Modulation Of Gut Microbiota Research Articles

Alisma plantago-aquatica polysaccharides ameliorate acetaminophen-induced acute liver injury by regulating hepatic metabolic profiles and modulating gut microbiota

Acetaminophen (APAP) has emerged as a predominant contributor to acute liver failure (ALF) in United States. Alismatis rhizoma, a commonly used traditional herbal medicine, contains small molecular components with extensive hepatoprotective activity. However, the specific role of Alismatis rhizoma polysaccharide (ARP) in liver protection remains unclear. ARP50 and ARP70, derived through graded alcohol precipitation and refinement, predominantly consisted of varying proportions of glucose, galactose, and arabinose. In vitro experiments on free radical scavenging demonstrated notable antioxidant capabilities of ARP50 and ARP70. To investigate the hepatoprotective effects, an APAP-induced acute liver injury (ALI) model was established in mice. ARP50 and ARP70 exerted dose-dependent therapeutic effects on APAP-induced liver injury. Further analysis of liver metabolites revealed that ARPs facilitated the reconstruction of the liver antioxidant system by modulating the metabolism network centered on l-glutamine. In addition, the abundance of gut microbiota was altered under the influence of ARPs. ARP50 significantly reduced the levels of Pseudarthrobacter and markedly increased the levels of Faecalibacterium，At the same time, ARP50 could increase the levels of acetic acid in the liver and serum. Meanwhile, ARP70 significantly increased the abundance of Dubosiella, Muribaculum, Ileibacterium, and Prevotellaceae UCG 001, while reducing the abundance of Escherichia Shigella and Pseudarthrobacter. The results indicated that ARPs could exert a protective effect against APAP-induced acute liver injury by reshaping the liver metabolic profile and modulating the gut microbiota.

Retraction Note: Dietary garcinol supplementation improves diarrhea and intestinal barrier function associated with its modulation of gut microbiota in weaned piglets

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s40104-020-0426-6.

Lactobacillus rhamnosus ZJUIDS07 ameliorates type 2 diabetes in mice through the microbiome-gut-pancreas axis

Diabetes mellitus is a chronic metabolic disease characterized by hyperglycemia, with its prevalence escalating. It exerts a profound impact on human health care and socio-economic development. Probiotics, known as natural, safe, and minimal side effects, have emerged as promising intervention agents to manage chronic diabetes. Our study aimed to explore the therapeutic potential of Lactobacillus rhamnosus ZJUIDS07 for mitigating T2D in mice induced by a high-fat diet (HFD) and streptozotocin (STZ). Administration of L. rhamnosus ZJUIDS07 led to a reduction in diabetic symptoms, including reversal of weight loss, improvement in hyperglycemia and insulin resistance, mitigation of disruptions in glucose and lipid metabolism, alleviation of pancreatic pathological damage, and reduction in oxidative stress and inflammation. Moreover, treatment with L. rhamnosus ZJUIDS07 could restore intestinal microbiota balance in T2D mice by altering the structure and composition of intestinal microbiota, and increased short-chain fatty acids (SCFAs) levels. Specifically, L. rhamnosus ZJUIDS07 significantly decreased the abundance of harmful bacteria like Staphylococcus, Corynebacterium, and Odoribacte, while increasing the abundance of beneficial bacteria (especially SCFAs-producing bacteria) such as Muribaculaceae_norank, Dubosiella, Clostridium sensu stricto 1, Lactobacillus, and Faecalibaculum. Our findings highlight that L. rhamnosus ZJUIDS07 represents a promising probiotic strategy for future treatment of T2D, and that the modulation of gut microbiota and their metabolites through the microbiome-gut-pancreas axis play a pivotal role for the antidiabetic effects of L. rhamnosus ZJUIDS07.

