Improved Gut Microbiota Research Articles

Lycium barbarum polysaccharides improve gut microbiota composition and alleviate pulmonary inflammatory damage in allergic asthma mice by inhibiting the IL-15RA/FUT2 pathway

This study examined the effects of Lycium barbarum polysaccharide (LBP) on the intestinal flora of mice with allergic asthma and its molecular mechanism on lung injury and inflammation. Bioinformatics analysis examined LBP targets for allergic asthma and the gut microbial ecosystem. IL-13 was used to create an in vitro cell model of allergic asthma in lung epithelial cell LA-4 and ovalbumin (OVA)-sensitized mice. LBP effects on inflammatory cell infiltration, mucus formation, proinflammatory factor release, and pulmonary epithelial fucosylation were examined after loss- and gain-function experiments. LBP therapy altered fecal microbial populations, decreased IL-15RA and FUT2 expression, and reduced pulmonary epithelial fucosylation in asthmatic mice. IL-15RA or FUT2 knockdown mimicked LBPs in asthmatic mice. More notably, LBPs or IL-15RA/FUT2 knockdown reduced pulmonary epithelial cell fucosylation. LBP reduces lung injury and inflammation in mice with allergic asthma by downregulating the IL-15RA/FUT2 pathway, inhibiting pulmonary epithelial fucosylation, and increasing anti-inflammatory intestinal flora.

Intestinal dysbiosis in heart failure - modulation of dysbiosis as a potential therapeutic target

The last decade has provided extensive information on the human gut microbiota. The microorganisms populating the gastrointestinal tract play important roles in maintaining the body's homeostasis. It turns out that the intestinal microbiota can affect many diseases from various branches of medicine. The importance of the function of the microflora can also affect cardiovascular diseases (CVD), including heart failure (HF). The microflora influences among other things, nutrient digestion, vitamin production or the production of bioactive metabolites including trimethylamine/trimethylamine N-oxide, short-chain fatty acids and bile acids. Therefore, changes in the composition of the intestinal microflora, defined as dysbiosis, have become one of the key pathogenic factors in many diseases. There is emerging evidence of a strong correlation between gut microflora and the occurrence of cardiovascular disease. In patients with cardiovascular disease and corresponding risk factors, the composition and proportions of the intestinal microflora differed significantly from healthy subjects. Differences in microbial composition and marked fluctuations in the levels of biomarkers such as TMAO, zonulin, LPS, SCFAs may become helpful in the diagnosis of cardiovascular diseases. For this reason, the intestinal microflora and its metabolic pathways have recently become the subject of numerous studies. A very important issue is the fact that it is possible to regulate the intestinal microflora through diet, the use of prebiotics, probiotics or influence through a much larger intervention - for example, fecal mass transplantation. These possibilities have become new strategies in the treatment of HF. The main purpose of this review is to summarize recent studies that illustrate the complex interactions between the microbiome and the occurrence of HF. Conclusions. The gut microbiota is a complex ecosystem of microorganisms that live in the human gut. The gut microbiota plays an important role in maintaining the body's health, including the cardiovascular system. Dysbiosis, or an imbalance in the gut microbiota, has been linked to the development of heart failure. Gut microbiota metabolites, such as trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and bile acids, can have harmful effects on the heart. Diet, probiotics, and fecal microbiota transplantation (FMT) are all potential interventions for improving gut microbiota and reducing the risk of heart failure. More research is needed to fully understand the role of gut microbiota in heart failure and to develop effective treatment strategies.

Dietary Curcumin Supplementation Could Improve Muscle Quality, Antioxidant Enzyme Activities and the Gut Microbiota Structure of Pelodiscus sinensis.

