An increasing number of studies have shown that obesity is the key etiological agent of cardiovascular diseases, nonalcoholic fatty liver disease, type 2 diabetes and several kinds of cancer and that gut microbiota change was one of the reasons suffering from obesity. At present, the gut microbiota has gained increased attention as a potential energy metabolism organ. Our recent study reported that cordycepin, a major bioactive component separated from Cordyceps militaris, prevented body weight gain in mice fed a high-fat diet directly acting to adipocytes, however, the effect of cordycepin regulating gut microbiota keeps unknown. In this research, we synthesized cordycepin (3-deoxyadenosine) by chemical methods and verified that cordycepin reduces body weight gain and fat accumulation around the epididymis and the kidneys of rats fed a high-fat diet. Furthermore, we used high-throughput sequencing on a MiSeq Illumina platform to test the species of intestinal bacteria in high-fat-diet-induced obese rats. We found that cordycepin modifies the relative abundance of intestinal bacteria in high-fat-diet-induced obese rats. However, cordycepin did not alter the variety of bacteria in the intestine. Cordycepin treatment dramatically reversed the relative abundance of two dominant bacterial phyla (Bacteroidetes and Firmicutes) in the high-fat-diet-induced obese rats, resulting in abundance similar to that of the chow diet group. Our study suggests that cordycepin can reduce body weight and microbiome done by cordycepin seems be a result among its mechanisms of obesity reduction.
Abstract Background: Recent studies have suggested an association between gut microbiota (GM) and venous thromboembolism (VTE). However, observational studies cannot indicate causality and population-level studies with a higher evidence level for causality are lacking. Therefore, our study aimed to explore the causal association of GM with VTE. Methods: This study utilized the summary-level data of respective genome-wide association study for 196 gut microbial taxa and VTE. Two-sample Mendelian randomization (MR) design was deployed and comprehensively sensitive analyses were followed to validate the robustness of results. We used the inverse-variance weighted (IVW) method, the weighted median method, weighted mode method, simple mode method, MR-Egger regression, MR-Egger intercept test, Cochrane’s Q-test, outlier test, and leave-one-out analysis as the primary analysis. Results: We identified suggestive associations between 17 bacterial traits and the risk of VTE. Porphyromonadaceae (IVW odds ratio (OR): 1.3729, p=0.0035) and Cyanobacteria (IVW OR: 1.2151, p=0.0048) were associated with increased risk of VTE. Three gut microbiota taxa (Eubacteriumrectalegroup (IVW OR: 1.0038, p=0.0278), Coprococcus2 (IVW OR: 1.0041, p = 0.0063), and LachnospiraceaeUCG001 (IVW OR: 1.0041, p=0.0009) were predicted to play a causal role in enhancing the risk of encompassing deep vein thrombosis. And three gut microbiota taxa (Christensenellaceae (IVW OR: 1.0023, p=0.0497), Streptococcaceae (IVW OR: 1.0031, p=0.0279), Victivallaceae (IVW OR: 1.0014, p=0.0493) were positively associated with pulmonary embolism. Conclusions: This study suggested the role of the specific GM on the risk for VTE, which may provide new ideas and a theoretical basis for the prevention and treatment of VTE in the future.