Gut microbiota modulation by L-Fucose as a strategy to alleviate Ochratoxin A toxicity on primordial follicle formation

In this study, we investigated the potential benefits of L-Fucose administration to pregnant mice exposed to Ochratoxin A (OTA), a widespread mycotoxin, producing ovarian damage in offspring. The results showmmced that administration of 3.5μg/d OTA induced alterations in intestinal tissues and gut microbiota of pregnant mice, leading to heightened local and systemic inflammation. This inflammatory affected the ovaries of their 3 dpp offspring, in which elevated levels of LPS and ROS were found associated to significant decreased oocyte count and impaired primordial follicle assembly. Moreover, mRNA Seq analysis showed significant changes in ovarian transcriptomes linked to various GO terms and KEGG pathways, notably ferroptosis, a recognized form of cell death observed. Interestingly, administration of 0.3g/kg b. w. L-Fucose following OTA exposure mitigated these effects on intestinal tissues and gut microbiota in mothers and on the offspring's ovaries. Similar benefits were obtained by gut microbiota transplantation from L-Fucose-treated pregnant females into OTA-exposed mothers. These findings suggest that inflammatory impact of OTA on maternal intestine/gut can pass to the fetus causing offspring ovary defects and support the use of L-Fucose as adjuvant to counteract the adverse effects of mycotoxins on the gut microbiota, particularly reference to those affecting reproductive organs. Environmental implicationMycotoxins are widely recognized as environmental pollutants. With the increasing intense of contradiction between the fact of mycotoxins pollution worldwide and the demand for feed/food safety, it is urgent to understand the toxicity mechanism and to develop the preventive measures and detoxification strategies. Reproductive toxicity causes harmful effects not only to animal themselves but also to their offspring, leading to adverse effects among several generations. Here we elaborate the reproductive injury induced by OTA and the potential of L-Fucose as a straightforward remedy against the deleterious effects of the mycotoxin.

Butyrate modulates gut microbiota and anti-inflammatory response in attenuating cisplatin-induced kidney injury.

In our previous research, we reported that administering probiotics Lactobacillus reuteri and Clostridium butyricum (LCs) before cisplatin treatment effectively modifies structures of the gut microbiota and restore ecological balance and significantly increases butyrate levels, a process closely associated with reducing cisplatin-induced nephrotoxicity. This study aims to investigate further whether the elevation of metabolite butyrate in the gut, promoted by probiotics LCs, can effectively mitigate the nephrotoxic effects of cisplatin and the progression of renal senescence in rats. Results show that butyrate administration significantly improved kidney function and decreased renal fibrosis in a dose-dependent manner compared to the cisplatin group. Its effects were associated with reductions in inflammatory responses, evidenced by decreased levels of key inflammatory markers, including KIM-1, MPO, NOX2, F4/80, and TGF-β1, alongside increased production of the anti-inflammatory cytokine IL-10. Furthermore, the butyrate intervention ameliorated cisplatin-induced gut microbiota dysbiosis, preserving the structure and diversity of healthy microbial communities. Specifically, we observed a decrease in the abundance of Escherichia_Shigella and Blautia, alongside an increase in the abundance of the butyrate-producing genus Roseburia. Notably, Escherichia_Shigella exhibited a positive correlation with the pro-inflammatory factor MPO, while displaying a negative correlation with the anti-inflammatory cytokine IL-10. Butyrate also attenuated the cisplatin-induced expression of senescence markers p21 and p16 in kidney tissue. It alleviated the cisplatin-increased senescence-associated beta-galactosidase activity and reactive oxygen species production in SV40 MES-13 cells. These results indicate that butyrate, derived from the gut microbiota, may exert a protective effect against cisplatin-induced kidney damage by regulating microbiota balance and anti-inflammatory effects.

Gastrointestinal health anti-diarrheal mixture relieves spleen deficiency-induced diarrhea through regulating gut microbiota

Abstract This study evaluated the therapeutic efficacy of the gastrointestinal health anti-diarrheal mixture (GHAM) on diarrhea induced by spleen deficiency, focusing on its modulation of gut microbiota. Using specific pathogen-free Wistar rats, a spleen deficiency model was created through senna leaf gavage. Rats were divided into control, model, positive control, and GHAM treatment groups. After a 14-day treatment, fecal samples were analyzed via 16S rDNA sequencing to assess microbiota alterations. GHAM significantly mitigated diarrhea and enhanced food intake and fecal quality. It increased the abundance of beneficial bacteria, such as Romboutsia and Clostridium_sensu_stricto_1, and decreased the levels of diarrhea-associated bacteria, such as Prevotellaceae and Bacillus, thereby improving microbiota functionality. GHAM’s modulation of gut microbiota structure and function effectively alleviated spleen deficiency-induced diarrhea, positioning it as a potential natural herbal treatment for gastrointestinal ailments. This study lays the groundwork for further exploration of GHAM’s regulatory impact on gut health.