This experiment aimed to assess the impact of different dietary curcumin (CM) levels on growth, muscle quality, serum-biochemical parameters, antioxidant-enzyme activities, gut microbiome, and liver transcriptome in Chinese soft-shelled turtles (Pelodiscus sinensis). Five experimental diets were formulated to include graded levels of curcumin at 0 (control, CM0), 0.5 (CM0.5), 1 (CM1), 2 (CM2) and 4 g/kg (CM4). Each diet was randomly distributed to quadruplicate groups of turtles (164.33 ± 5.5 g) for 6 weeks. Our findings indicated that dietary curcumin supplementation did not have a significant influence on growth performance (p > 0.05); however, it significantly improved the muscular texture profiles (p < 0.05). Serum total superoxide dismutase (SOD), liver catalase (CAT), and total antioxidant capacity (T-AOC) activities increased significantly as dietary curcumin levels rose from 0.5 to 4 g/kg (p < 0.05). Dietary curcumin supplementation improved gut microbiota composition, as evidenced by an increase in the proportion of dominant bacteria such as Lactobacillus and Flavobacterium. Liver transcriptome analysis revealed that curcumin altered metabolic pathways in the liver. In conclusion, based on the evaluation of the activities of SOD in serum and CAT in liver under current experimental design, it was determined that the appropriate dietary curcumin supplementation for Chinese soft-shelled turtles is approximately 3.9 g/kg.

Holothurian Wall Hydrolysate Ameliorates Cyclophosphamide-Induced Immunocompromised Mice via Regulating Immune Response and Improving Gut Microbiota.

Some biologically active compounds isolated from sea cucumbers stimulate the body's immune response by activating immune cells. Immune function is closely related to the integrity intestinal barrier and balanced gut microbiota. However, it is unknown whether the daily administration of holothurian wall hydrolysate (HWH) ameliorated intestinal dysbiosis and barrier injury induced by immunodeficiency. This study aimed to investigate the immunomodulatory effect and the underlying mechanism of HWH in cyclophosphamide (CTX)-induced immunocompromised mice. BALB/c mice received CTX (80 mg/kg, intraperitoneally) once a day for 3 days to induce immunodeficiency, and then they received the oral administration of HWH (80 or 240 mg/kg) or levamisole hydrochloride (LH, 40 mg/kg, positive control), respectively, once a day for 7 days. We utilized 16S rRNA sequencing for microbial composition alterations, histopathological analysis for splenic and colonic morphology, Western blotting for expressions of tight junction proteins (TJs), and quantitative real-time (qRT)-PCR for measurements of pro-inflammatory cytokines. HWH attenuated the immune organ damage induced by CTX, increased the secretions of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α, and promoted the recovery of goblet cells and the production of TJs (claudin-1, occludin, and ZO-1) in the colon of the immunocompromised mice. Moreover, HWH promoted the growth of beneficial microorganisms such as Lactobacillus, Lachnospiraceae, Christensenellaceae, and Bifidobacterium, while it suppressed the populations of Ruminococcus, Staphylococcus, and Streptococcus. These results demonstrate that HWH elicits intestinal mucosal immunity, repairs the damage to intestinal mucosal integrity, and normalizes the imbalanced intestinal microbial profiles in immunocompromised mice. It may be helpful to identify the biological activities of HWH to support its potential use in new prebiotics, immunomodulatory agents, and medical additives for intestinal repair.

Enhancing NKT cell-mediated immunity against hepatocellular carcinoma: Role of XYXD in promoting primary bile acid synthesis and improving gut microbiota

Ethnopharmacological relevance‘Xiayuxue decoction’ (XYXD) is a traditional Chinese medicine compound, composing of three natural medicines: Rheum officinale Baill., Prunus persica (L.) Batsch and Eupolyphaga sinensis Walker. It is derived from the famous traditional Chinese medical classics ‘Jingui Yaolue’ and has been used for thousands of years. In the Guidelines for the Diagnosis and Treatment of Primary liver Cancer issued by China's Health Commission, XYXD was applied in the treatment of primary liver cancer. Aim of the studyTo clarify the pharmacodynamic material basis and mechanism of XYXD in the treatment of hepatocellular carcinoma (HCC). Materials and methodsFirstly, the active components of XYXD and its distribution in vivo were identified by Ultraperformance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS). Then, the effective components and mechanism of XYXD against HCC were explored by network pharmacology combined with cell experiments in vitro. Furthermore, the anti-HCC effect of XYXD was determined by animal experiments in vivo. Metagenomic sequencing was used to detect its effect in gut microbiota, and targeted metabolism was used to detect the changes of bile acids in the liver. Finally, the related targets of NKT cell immune function activation were detected by RT-qPCR and Elisa. ResultsA total of 113 active ingredients in XYXD were identified, and the distribution of active ingredients in blood, liver, tumor, cecum, intestinal contents and feces was clarified. The circulation process and active ingredient group of XYXD were preliminarily clarified. In addition, we found five anti-HCC active ingredients in XYXD through network pharmacology combined with cell experiments in vitro, among which aloe emodin had the most significant effect, and predicted the potential mechanism of XYXD against HCC through NKT cell pathway. Moreover, the inhibitory effect of XYXD on liver tumor growth was clarified by animal experiments in vivo. The mechanism was mainly to promote the production of bile salt hydrolase (BSH) by increasing the abundance of Bacteroides and Lactobacillus, BSH converts conjugated bile acids into primary bile acids, and reduces the conversion of primary bile acids to secondary bile acids by reducing the abundance of Eubacterium, thereby increasing the content of primary bile acids. Primary bile acids trigger NKT cells in the liver to produce interferon-γ to exert anti-HCC immune effects. ConclusionThis study found that the traditional Chinese herbal formula XYXD can trigger the immune effect of NKT cells against HCC by regulating the interaction between gut microbiota and bile acids.

