H. pylori in young patients with proton pump inhibitor-dependent GERD who, in the absence of anti-reflux surgery, are faced with the likelihood of long-term medical therapy.

Therapeutic efficacy of hyperimmune bovine colostrum treatment against clinical and subclinical Cryptosporidium serpentis infections in captive snakes

Therapy based on the protective passive immunity of Hyperimmune Bovine Colostrum (HBC) (raised against Cryptosporidium parvum in dairy cows immunized during gestation) was tested for heterologous efficacy in subclinical and clinical infections of 12 captive snakes with C. serpentis. Six gastric HBC treatments of 1% snake weight at 1-week intervals each, have histologically cleared C. serpentis in three subclinically infected snakes, and regressed gastric histopathological changes in one of these snakes. In all snakes, each subsequent HBC treatment significantly decreased the number of oocysts recovered in gastric lavage eluants ( P<0.03). The treatments induced oocyst-negative gastric eluants and stools in all snakes, and improved clinical signs of infection. Clinically infected snakes displayed severe histopathological changes in the gastric region; however, the numbers of developmental stages of C. serpentis were moderate. Considering the severity of pathology, much lower than expected pathogen numbers were observed, and it is believed that clinically infected snakes did not have enough time to repair tissue damage that had occurred over the years of infection. As the HBC treatment was safe and highly efficacious, it is recommended to gastrically administer the HBC therapeutically to snakes that are clinically or subclinically infected with C. serpentis. Hyperimmune bovine colostrum can also be used in snake supportive therapy or prophylaxis.