Roles of the gut microbiota in human neurodevelopment and adult brain disorders

Growing evidence demonstrates the connection between gut microbiota, neurodevelopment, and adult brain function. Microbial colonization occurs before the maturation of neural systems and its association with brain development. The early microbiome interactions with the gut-brain axis evolved to stimulate cognitive activities. Gut dysbiosis can lead to impaired brain development, growth, and function. Docosahexaenoic acid (DHA) is critically required for brain structure and function, modulates gut microbiota, and impacts brain activity. This review explores how gut microbiota influences early brain development and adult functions, encompassing the modulation of neurotransmitter activity, neuroinflammation, and blood-brain barrier integrity. In addition, it highlights processes of how the gut microbiome affects fetal neurodevelopment and discusses adult brain disorders.

Dose-dependent effects of anthocyanin-rich extracts on obesity-induced inflammation and gut microbiota modulation.

Obesity and its associated inflammatory state pose a significant health burden. Anthocyanins, bioactive compounds found in fruits and vegetables, have garnered interest in their potential to attenuate these conditions. Understanding the dose-dependent response of anthocyanins is essential for optimizing their therapeutic potential in preventing and managing obesity. This comprehensive review explores the current knowledge on the dose-dependent effects of anthocyanins on obesity in both human and animal models, analyzing the structure and mechanism of absorption of these compounds. The article also highlights the diverse mechanisms underlying anthocyanin action, the symbiosis between anthocyanins and gut microbiota impacting metabolite production, influencing diverse health outcomes, modulating cytokines, and activating anti-inflammatory pathways. Additionally, their impact on energy metabolism and lipid regulation is discussed, highlighting potential contributions to weight management through AMPK and PPARγ pathways. Despite promising results, dose-dependent effects are fundamental considerations, with some studies indicating less favorable outcomes at higher doses. Future research should focus on optimizing dosages, accounting for individual responses, and translating findings into effective clinical applications for obesity management.

Ruminococcus gnavus in the gut: driver, contributor, or innocent bystander in steatotic liver disease?

The human gut microbiome plays a crucial role in regulating intestinal and systemic health, impacting host immune response and metabolic function. Dysbiosis of the gut microbiome is linked to various diseases, including steatotic liver diseases. Metabolic dysfunction-associated steatotic liver disease (MASLD), a chronic liver disease characterized by excess hepatic lipid content and impaired metabolism, is the leading cause of liver disease worldwide. Among the gut microbes, Ruminococcus gnavus (R. gnavus) has garnered attention for its association with inflammatory and metabolic diseases. While R. gnavus abundance correlates to liver fat accumulation, further research is needed to identify a causal role or therapeutic intervention in steatotic liver disease. This review surveys our current understanding of R. gnavus in the development and progression of steatotic liver diseases, highlighting its potential mechanisms through metabolite secretion, and emphasizes the need for comprehensive microbiome analyses and longitudinal studies to better understand R. gnavus' impact on liver health. This knowledge could pave the way for targeted interventions aimed at modulating gut microbiota to treat and prevent MASLD and its comorbidities.