Protective effects of yeast extract against alcohol-induced liver injury in rats.

Oxidative stress, inflammatory response, and gut-liver axis dysbiosis have been suggested as the primarily involved in the pathogenesis of alcoholic liver injury. Previous research established that yeast extract (YE) has antioxidant, immune-boosting or microbiota-regulating properties. However, there is currently lack of information regarding the efficacy of YE on alcoholic liver injury. This study seeks to obtain data that will help to address this research gap using a Wistar male rat experimental model. Histologic and biochemical analysis results showed that the groups treated with both low-dose yeast extract (YEL) and high-dose yeast extract (YEH) had lower degrees of alcohol-induced liver injury. The abundance of Peptococcus and Ruminococcus reduced in the low-dose yeast extract (YEL) group, while that of Peptococcus, Romboutsia, Parasutterella, and Faecalibaculum reduced in the high-dose (YEH) group. Furthermore, Spearman analysis showed that the gut microbes were significantly associated with several liver-related indicators. For the analysis of differential metabolites and enriched pathways in the YEL group, the abundance of lysophosphatidylcholine (16:0/0:0) significantly increased, and then the levels of histamine, adenosine and 5' -adenine nucleotide were remarkedly elevated in the YEH group. These findings suggest that both high and low doses of YE can have different protective effects on liver injury in alcoholic liver disease (ALD) rats, in addition to improving gut microbiota disorder. Besides, high-dose YE has been found to be more effective than low-dose YE in metabolic regulation, as well as in dealing with oxidative stress and inflammatory responses.

Dietary pulses as a means to improve the gut microbiome, inflammation, and appetite control in obesity.

A dysbiotic intestinal microbiome has been linked to chronic diseases such as obesity, which may suggest that interventions that target the microbiome may be useful in treating obesity and its complications. Appetite dysregulation and chronic systemic low-grade inflammation, such as that observed in obesity, are possibly linked with the intestinal microbiome and are potential therapeutic targets for the treatment of obesity via the microbiome. Dietary pulses (e.g., common beans) are composed of nutrients and compounds that possess the potential to modulate the gut microbiota composition and function which can in turn improve appetite regulation and chronic inflammation in obesity. This narrative review summarizes the current state of knowledge regarding the connection between the gut microbiome and obesity, appetite regulation, and systemic and adipose tissue inflammation. More specifically, it highlights the efficacy of interventions employing dietary common beans as a means to improve gut microbiota composition and/or function, appetite regulation, and inflammation in both rodent obesity and in humans. Collectively, results presented and discussed herein provide insight on the gaps in knowledge necessary for a comprehensive understanding of the potential of beans as a treatment for obesity while highlighting what further research is required to gain this understanding.

