Helicobacter pylori infection: a dynamic process from diagnosis to treatment.

Helicobacter pylori, a gram-negative microaerophilic pathogen, causes several upper gastrointestinal diseases, such as chronic gastritis, peptic ulcer disease, and gastric cancer. For the diseases listed above, H. pylori has different pathogenic mechanisms, including colonization and virulence factor expression. It is essential to make accurate diagnoses and provide patients with effective treatment to achieve positive clinical outcomes. Detection of H. pylori can be accomplished invasively and noninvasively, with both having advantages and limitations. To enhance therapeutic outcomes, novel therapeutic regimens, as well as adjunctive therapies with probiotics and traditional Chinese medicine, have been attempted along with traditional empiric treatments, such as triple and bismuth quadruple therapies. An H. pylori infection, however, is difficult to eradicate during treatment owing to bacterial resistance, and there is no commonly available preventive vaccine. The purpose of this review is to provide an overview of our understanding of H. pylori infections and to highlight current treatment and diagnostic options.

Research on antibiotic resistance in Helicobacter pylori: a bibliometric analysis of the past decade.

Resistance of Helicobacter pylori (H. pylori) to antibiotics has reached alarming levels worldwide, and the efficacy of the H. pylori eradication treatment has decreased dramatically because of antibiotic resistance. To gain a more comprehensive understanding of the development status, research hotspots, and future trends related to H. pylori antibiotic resistance, we conducted a thorough retrospective analysis via the bibliometrics method. We searched the Science Citation Index Expanded of the Web of Science Core Collection for all pertinent articles on H. pylori antibiotic resistance from 2013 to 2022. R-bibliometrix, CiteSpace, and VOSviewer tools were utilized to depict statistical evaluations in order to provide an unbiased presentation and forecasts in the field. We incorporated a total of 3,509 articles related to H. pylori antibiotic resistance. Publications were inconsistent prior to 2017, but steadily increased after 2017. China generated the most papers and the United States of America received the most citations and the highest H-index. Baylor College of Medicine was the most influential institution in this field, with the highest number of publications and citations, as well as the highest H-index. Helicobacter was the most productive journal, followed by the World Journal of Gastroenterology and Frontiers in Microbiology. The World Journal of Gastroenterology had the highest citation. Graham, David Y was the most productive and cited author. Clarithromycin resistance, prevalence, gastric cancer, quadruple therapy, sequential therapy, 23S rRNA, whole genome sequencing, bismuth, and probiotics appeared with a high frequency in the keywords. The top keywords with the highest citation bursts were vonoprazan, RdxA, biofilm formation, and fatty acid chain. Our research illustrated a multi-dimensional facet and a holistic knowledge structure for H. pylori antibiotic resistance research over the past decade, which can serve as a guide for the H. pylori research community to conduct in-depth investigations in the future.

Kappaphycus Alvarezii Compound Powder Prevents Chemotherapy-Induced Intestinal Mucositis in BALB/c Mice.

This study aimed to formulate Kappaphycus alvarezii compound powder containing Kappaphycus alvarezii powder (KP), cooked sorghum powder (SP), and longan powder (LP); which was evaluated for its therapeutic effects against chemotherapy-induced intestinal mucosal injury (CIMI). Based on rheological properties, sensory evaluation, and antioxidant activity and using single factor and response surface methodology, the optimal formula to develop the compound powder was determined to be 35% KP, 30% SP, 5% LP, and 30% xylitol. Thereafter, the efficacy of the compound powder was tested by feeding BALB/c mice with diets supplemented with the Kappaphycus alvarezii compound powder (3% and 5%) for 14 consecutive days. The chemotherapeutic drug 5-fluorouracil was intraperitoneally injected (50 mg/kg) in the mice to induce CIMI for the last three consecutive days. Compared to the CIMI mice, those fed 5% Kappaphycus alvarezii compound powder (HC) showed significantly improved the intestinal injury, increased mucin-2 secretion, and reduced TNF-α, IL-1ß, IL-6, LT, and COX-2 levels. Furthermore, HC intake significantly reduced the Firmicutes-to-Bacteroidetes ratio, promoted the growth of beneficial bacteria, such as Alloprevotella, and inhibited the growth of harmful bacteria, such as Clostridium. In conclusion, HC has a protective effect against CIMI and provides a novel dietary strategy for patients undergoing chemotherapy.

Sun-Dried and Air-Dried Kappaphycus alvarezii Attenuates 5-Fluorouracil-Induced Intestinal Mucositis in Mice.