Clerodendranthus spicatus [Orthosiphon aristatus (Blume) Miq.] maintains uric acid homeostasis via regulating gut microbiota and restrains renal inflammation in hyperuricemic nephropathy

IntroductionThe kidney damage caused by the deposition of uric acid in the kidneys is of urgent need for new treatment drugs due to its complex pathogenesis. Orthosiphon aristatus (Blume) Miq. Also known as C. spicatus, which has a significant therapeutic effect on hyperuricemia nephropathy (HN), however, the specific mechanism of its action is still unknown.MethodsThe HN mice model was constructed using adenine (AD) and potassium oxonate (PO), and serum biochemical indexes, kidney pathological changes, xanthine oxidase (XOD) activity in the liver, and renal protein expressions of phosphoribose pyrophosphate synthetase (PRPS) and uric acid transporter were detected. The effects of C. spicatus on uric acid lowering, anti-inflammation, and renal protection of HN mice were verified. The effect of C. spicatus on gut microbiota was assessed by 16 S rRNA sequencing. Establish pseudo-sterile mice through the combined treatment of ampicillin, neomycin, and vancomycin to verify the role of gut microbiota in improving HN in C. spicatus.ResultsIn HN mice, C. spicatus could significantly reduce serum uric acid levels and improve renal function. In addition, C. spicatus modulated gut microbiota and decreased the relative abundance of Bacteroides, Prevotellaceae_UCG-001 and Alistipes, and increased the abundance of Alloprevotella and Lachnospiraceae_NK4A136_group.C.spicatus altered the expression of the renal urate transporter and key enzymes in hepatic urate synthesis, leading to a decrease in serum uric acid levels. C. spicatus alleviated kidney inflammation by inhibiting the activation of the NLRP3 and TLR4/MYD88 inflammatory pathways, and reduced the level of kidney inflammatory factors. It also improved kidney damage by inhibiting the process of renal epithelial-mesenchymal transition, and improved kidney fibrosis. In pseudo-sterile HN mice, without the effect of gut microbiota, the uric acid lowering, anti-inflammatory, and renal fibrosis improving effects of C. spicatus were significantly reduced.ConclusionOur results demonstrated that C. spicatus could reduce uric acid levels, anti-inflammatory effects, and improve HN by regulating the gut microbiota. This provides a novel scientific basis for the clinical application of C. spicatus.

Unveiling the Potential of Probiotics in Osteoarthritis Management.

Osteoarthritis (OA), a highly prevalent degenerative joint disease, is of increasing concern due to its debilitating nature and negative impact on quality of life. Recent investigations have explored the therapeutic potential of probiotics to alleviate OA. This review summarizes the emerging evidence for the potential role of probiotics in managing OA symptoms and disease progression. The link between gut dysbiosis and chronic inflammation, a key player in OA progression is discussed in this review. Probiotics may modulate gut microbiota composition, potentially reducing systemic inflammation and alleviating OA symptoms, including joint pain and function. Possible mechanisms through which probiotics may exert these effects, including dampening inflammatory pathways and enhancing intestinal barrier integrity have been highlighted. Promising results from preclinical and clinical studies investigating the specific beneficial effects of specific probiotic strain(s) for OA management have been highlighted. Finally, limitations in current research and future directions, emphasizing the need for well-designed, large-scale clinical trials to definitively establish the therapeutic potential of probiotics in OA treatment have been discussed.

Microbiota modulation by the inclusion of Tenebrio molitor larvae as alternative to fermented soy protein concentrate in growing pigs diet.

Tenebrio molitor meal represents a promising protein source for animal nutrition due to its low environmental impact and high nutritional value. To date, there is limited data in the literature regarding the effects of Tenebrio molitor meal on the modulation of gut microbiota in growing animals, with most results focusing on poultry rather than pigs. The aim of this study was to evaluate the effects of replacing fermented soy protein concentrate with Tenebrio molitor meal on gut microbiota and feed digestibility in growing pigs. A total of 14 growing pigs (80 ± 2 days old) were randomly allotted to two groups: the control group (CON) was fed a commercial diet containing 4% fermented soy protein concentrate (48% crude protein), and the treatment group (TM) was fed a basal diet containing 5% of T. molitor larvae meal formulated to be isonitrogenous and isoenergetic. The study lasted 28 days. Animals were weekly weighted and feed refuse was routinely measured. Fecal, blood samples, and rectal swabs were collected for analysis. No differences were observed in growth and diet digestibility for the protein and lipid components throughout the trial. No differences in the serum concentrations of albumin, globulin, urea, and interleukin-6 were registered in both groups, suggesting an unaltered health status. The TM group showed a significant difference in the beta diversity index considering the total duration of the trial (treatment effect evaluated with PERMANOVA, R2 0.0771, p value = 0.0099) showing an increased abundance of Elusimicrobium spp. and a decrease in Asteroplasma spp. in TM compared to the CON group (p < 0.05). Obtained findings indicate that 5% T. molitor meal can be included as a partial replacement for soy in growing pig formula without impairing pig growth and gut microbiota composition.