Effects of the Phytocompound Combination against Dysbiosis Induced by AGE-Rich High-fat Diet in Mice

Background and Aims: The composition of the Microbiota can be influenced by various lifestyle and environmental factors, including diet. We designed a study to investigate the improving effects of plant extract, the combination of turmeric, ginger, boswellia, and cat’s claw on the abundance of key members of the gut microbiota, Bacteroidetes, Akkermansia muciniphila (A. muciniphila), Faecalibacterium prausnitzii (F. prausnitzii), Firmicutes and Bifidobacterium in mice treated with advanced glycation end products (AGE) rich high-fat diet (HFD).&#x0D; Materials and Methods: Eighteen 2-month age male C57BL/6 mice were adopted to a regular diet for 1 week and then fed with an HFD or regular diet. After 8 weeks of diet, animals received plant extract concurrently with HFD for 8 weeks. Stools were taken, DNA of stool samples was extracted, and qPCR of 16s rDNA universal primers was performed. Then the effect of plant extract on dysbiosis induced by AGE-rich HFD was accessed.&#x0D; Results: Our results revealed the frequencies of Bacteroidetes (p=0.001), A. muciniphila (p= 0.0005), F. prausnitzii (p&lt;0.0001), and Bifidobacterium (p= 0.0008) were reduced, whereas the frequency of Firmicute was increased in the AGE-rich HFD group. A significant increase in the F/B ratio was observed in the HFD group than in the regular diet group (p= 0.0003). plant extract reduced the F/B ratio and improved gut microbiota homeostasis. &#x0D; Conclusion: Plant extract restored gut microbiota patterns in HFD-treated mice. It seems more studies are required to prove the application of plant extracts for modulating the gut microbiota as a promising new biomarker with potential for therapeutic applications.

Dietary components regulate chronic diseases through gut microbiota: a review.

In recent years, gut microbiota as an immune organ has gradually become the mainstream of research. When the composition of the gut microbiota is changed significantly, this may affect human health. This review details the major microbiota composition and metabolites in the gut and discusses chronic diseases based on gut dysbiosis, including obesity, liver injury, colon cancer, atherosclerosis, and central nervous system diseases. We comprehensively summarize the changes in abundance of relevant gut microbiota by ingesting different diet components (such as food additives, dietary polyphenols, polysaccharides, fats, proteins) and their influence on the microbial quorum sensing system, thereby regulating related diseases. We believe that quorum sensing can be used as a new entry point to explain the mechanism of ingesting dietary components to improve gut microbiota and thereby regulate related diseases. This review hopes to provide a theoretical basis for future research on improving disease symptoms by ingesting functional foods containing dietary components. © 2023 Society of Chemical Industry.

Prebiotic Supplementation during Lactation Affects Microbial Colonization in Postnatal-Growth-Restricted Mice.

An inadequate perinatal nutritional environment can alter the maturation of the intestinal barrier and promote long-term pathologies such as metabolic syndrome or chronic intestinal diseases. The intestinal microbiota seems to play a determining role in the development of the intestinal barrier. In the present study, we investigated the impact of consuming an early postnatal prebiotic fiber (PF) on growth, intestinal morphology and the microbiota at weaning in postnatal-growth-restricted mice (PNGR). Large litters (15 pups/mother) were generated from FVB/NRj mice to induce PNGR at postnatal day 4 (PN4) and compared to control litters (CTRL, 8 pups/mother). PF (a resistant dextrin) or water was orally administered once daily to the pups from PN8 to PN20 (3.5 g/kg/day). Intestinal morphology was evaluated at weaning (PN21) using the ileum and colon. Microbial colonization and short-chain fatty acid (SCFA) production were investigated using fecal and cecal contents. At weaning, the PNGR mice showed decreased body weight and ileal crypt depth compared to the CTRL. The PNGR microbiota was associated with decreased proportions of the Lachnospiraceae and Oscillospiraceae families and the presence of the Akkermansia family and Enterococcus genus compared to the CTRL pups. The propionate concentrations were also increased with PNGR. While PF supplementation did not impact intestinal morphology in the PNGR pups, the proportions of the Bacteroides and Parabacteroides genera were enriched, but the proportion of the Proteobacteria phylum was reduced. In the CTRL pups, the Akkermansia genus (Verrucomicrobiota phylum) was present in the PF-supplemented CTRL pups compared to the water-supplemented ones. PNGR alters intestinal crypt maturation in the ileum at weaning and gut microbiota colonization. Our data support the notion that PF supplementation might improve gut microbiota establishment during the early postnatal period.

Oligosaccharides as Potential Regulators of Gut Microbiota and Intestinal Health in Post-COVID-19 Management.