5-fluorouracil (5-FU)-induced intestinal mucositis (IM) often makes chemotherapy patients suffer from physical and psychological suffering. Kappaphycus alvarezii (KA) is known for its potent multiple biological activities from decades. In the current study, we explored the effect of sun-dried and air-dried Kappaphycus alvarezii as a whole food supplement on 5-FU-induced IM. Diets supplemented with sun-dried Kappaphycus alvarezii (SKA, 3%), air-dried Kappaphycus alvarezii (AKA, 3%), and 5-aminosalicylic acid (0.005%) for consecutive14 days. While intraperitoneal injection of 5-FU (50 mg/kg) induced IM for last three consecutive days, and IM was assessed by the disease activity index (DAI) and inflammatory cytokine levels. Pretreatment of KA could alleviate phenotypic index, inhibit the increase of DAI, and reverse villus/crypt ratio. On the 14th day, AKA significantly increased the weight growth rate of the mice. The intervention of SKA significantly reduced the level of TNF-α and IL-1ß (P < 0.01, P < 0.01), while the intervention of AKA significantly inhibited the level of TNF-α, IL-1ß, and LT (P < 0.01, P < 0.01, P < 0.001). Therefore, these results showed that KA as a whole food supplement might be prevent the 5-FU-induced IM. For the first time suggest that the use of AKA might be more effective than SKA despite exact mechanism still needs further study.

Selenium Forms and Dosages Determined Their Biological Actions in Mouse Models of Parkinson's Disease.

Selenium (Se), an essential antioxidant trace element, is reported to play a role in Parkinson's disease (PD). However, there is a lack of systematic studies on different Se forms against PD. Our study is designed to compare the neuroprotective effects of inorganic and organic Se in two classical PD mice models and investigate the underlying mechanisms for their potentially differential actions against PD. In this study, different dosages of inorganic sodium selenite (Se-Na) or organic seleno-L-methionine (Se-Met) were fed to either acute or chronic PD mice models, and their neuroprotective effects and mechanisms were explored and compared. Se-Na provided better neuroprotective effects in PD mice than Se-Met administered at the same but at a relatively low Se dosage. Se-Na treatment could influence GPX activities but not their mRNA expressions in the midbrains of PD mice. The enhanced GPX activities caused by Se-Na, but not Se-Met, in PD mice could be the major reason for the positive actions of inorganic Se to prevent dopaminergic neuronal loss in this study. In vivo bio-distribution experiments found MPTP injection greatly changed Se bio-distribution in mice, which led to reversed alterations in the bioavailability of Se-Met and Se-Na. Se-Na had higher bioavailability than Se-Met in PD mice, which could explain its better neuroprotective effects compared to Se-Met. Our results proved that Se forms and dosages determined their biological actions in mouse models of PD. Our study will provide valuable scientific evidence to researchers and/or medical professionals in using Se for PD prevention or therapy.

Sargassum fusiforme together with turmeric extract and pomegranate peel extract alleviates obesity in high fat-fed C57BL/6J mice.

Sargassum fusiforme, a nutritious edible brown alga, has been widely suggested to play an important role in the development of functional food because of its multiple biological activities. The aim of this study was to explore the anti-obesity effect of the combination of Sargassum fusiforme with extracts of fruit and vegetable by comparing the effects of Sargassum fusiforme (S), Sargassum fusiforme together with pomegranate peel extract (SP), Sargassum fusiforme together with turmeric extract (ST) and Sargassum fusiforme together with turmeric extract and pomegranate peel extract (C) on diet-induced obese C57BL/6J mice. Long-term consumption of a high-fat diet can lead to high levels of blood lipid, increase adipocyte size, and cause lipid metabolism dysfunction and gut microbiota dysbiosis. According to the results of the experiments, SP and ST were more effective in reducing lipid levels and fat accumulation than S; and, C exhibited the strongest efficacy compared with the other three supplements. ST and C also regulated adipocytokines and had significant effects on the gene expression of lipid metabolism. We also found that C alleviated the imbalance of intestinal flora caused by a high-fat diet to a certain extent. In conclusion, SP, ST and C have anti-obesity potentials, which can be used as alternative ingredients in the formula of functional food for obese people.

Bacterial Characteristics in Intestinal Contents of Antibiotic-Associated Diarrhea Mice Treated with Qiweibaizhu Powder.