Objective: To explore the trends and distribution of chronic obstructive pulmonary disease (COPD) mortality of the residents with different characteristics from 2000 to 2016 in Tianjin. Methods: COPD mortality data in 2000-2016 were from Tianjin population based mortality surveillance system. The mortality rate of COPD, difference in the rate by gender, age, and geographic distribution, and the trend over years were analyzed. Age-sex-standardized mortality rates of COPD were calculated using the year 2000 world standard population. Joinpoint regression and Cochran-Armitage trend analysis were used to examine the trend of mortality. Results: The crude COPD mortality rate in Tianjin decreased from 57.57/100 000 in 2000 to 28.23/100 000 in 2016 (annual percent change (APC)=-5.01%, Z=-64.76, P<0.001), and the standardized mortality rate decreased from 56.53/100 000 in 2000 to13.88/100 000 in 2016 (APC=-9.17%, Z=-100.83, P<0.001). The crude COPD mortality rate of males decreased from 54.57/100 000 to 27.77/100 000 (APC=-4.89%, Z=-43.63, P<0.001) and the standardized mortality rate decreased from 57.52/100 000 to 14.63/100 000 (APC=-9.07%, Z=-71.48, P<0.001). The crude COPD mortality rate of females decreased from 60.63/100 000 to 28.68/100 000 (APC=-5.12%, Z=-47.92, P<0.001) and the standardized mortality rate decreased from 55.53/100 000 to 13 13/100 000 (APC=-9.27%, Z=-71.13, P<0.001). The crude mortality rate of COPD in urban areas decreased from 45.07/100 000 to 19.54/100 000 (APC=-5.35%, Z=-42.38, P<0.001) and the standardized mortality rate decreased from 39.24/100 000 to 7.45/100 000 (Z=-63.97, P<0.001, APC=-10.22%). The crude mortality rate of COPD in rural areas decreased from 70.20/100 000 to 37.24/100 000 (APC=-4.77%, Z=-48.77, P<0.001) and the standardized mortality rate decreased from 78.88/100 000 to 25.70/100 000 (APC=-7.59%, Z=-72.43, P<0.001). The COPD mortality rate in rural areas was higher than that in urban areas (P<0.001). The COPD mortality rate in 35 years old and over decreased from 2000 to 2016 (P<0.001). Conclusion: The COPD mortality in Tianjin decreased from 2000 to 2016. More efforts are need to reduce COPD mortality in Tianjin, in particular people in rural areas.目的： 了解2000-2016年天津市居民慢性阻塞性肺疾病（COPD）死亡率及其变动趋势。 方法： 采用天津市全死因监测管理系统收集2000-2016年天津市居民COPD死亡情况，统计天津市居民COPD死亡率，比较不同年龄、性别以及地区之间死亡率的差异，并分析其变化趋势。采用2000年世界标准人口计算年龄别、性别标化死亡率。采用Joinpoint回归和Cochran-Armitage趋势检验进行趋势分析。 结果： 2000-2016年COPD死亡率为57.57/10万~28.23/10万，呈下降趋势[年度变化百分比（APC）=-5.01%；Z=-64.76，P<0.001]；标化死亡率为56.53/10万~13.88/10万，呈下降趋势（APC=-9.17%，Z=-100.83，P<0.001）。2000-2016年男性COPD死亡率为54.57/10万~27.77/10万，呈下降趋势（APC=-4.89%，Z=-43.63，P<0.001）；标化死亡率为57.52/10万~14.63/10万，呈下降趋势（APC=-9.07%，Z=-71.48，P<0.001）。2000-2016年女性COPD死亡率为60.63/10万~28.68/10万，呈下降趋势（APC=-5.12%，Z=-47.92，P<0.001）；标化死亡率为55.53/10万~13.13/10万，呈下降趋势（APC=-9.27%，Z=-71.13，P<0.001）。2000-2016年天津市城市COPD死亡率为45.07/10万~19.54/10万，呈下降趋势（APC=-5.35%，Z=-42.38，P<0.001）；标化死亡率为39.24/10万~7.45/10万，呈下降趋势（APC=-10.22%，Z=-63.97，P<0.001）。2000-2016年天津市农村COPD死亡率为70.20/10万~37.24/10万，呈下降趋势（APC=-4.77%，Z=-48.77，P<0.001）；标化死亡率为78.88/10万~25.70/10万，呈下降趋势（APC=-7.59%，Z=-72.43，P<0.001）。各年份农村COPD死亡率均明显高于城市地区（P<0.001）。2000-2016年，除了<35岁组，其他各年龄组COPD死亡率均呈下降趋势（P<0.001）。 结论： 2000-2016年期间天津市居民COPD死亡率呈明显的下降趋势特点。农村人群为COPD死亡高发人群。.
The global incidence of inflammatory bowel disease (IBD) has increased rapidly in recent years, but its exact etiology remains unclear. In the past decade, IBD has been reported to be associated with dysbiosis of gut microbiota. Although not yet proven to be a cause or consequence of IBD, the common hypothesis is that at least some alterations in the microbiome are protective or pathogenic. Furthermore, intestinal epithelial cells (IECs) serve as a protective physical barrier for gut microbiota, essential for maintaining intestinal homeostasis and actively contributes to the mucosal immune system. Thus, dysregulation within the intestinal epithelium increases intestinal permeability, promotes the entry of bacteria, toxins, and macromolecules, and disrupts intestinal immune homeostasis, all of which are associated with the clinical course of IBD. This article presents a selective overview of recent studies on bacterial mechanisms that may be protective or promotive of IBD in biological models. Moreover, we summarize and discuss the recent discovery of key modulators and signaling pathways in the IECs that could serve as potential IBD therapeutic targets. Understanding the role of the IECs in the pathogenesis of IBD may help improve the understanding of the inflammatory process and the identification of potential therapeutic targets to help ameliorate this increasingly common disease.