The COVID-19 pandemic has had a profound impact worldwide, resulting in long-term health effects for many individuals. Recently, as more and more people recover from COVID-19, there is an increasing need to identify effective management strategies for post-COVID-19 syndrome, which may include diarrhea, fatigue, and chronic inflammation. Oligosaccharides derived from natural resources have been shown to have prebiotic effects, and emerging evidence suggests that they may also have immunomodulatory and anti-inflammatory effects, which could be particularly relevant in mitigating the long-term effects of COVID-19. In this review, we explore the potential of oligosaccharides as regulators of gut microbiota and intestinal health in post-COVID-19 management. We discuss the complex interactions between the gut microbiota, their functional metabolites, such as short-chain fatty acids, and the immune system, highlighting the potential of oligosaccharides to improve gut health and manage post-COVID-19 syndrome. Furthermore, we review evidence of gut microbiota with angiotensin-converting enzyme 2 expression for alleviating post-COVID-19 syndrome. Therefore, oligosaccharides offer a safe, natural, and effective approach to potentially improving gut microbiota, intestinal health, and overall health outcomes in post-COVID-19 management.

Natural emulsifiers lecithins preserve gut microbiota diversity in relation with specific faecal lipids in high fat-fed mice

Synthetic emulsifiers promote metabolic syndrome and considerably alter gut microbiota. Data is lacking regarding natural emulsifiers like plant lecithins, a polar lipid-rich source of 18:3n-3 PUFA (ALA). For 13 weeks, male Swiss mice were fed ALA-replete semi-synthetic high-fat diet (HFD) including lecithin from rapeseed (RL) or soy, vs 2 HFD-controls devoid of lecithin (ALA-replete; low-ALA), vs Chow. Lecithins did not enhance HFD-induced adiposity nor increased inflammation, did not alter gut barrier markers and caecal bile acids, and contributed to n-3 PUFA status. Lecithins improved gut microbiota diversity. RL (10% in fat) even restored α-diversity similar to Chow, increased Lachnospiraceae NK4A136, Lactobacillus and Ruminococcaceae UCG-014 groups, and decreased Blautia genus bacteria. The abundance of most beneficial lecithin-enhanced bacteria was positively correlated to the amount of faecal polar lipid-bound ALA. These findings show that lecithins can beneficially affect the gut microbiota in association with changes in lipid residues in the distal gut.

Oral and Topical Probiotics and Postbiotics in Skincare and Dermatological Therapy: A Concise Review.

The skin microbiota is a pivotal contributor to the maintenance of skin homeostasis by protecting it from harmful pathogens and regulating the immune system. An imbalance in the skin microbiota can lead to pathological conditions such as eczema, psoriasis, and acne. The balance of the skin microbiota components can be disrupted by different elements and dynamics such as changes in pH levels, exposure to environmental toxins, and the use of certain skincare products. Some research suggests that certain probiotic strains and their metabolites (postbiotics) may provide benefits such as improving the skin barrier function, reducing inflammation, and improving the appearance of acne-prone or eczema-prone skin. Consequently, in recent years probiotics and postbiotics have become a popular ingredient in skincare products. Moreover, it was demonstrated that skin health can be influenced by the skin-gut axis, and imbalances in the gut microbiome caused by poor diet, stress, or the use of antibiotics can lead to skin conditions. In this way, products that improve gut microbiota balance have been gaining attention from cosmetic and pharmaceutical companies. The present review will focus on the crosstalk between the SM and the host, and its effects on health and diseases.

Ginger essential oil and citral ameliorates atherosclerosis in ApoE−/− mice by modulating trimethylamine-N-oxide and gut microbiota

Recently, the role of the gut microbiota in diseases, including cardiovascular disease (CVD), has gained considerable research attention. Trimethylamine-N-oxide (TMAO), which is formed during ʟ-carnitine metabolism, promotes the formation of atherosclerotic plaques, causing thrombosis. Here, we elucidated the anti-atherosclerotic effect and mechanism of ginger (Zingiber officinale Roscoe) essential oil (GEO) and its bioactive compound citral in Gubra Amylin NASH (GAN) diet with ʟ-carnitine-induced atherosclerosis female ApoE−/− mice. Treatment with GEO at both low and high doses and citral inhibited the formation of aortic atherosclerotic lesions, improved plasma lipid profile, reduced blood sugar, improved insulin resistance, decreased plasma TMAO levels, and inhibited plasma inflammatory cytokines, especially interleukin-1β. Additionally, GEO and citral treatment modulated gut microbiota diversity and composition by increasing the abundance of beneficial microbes and decreasing the abundance of CVD-related microbes. Overall, these results showed that GEO and citral may serve as potential dietary supplements for CVD prevention by improving gut microbiota dysbiosis.