Phenolics-Rich Extract from Agarwood Leaf-Tea Alleviate Dextran Sulfate Sodium (DSS)-Induced Ulcerative Colitis Via Modulating Intestinal Barrier Function, Liver Inflammation, and Gut Microbiota.

At present, the incidence rate of ulcerative colitis (UC) continues to increase, causing a global burden. In addition, therapeutic drugs have great side effects. According to modern pharmacology, agarwood leaves have anti-inflammatory, antibacterial, hypoglycemic, and lipid-lowering effects. Therefore, this experiment on DSS induced colitis treatment of polyphenolic substances in agarwood leaves is feasible and in line with the current hot topic of using natural substances instead of drugs for treatment. ALP supplementation promotes the expression of tight junction proteins occludin and Zonula occludens protein 1 (ZO-1) on colonic tissues, repairs the intestinal barrier, and relieves further colonic tissue damage. Besides, ALP effectively inhibits the activation of nuclear factor kappa-B (NF-кB) signaling pathway and reduces the release of proinflammatory cytokines. Moreover, ALP reverses the alteration of gut microbiota in the colitic mice by increasing the abundances of Parabacteroides, Chlamydia, and Lachnospiraceae, and decreasing the abundances of Bacteroides and Phocaeicola. Furthermore, the correlation analysis suggested that ALP can attenuate DSS-induced UC, which is probably related to the alterations in the gut microbiota. ALP can ameliorate DSS-induced UC by modulating gut microbiota, intestinal barrier function, and inflammatory responses.

Microbiota and social behavior alterations in a mouse model of down syndrome: Modulation by a synbiotic treatment

Sex differences in the composition and functionality of gut microbiota are an emerging field of interest in neurodevelopmental disorders, as they may help in understanding the phenotypic disparities between males and females. This study aimed to characterize sex-related specific alterations in gut microbiota composition in a mouse model of Down syndrome (Ts65Dn mice, TS mice) through the sequencing of the PCR-amplified 16S ribosomal DNA fraction. Moreover, it intended to examine whether the modulation of gut microbiota by the administration of a synbiotic (SYN) treatment would be beneficial for the behavioral alterations observed in male and female TS mice. Our results show that male, but not female, TS mice exhibit alterations in beta diversity compared to their wild-type (WT) littermates. Sex-dependent differences are also observed in the relative abundance of the classes Bacilli and Clostridia. Administering the SYN effectively counteracts hypersociability in females, and normalizes the overall abundance of Bacilli, specifically by increasing Lactobacillaceae. On the contrary, it rescues emotional recognition deficits in male TS mice and increases the relative abundance of the families Lactobacillaceae, Streptococcaceae and Atopobiaceae. In addition, a metagenome KEGG analysis of differentially enriched pathways shows relevant changes in the cofactor biosynthesis and the amino acid synthesis categories. Finally, following SYN treatment, both male and female TS mice exhibit a robust increase in propionic acid levels compared to WT littermates. These findings suggest sex-specific mechanisms that could link gut microbiota composition with behavior in TS mice, and underscore the potential of targeted gut microbiota interventions to modulate social abnormalities in neurodevelopmental disorders.

Effect of Brassica rapa L. Polysaccharide on Lewis Lung Cancer Mice by Inflammatory Regulation and Gut Microbiota Modulation.