Abstract: Allergy rhinitis (AR) is becoming more common and has serious medical and societal consequences. Sneezing, paroxysmal nasal blockage, nasal itching, mucosal edema, coughing, and rhinorrhea are symptoms of this type I allergic immunological illness. Immunoglobulin E-mediated inflammation is the cause of it. Because AR is prone to recurrent attacks, extended medication therapy may impair its effectiveness. In addition to negatively affecting the patients' physical health, this can also negatively impact their mental health. During AR development, there are inflammatory and oxidative stress responses that are linked to problems in a number of signal transduction pathways. By using the terms "allergic rhinitis", "traditional Chinese medicine", "inflammation", and "oxidative stress", we screened for pertinent research published over the previous five years in databases like PubMed. We saw that NF-KB, TLR, IL-33/ST2, PI3K/AKT, MAPK, and Nrf2 are some of the most important inflammatory and oxidative stress pathways in AR. Studies have revealed that antioxidant and anti-inflammatory therapy reduced the risk of AR and was therapeutic; however, the impact of the therapy varies widely. The Chinese medical system places a high value on traditional Chinese medicine (TCM), which has been there for virtually all of China's 5000-year history. By influencing signaling pathways related to inflammation and oxidative stress, Chinese herbal medicine and its constituent compounds have been shown to prevent allergic rhinitis. This review will focus on this evidence and provide references for clinical treatment and scientific research applications. Keywords: allergic rhinitis, traditional Chinese medicine, inflammatory, oxidative stress, signaling pathways
Correction for ‘Heat-treated foxtail millet protein delayed the development of pre-diabetes to diabetes in mice by altering gut microbiota and metabolomic profiles’ by Han Wang et al. , Food Funct. , 2023, 14 , 4866–4880, https://doi.org/10.1039/D3FO00294B.
Background Peptic ulcer disease (PUD) is a multi-cause illness with an unknown role for gastric flora and metabolism in its pathogenesis. In order to further understand the pathogenesis of gastric flora and metabolism in PUD, this study used histological techniques to analyze the microbiome and metabolome of gastric biopsy tissue. In this paper, our work described the complex interactions of phenotype-microbial-metabolite-metabolic pathways in PUD patients at different pathological stages. Methods Gastric biopsy tissue samples from 32 patients with chronic non-atrophic gastritis, 24 patients with mucosal erosions, and 8 patients with ulcers were collected for the microbiome. UPLC-MS metabolomics was also used to detect gastric tissue samples. These datasets were analyzed individually and integrated using various bioinformatics methods. Results Our work found reduced diversity of gastric flora in patients with PUD. PUD patients at different pathological stages presented their own unique flora, and there were significant differences in flora phenotypes. Coprococcus_2 , Phenylobacterium , Candidatus_Hepatoplasma , and other bacteria were found in the flora of people with chronic non-atrophic gastritis (HC). The representative flora of mucosal erosion (ME) had uncultured_bacterium_c_Subgroup_6 , Sphingomonadaceae, Xanthobacteraceae , and uncultured_bacterium_f_Xanthobacteraceae. In comparison, the characteristic flora of the PUD group was the most numerous and complex, including Ruminococcus_2 , Agathobacter , Alistipes , Helicobacter , Bacteroides and Faecalibacterium . Metabolomics identified and annotated 66 differential metabolites and 12 significantly different metabolic pathways. The comprehensive analysis correlated microorganisms with metabolites at different pathological stages and initially explored the complex interactions of phenotype-microbial-metabolite-metabolic pathways in PUD patients at different pathological stages. Conclusion Our research results provided substantial evidence to support some data on the analysis of the microbial community and its metabolism in the stomach, and they demonstrated many specific interactions between the gastric microbiome and the metabolome. Our study can help reveal the pathogenesis of PUD and indicate plausible disease-specific mechanisms for future studies from a new perspective.
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