Hydrogen gas ameliorates acute alcoholic liver injury via anti-inflammatory and antioxidant effects and regulation of intestinal microbiota

Alcoholic liver disease (ALD) is a globally prevalent liver-related disorder characterized by severe oxidative stress and inflammatory liver damage, for which no effective treatment is currently available. Hydrogen gas (H2) has been demonstrated to be an efficient antioxidant in various diseases in animals as well as humans. However, the protective effects of H2 on ALD and its underlying mechanisms remain to be elucidated. The present study demonstrated that H2 inhalation ameliorated liver injury, and attenuated liver oxidative stress, inflammation, and steatosis in an ALD mouse model. Moreover, H2 inhalation improved gut microbiota, including increasing the abundance of Lachnospiraceae and Clostridia, and decreasing the abundance of Prevotellaceae and Muribaculaceae, and also improved intestinal barrier integrity. Mechanistically, H2 inhalation blocked activation of the LPS/TLR4/NF-κB pathway in liver. Notably, it was further demonstrated that the reshaped gut microbiota may accelerate alcohol metabolism, regulate lipid homeostasis and maintain immune balance by bacterial functional potential prediction (PICRUSt). Fecal microbiota transplantation from mice that had undergone H2 inhalation significantly alleviated acute alcoholic liver injury. In summary, the present study showed that H2 inhalation alleviated liver injury by reducing oxidative stress and inflammation, while also improving intestinal flora and enhancing the intestinal barrier. H2 inhalation may serve as an effective intervention for preventing and treating ALD in a clinical context.

Urolithin A Alleviates Colitis in Mice by Improving Gut Microbiota Dysbiosis, Modulating Microbial Tryptophan Metabolism, and Triggering AhR Activation

Urolithin A (UroA) is a microbial metabolite derived from ellagitannins and ellagic acid with good bioavailability. In this study, we explored the anticolitis activity of UroA and clarified the mechanism by 16S rDNA sequencing and metabonomics. UroA alleviated dextran sulfate sodium (DSS)-induced colitis in mice, characterized by a decreased disease activity index, increased colon length, and improved colonic histopathological lesions, along with inhibited phosphorylation of the mitogen-activated protein kinase signaling pathway. In addition, UroA improved gut microbiota dysbiosis and modulated the microbiota metabolome. Furthermore, targeted metabolomics focused on tryptophan catabolites showed that UroA significantly increased the production of indole-3-aldehyde (IAld) and subsequently led to increased colonic expression of aryl hydrocarbon receptor (AhR) and promoted the serum content of IL-22 in mice with colitis. Collectively, our data identified a novel anticolitis mechanism of UroA by improving gut microbiota dysbiosis, modulating microbial tryptophan metabolism, promoting IAld production, and triggering AhR/IL-22 axis activation. However, a limitation noted in this study is that these beneficial effects of UroA were found at 50 μM in vitro and 20 mg/kg in vivo, which were nonphysiological concentrations.

A new strategy to alleviate the obesity induced by endocrine disruptors-A unique lysine metabolic pathway of nanoselenium Siraitia grosvenorii to repair gut microbiota and resist obesity.

Obesity caused by endocrine disruptors (EDCs) has become a hot topic threatening human health. Recently, Nanoselenium Siraitia grosvenorii (NSG) has been shown to have potential health-modulating uses. Based on the results of 16S rRNA sequencing and metabolomics analysis, NSG has the unique function of improving gut microbiota and inhibiting obesity. Specifically, NSG can enhance gut microbiota diversity and change their composition. A significant positive correlation exists between the liver change in lysine and the high-importance dominant species ([Ruminococcus]_gnavus, Alistipes_finegoldii, etc.). NSG metabolites analysis showed that the lysine level increased by 44.45% and showed a significantly negatively correlated with (TG, TC, Leptin, etc.). Significantly, NSG reduces the degradation of lysine metabolism in the liver and inhibits fatty acid β-oxidation. In addition, NSG decreased Acetyl-CoA levels by 24% and regulated the downregulation of TCA genes (CS, Ogdh, Fh1, and Mdh2) and the upregulation of ketone body production genes (BDH1). NSG may have a positive effect on obesity by reducing the participation of Acetyl-CoA in the TCA cycle pathway and enhancing the ketogenic conversion of Acetyl-CoA. In conclusion, the results of this study may provide a new dietary intervention strategy for preventing endocrine disruptor-induced obesity.