BACKGROUND Qiweibaizhu powder (QWBZP) is a classical prescription of traditional Chinese medicine (TCM) to treat diarrhea in pediatric patients. Its use in health care practices and interventions has shown its effect on antibiotic-associated diarrhea (AAD). It is known that the occurrence of AAD is related to an imbalance of intestinal micro-ecology. Previous studies found that QWBZP could regulate the amount of some cultured microbes and the activities of lactase and sucrase in AAD mice. In order to investigate the treatment mechanism of QWBZP on AAD, we studied the effect of QWBZP on intestinal bacteria in a community of AAD mice. MATERIAL AND METHODS AAD mice were established by administrating the mixture of gentamycin sulfate and cefradine at the dose of 23.33 mL·kg⁻¹·d⁻¹ for 5 days. Then the AAD mice were gavaged with QWBZP decoction for 4 days and gradually recovered to a normal status. On the tenth day, the intestinal contents of mice were collected, and then the DNA was extracted for 16S rRNA sequencing followed by analysis. RESULTS The analysis of bacterial 16S rRNA sequencing showed the Simpson index was decreased and the Shannon index was increased in AAD mice treated with QWBZP compared to the model group; there was no significant difference between the control group and the treatment group (P>0.05). Principle co-ordinates analysis (PCoA) indicated that there was a shorter distance between the control group and the treatment group than that between the control group and model group. At the phylum level, use of antibiotics decreased the relative abundance of Actinobacteria, Bacteroidetes, and Proteobacteria, but increased the abundance of Firmicutes and Verrucomicrobia, and the reverse changes occurred after treated with QWBZP. At the genus level, the abundance of Bacteroides and Ochrobacitrum increased in the model group, while an opposite result was observed in the treatment group. Moreover, the relative abundance of Osillospira decreased in the model group and increased in the treatment group. Genus Dorea, Coprococcus and Blautia in the model group were higher than those in the control group and further increased in the treatment group. CONCLUSIONS These results indicated that QWBZP improved the diarrhea syndrome with restoring the diversity and adjusting the structures of bacteria in mice intestine, which might reveal the therapeutic mechanism of QWBZP on treating AAD.

Atractylenolide I stimulates intestinal epithelial repair through polyamine-mediated Ca2+ signaling pathway.

BACKGROUND: An impairment of the integrity of the mucosal epithelial barrier can be observed in the course of various gastrointestinal diseases. The migration and proliferation of the intestinal epithelial (IEC-6) cells are essential repair modalities to the healing of mucosal ulcers and wounds. Atractylenolide I (AT-I), one of the major bioactive components in the rhizome of Atractylodes macrocephala Koidz. (AMR), possesses multiple pharmacological activities. This study was designed to investigate the therapeutic effects and the underlying molecular mechanisms of AT-I on gastrointestinal mucosal injury. METHODS: Scratch method with a gel-loading microtip was used to detect IEC-6 cell migration. The real-time cell analyzer (RTCA) system was adopted to evaluate IEC-6 cell proliferation. Intracellular polyamines content was determined using high performance liquid chromatography (HPLC). Flow cytometry was used to measure cytosolic free Ca2+ concentration ([Ca2+]c). mRNA and protein expression of TRPC1 and PLC-γ1 were determined by real-time PCR and Western blotting assay respectively. RESULTS: Treatment of IEC-6 cells with AT-I promoted cell migration and proliferation, increased polyamines content, raised cytosolic free Ca2+ concentration ([Ca2+]c), and enhanced TRPC1 and PLC-γ1 mRNA and protein expression. Depletion of cellular polyamines by DL-a-difluoromethylornithine (DFMO, an inhibitor of polyamine synthesis) suppressed cell migration and proliferation, decreased polyamines content, and reduced [Ca2+]c, which was paralleled by a decrease in TRPC1 and PLC-γ1 mRNA and protein expression in IEC-6 cells. AT-I reversed the effects of DFMO on polyamines content, [Ca2+]c, TRPC1 and PLC-γ1 mRNA and protein expression, and restored IEC-6 cell migration and proliferation to near normal levels. CONCLUSION: Our data demonstrate that AT-I stimulates intestinal epithelial cell migration and proliferation via the polyamine-mediated Ca2+ signaling pathway. Therefore, AT-I may have the potential to be further developed as a promising therapeutic agent to treat diseases associated with gastrointestinal mucosal injury, such as inflammatory bowel disease and peptic ulcer.

Buyang Huanwu Decoction Ameliorates Poststroke Depression via Promoting Neurotrophic Pathway Mediated Neuroprotection and Neurogenesis.

Objective. The aim of the present research is to investigate the therapeutic effect of Buyang Huanwu Decoction (BHD) in poststroke depression (PSD) animal model and illustrate its underlying mechanism via promoting neurotrophic pathway mediated neuroprotection and neurogenesis. Methods. To induce PSD rat model, isolation housed rats that received middle cerebral artery occlusion (MCAO) surgery successively suffered from chronic mild stress (CMS) treatment for consecutive twenty-one days. Meanwhile, rats were correspondingly given vehicle, BHD, and fluoxetine. Then, neurologic function was scored and depressive-like behaviors were assessed by sucrose preference test, locomotor activity, novelty-suppressed feeding test, and forced swim test. Thereafter, the neuroprotection and neurogenesis related molecular markers and signaling were detected. Results. We firstly observed a significant neurological function recovery and antidepressants effect of BHD after MCAO together with CMS treatment. Our study also found that treatment with BHD and fluoxetine can significantly rescue neurons from apoptosis and promote neurogenesis in the CA3 and DG regions in the hippocampus. Notably, BHD and fluoxetine treatment can activate BDNF/ERK/CREB signaling. Conclusion. The results suggest that BHD is a promising candidate for treating PSD. Its curative effects can be attributed to neurotrophic pathway mediated neuroprotection and neurogenesis.