Lung cancer is the leading cause of cancer-related fatalities globally, related to inflammatory and gut microbiota imbalance. Brassica rapa L. polysaccharide (BP) is a functional compound, which is utilized by the gut microbiota to regulate immunity and metabolism. However, the effect of BP on lung cancer and whether it affects the "gut-lung" axis remains unclear. This study explored the intervention of BP in Lewis lung cancer (LLC) mice and its effect on the gut microbiota. The results revealed that BP reduced tumor weight and downregulated the expression of Ki67 protein. Additionally, BP reduced the content of inflammatory factors and growth factors, promoting tumor cell apoptosis and inhibiting the growth of LLC. The intervention of BP suppressed intestinal inflammation, preserved intestinal barrier integrity, and augmented the level of beneficial microbiota, such as Blautia and Bifidobacterium. Furthermore, BP significantly increased the production of short-chain fatty acids (SCFAs), particularly butyrate and propionate. A correlation analysis showed significant correlations among the gut microbiota, SCFAs, inflammatory factors, and tight junction proteins. A functional analysis indicated that BP promoted amino acid metabolism and fatty acid metabolism. These findings suggested that BP had the potential to act as prebiotics to prevent disease and improve lung cancer progression by regulating the gut microbiota.

Modulation of Canine Gut Microbiota by Prebiotic and Probiotic Supplements: A Long-Term In Vitro Study Using a Novel Colonic Fermentation Model.

The gut microbiota plays a crucial role in dogs' health, influencing immune function, digestion, and protection against pathogens. This study evaluates the effects of three canine dietary supplements-Microbiotal (prebiotic), Lactobacillus reuteri (probiotic), and a combination of both-on the gut microbiota composition of a healthy canine donor using an in vitro colonic fermentation model. The SCIME™ platform, adapted to simulate the canine gastrointestinal tract, was used to monitor microbial shifts in the luminal and mucosal environments of the proximal and distal colon over a 2-week treatment period. The microbial communities were analyzed using 16S rRNA sequencing to assess changes at various taxonomic levels. Alpha- and beta-diversity indices were calculated, while LEfSe and treeclimbR were employed to identify taxa-driving microbial shifts. Results indicated that all treatments led to significant modulations in key microbial groups, with enrichment of Limosilactobacillus, Bifidobacterium, Prevotella, and Faecalibacterium. These changes suggest improved saccharolytic fermentation and butyrate production, particularly when prebiotics and probiotics were co-administered. This study highlights the promising benefits of combined prebiotic and probiotic supplementation in promoting gut health and microbial diversity, providing a basis for future studies targeting the metabolic activity of the gut microbiota using the same supplements and technology.

Limosilactobacillus reuteri ameliorates maternal separation stress in newborn mice and alters subsequent adult behaviour.

Maternal separation (MS) in mice results in behavioral deficits and gut microbiota dysbiosis that all persist into adulthood. Limosilactobacillus reuteri DSM 17938 modulates gut microbiota, alters systemic metabolites, and facilitates immune regulation. To assess the effect of DSM 17938 on biochemical and behavioural stress-associated changes, newborn mice were exposed to unpredictable MS (MSU) daily from day 7 to day 20 of life, with intragastric administration of DSM 17938 or PBS as control. Body weight, brain levels of cholecystokinin (CCK), glial fibrillary acidic protein (GFAP), corticosterone, and stool microbiota were assessed at day 21. Behaviour tests including Y-maze (YMT), Tail Suspension (TST), and Open Field (OFT) were evaluated in adult mice. MSU resulted in a decrease in early postnatal growth, which improved with DSM 17938. Reduced CCK and increased corticosterone brain levels due to MSU were reversed by DSM 17938. GFAP levels increased with MSU, indicating that the decreased brain CCK was likely secondary to neuronal damage. DSM 17938 treated offspring demonstrated better cognitive function and less anxious behaviour in adult behaviour tests. DSM 17398 corrected stress related gut microbial dysbiosis. In conclusion, early life modulation of gut microbiota by DSM 17938 had beneficial effects on stress-associated physical and biochemical changes caused by MS in neonates and on subsequent adult behaviour.