Role of in vitamin D in irritable bowel syndrome.

Irritable bowel syndrome (IBS) is a common chronic functional gastrointestinal disorder affecting 10%-22% of adults. Its development is closely related to the gut microbiota, and the inflammatory and immune responses triggered by the gut microbiota can lead to IBS. Vitamin D (VD) effectively treats IBS with fewer side effects by improving gut microbiota, immune regulation, and anti-inflammatory effects. In the future, it is necessary to carry out epidemiological studies on the relationship between VD and IBS, clinical studies on the efficacy of supplementing VD to improve IBS, and animal studies on the mechanism of VD improving IBS. Therefore, this paper discussed the relationship between VD and IBS.

Multi-omics reveals Dengzhan Shengmai formulation ameliorates cognitive impairments in D-galactose-induced aging mouse model by regulating CXCL12/CXCR4 and gut microbiota.

Dengzhan Shengmai (DZSM), a traditional Chinese medicine formulation, has been administered extensively to elderly individuals with cognitive impairment (CI). However, the underlying mechanisms by which Dengzhan Shengmai improves cognitive impairment remains unknown. This study aimed to elucidate the underlying mechanism of the effect of Dengzhan Shengmai on aging-associated cognitive impairment via a comprehensive combination of transcriptomics and microbiota assessment. Dengzhan Shengmai was orally administered to a D-galactose-induced aging mouse model, and evaluation with an open field task (OFT), Morris water maze (MWM), and histopathological staining was performed. Transcriptomics and 16S rDNA sequencing were applied to elucidate the mechanism of Dengzhan Shengmai in alleviating cognitive deficits, and enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (PCR), and immunofluorescence were employed to verify the results. The results first confirmed the therapeutic effects of Dengzhan Shengmai against cognitive defects; specifically, Dengzhan Shengmai improved learning and impairment, suppressed neuro loss, and increased Nissl body morphology repair. Comprehensive integrated transcriptomics and microbiota analysis indicated that chemokine CXC motif receptor 4 (CXCR4) and its ligand CXC chemokine ligand 12 (CXCL12) were targets for improving cognitive impairments with Dengzhan Shengmai and also indirectly suppressed the intestinal flora composition. Furthermore, in vivo results confirmed that Dengzhan Shengmai suppressed the expression of CXC motif receptor 4, CXC chemokine ligand 12, and inflammatory cytokines. This suggested that Dengzhan Shengmai inhibited CXC chemokine ligand 12/CXC motif receptor 4 expression and modulated intestinal microbiome composition by influencing inflammatory factors. Thus, Dengzhan Shengmai improves aging-related cognitive impairment effects via decreased CXC chemokine ligand 12/CXC motif receptor 4 and inflammatory factor modulation to improve gut microbiota composition.

Research progress on the relationship between gut microbiota dysbiosis and osteoarthritis

To introduce the research progress on the relationship between gut microbiota dysbiosis and osteoarthritis (OA), focus on the possible mechanism of gut microbiota dysbiosis promoting OA, and propose a new therapeutic direction. The domestic and foreign research literature on the relationship between gut microbiota dysbiosis and OA was reviewed. The role of the former in the occurrence and development of OA and the new ideas for the treatment of OA were summarized. The gut microbiota dysbiosis promotes the development of OA mainly in three aspects. First, the gut microbiota dysbiosis destroys intestinal permeability and causes low-grade inflammation, which aggravate OA. Secondly, the gut microbiota dysbiosis promotes the development of OA through metabolic syndrome. Thirdly, the gut microbiota dysbiosis is involved in the development of OA by regulating the metabolism and transport of trace elements. Studies have shown that improving gut microbiota dysbiosis by taking probiotics and transplanting fecal microbiota can reduce systemic inflammation and regulate metabolic balance, thus treating OA. Gut microbiota dysbiosis is closely related to the development of OA, and improving gut microbiota dysbiosis can be an important idea for OA treatment.