Harnessing Ginger’s Healing Power: A Natural Remedy for Gastrointestinal Inflammation, Revitalizing Digestive Health

This paper explores the anti-inflammatory of ginger, emphasizing its role in managing gastrointestinal conditions such as inflammatory disease and gastritis. Active compounds in ginger, including gingerols and shogaols, are shown to inhibit key inflammatory pathways, reduce oxidative stress, and modulate gut microbiota, which collectively contribute to alleviating symptoms like abdominal pain, bloating and nausea. Clinical trials have further supported the beneficial effects of ginger in enhancing digestive enzyme activity and improving gastric motility, making it a valuable natural remedy for gastrointestinal discomfort. Overall, ginger's ability to modulate both inflammation and oxidative stress positions it as a promising adjunct or alternative treatment for gastrointestinal disorders. This paper provides a comprehensive overview of the current evidence supporting ginger's therapeutic potential and suggests areas for future research to fully elucidate its mechanisms of action and clinical applications in digestive health.

Extraction and Identification of Polysaccharide from Lentinus edodes and Its Effect on Immunosuppression and Intestinal Barrier Injury Induced by Cyclophosphamide.

Lentinus edodes serves as a significant source of both medicine and food, with its key component, lentinan (LNT), recognized as an effective immunomodulator. However, the mechanisms by which it regulates immune and intestinal functions under conditions of immunosuppression remain unclear. This study aims to investigate the components of lentinan and examine its potential effects on countering cyclophosphamide (CP)-induced immunosuppression, intestinal barrier damage, and dysregulation of gut microbiota. In this study, the effects of LNT were evaluated by serological indicators, histopathological changes in ileum, tight-junction-related protein expression, cytokine expression levels, and gut microbiota 16S rRNA gene sequencing. We found that LNT was effective in mitigating the abnormalities in body weight, immune organ index, and serum levels of IL-6, IL-2, IFN-γ, and IgG in mice induced by CP (p < 0.05). Furthermore, LNT demonstrated the ability to alleviate intestinal barrier damage induced by CP by increasing the mRNA levels of TNF-α, IL-1β, IFN-γ, Occludin, and ZO-1 (p < 0.05). Additionally, 16S rRNA gene sequencing revealed that LNT also normalized the disrupted abundance of Firmicutes, Proteobacteria, and Bacteroidets caused by CP. This restoration brought the gut microbiota back to normal levels and increased the abundance of certain tumor-inhibiting bacteria, such as Alistipes. Overall, lentinan demonstrated the ability to reverse the immunosuppressive effects induced by cyclophosphamide and modulate gut microbiota to restore a healthy microbial balance.

Managing Type 2 Diabetes Mellitus via the Regulation of Gut Microbiota: A Chinese Medicine Perspective.

Type 2 Diabetes Mellitus (T2DM) is a metabolic disorder characterized by insulin resistance and inadequate insulin production. Given the increased frequency of T2DM and the health issues it can cause, there is an increasing need to develop alternative T2DM management strategies. One such approach is Chinese Medicine (CM), a complementary therapy widely used in T2DM treatment. Given the emphasis on gut microbiota in current research, studying CM in the treatment of T2DM via gut microbiota modulation could be beneficial. Scope and approach: The use of various CM methods for managing T2DM via gut microbiota modulation is highlighted in this review. Following an introduction of the gut microbiota and its role in T2DM pathogenesis, we will review the potential interactions between gut microbiota and T2DM. Thereafter, we will review various CM treatment modalities that modulate gut microbiota and provide perspectives for future research. Key findings and discussion: In T2DM, Akkermansia, Bifidobacterium, and Firmicutes are examples of gut microbiota commonly imbalanced. Studies have shown that CM therapies can modulate gut microbiota, leading to beneficial effects such as reduced inflammation, improved metabolism, and improved immunity. Among these treatment modalities, Chinese Herbal Medicine and acupuncture are the most well-studied, and several in vivo studies have demonstrated their potential in managing T2DM by modulating gut microbiota. However, the underlying biomolecular mechanisms of actions are not well elucidated, which is a key area for future research. Future studies could also investigate alternate CM therapies such as moxibustion and CM exercises and conduct large-scale clinical trials to validate their effectiveness in treatment.