INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2024
·
IF 7.7
Li Li,Mingjie Xia,Lina Yang,Yutang He,He Liu,Mengxi Xie,Miao Yu
Polysaccharides impact intestinal fermentation and regulate interfacial properties which affect absorption and transportation. Short-chain fatty acids (SCFAs), the main metabolites of soy hull polysaccharide lysate, are readily absorbed by the body and perform various physiological functions. We analysed the interfacial properties and transport of soy hull polysaccharide-derived SCFAs in the Caco-2 cell model to clarify the transmembrane transport mechanism. The results showed that the interfacial properties of the co-culture system were influenced by both transit time and concentration of SCFAs, the uptake and transit rates of SCFAs at 1–3 h increased significantly with time ( P < 0.05). With increasing transit time and concentration, the transit rates of SCFAs on the apical side (AP) → basolateral side (BL) and BL → AP sides increased and then stabilised, the transit rate of the AP → BL side was higher than that of the BL → AP side. Proteomic analysis showed that soy hull polysaccharide-derived SCFAs resulted in the differential expression of 285 upregulated and 501 downregulated after translocation across Caco-2 cells. The differentially expressed proteins were mainly enriched in ribosomes, oxidative phosphorylation, nuclear transport, and SNARE vesicular transport. This study lays the theoretical foundation for understanding the structure-activity relationship of soy hull polysaccharides in the intestine.
研究领域:
营养学
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胃肠病学
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分子生物学
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细胞生物学
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蛋白质组学
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DOI
PubMed
高影响因子
Frontiers in Microbiology
·
2025
·
IF 4.5
Lin Lin,Siyuan Li,Que Liu,Xingxing Zhang,Ying Xiong,Shaoyun Zhao,Liyue Cao,Jiaxuan Gong,Yaping Liu,Rong Wu
Objective: This study aimed to investigate the potential relation between the retarded growth of skeletal muscle (SM) and dysbiosis of gut microbiota (GM) in children with asthma, and to explore the potential action mechanisms of traditional pediatric massage (TPM) from the perspective of regulating GM and short-chain fatty acids (SCFAs) production by using an adolescent rat model of asthma.Methods: Male Sprague-Dawley rats aged 3weeks were divided randomly into the 5 groups (n=6~7) of control, ovalbumin (OVA), OVA + TPM, OVA + methylprednisolone sodium succinate (MP) and OVA + SCFAs. Pulmonary function (PF) was detected by whole body plethysmograph, including enhanced pause and minute ventilation. Airway allergic inflammation (AAI) status was assessed by concentrations of OVA-specific immunoglobulin E in plasma, interleukin (IL)-4 and IL-1β in bronchoalveolar lavage fluid via ELISA assay. SM mass was assessed by using cross-sectional areas of diaphragm muscle and gastrocnemius via hematoxylin and eosin staining. GM and SCFAs production were detected by 16S rDNA sequencing and GC-MS, respectively. The protein and gene expressions of free fatty acid receptor 2 in SM were detected by using immunohistochemical staining and qRT-PCR, respectively. qRT-PCR was used to detect other relative gene expressions that were closely related with SM mass. The activity of insulin-like growth factor-1 (IGF-1)/protein kinase B (PKB/AKT) pathway in SM was detected by western blotting test.Results: OVA exposure caused obvious AAI and poor PF in adolescent rats. OVA-exposed adolescent rats had a retarded growth of SM mass and inhibited activity of IGF-1/AKT pathway, which was related with GM dysbiosis, reduced SCFAs production and FFAR2 expressions in SM. TPM efficiently enhanced the SM mass, along with alleviating AAI and improving PF. TPM activated IGF-1/AKT pathway in SM, which was closely related with correcting GM dysbiosis, enhanced SCFAs production and FFAR2 expressions.Conclusion: The retarded growth of SM mass and inhibition of IGF-1/AKT pathway existed in OVA-exposed adolescent rats, which was related with GM dysbiosis, reduced SCFAs production and FFAR2 expressions in SM. TPM efficiently enhanced the SM mass, at least, partially via regulating GM, enhancing SCFAs production and activating FFAR2-IGF-1/AKT pathway.
研究领域:
儿科学
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免疫学
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药理学
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微生物学
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肌肉骨骼系统
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DOI
PubMed
高影响因子
Communications Biology
·
2025
·Vol. 8
·期 1
·1-17
·
IF 5.1
Wang He,Kang Tianyang,Li Weiwei
Gestational diabetes during pregnancy is associated with an increased risk of developmental abnormalities in offspring, but the underlying mechanisms remain unclear. It is not known how maternal metabolism and gut microbes influence kidney development in the fetus. Here we show that gestational diabetes alters maternal gut microbiota and reduces the production of key fatty acids that normally support kidney development in offspring. We find that these changes impair a molecular pathway involving the receptor GPR43 , which promotes the growth and migration of kidney cells. In a mouse model, restoring short-chain fatty acids or transferring gut bacteria from healthy donors improves kidney development in offspring, while blocking GPR43 reverses this effect. This study reveals a previously unknown link between maternal gut metabolism and fetal kidney formation and may guide future strategies to prevent congenital kidney disorders in children born to mothers with gestational diabetes.
研究领域:
发育生物学
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微生物学
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代谢学
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分子生物学
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肾脏病学
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妇产科学
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DOI
PubMed
高影响因子
npj Science of Food
·
2026
·
IF 9.7
Zhi Dandan,He Xiying,Yang Linfu,Gong Xueyang,Xue Yunfei,Wang Shuang,Wen Xin,Guan Zhibin,Zhao Hongmu,Dong Kun,Tian Yakai
The incidence of hyperlipidemia, a lipid metabolic disorder, continues to increase globally, but current pharmacological therapies are often limited by adverse effects. Royal jelly acid, a unique monounsaturated fatty acid (MUFA) derived from royal jelly, shows therapeutic promise against hyperlipidemia; however, its direct targets and regulatory mechanisms remain unclear. In a diet-induced rat model of hyperlipidemia, royal jelly acid exhibited favorable safety and significantly improved body weight, serum lipid indices, hepatic enzyme activity, and antioxidant capacity, while alleviating hepatic lipid droplet accumulation. Royal jelly acid significantly increased the abundance of short-chain fatty acid (SCFA)-producing intestinal microorganisms, promoted SCFA production, and restored hyperlipidemia-associated intestinal microbial imbalance. Liver transcriptomic and plasma metabolomic analyses demonstrated that royal jelly acid regulated genes involved in glycolipid metabolism, oxidative stress, and inflammatory responses, as well as multiple key metabolites. Integrated multi-omics analysis and molecular docking confirmed that the glycerophospholipid metabolic pathway represents the core metabolic axis mediating these protective effects. Royal jelly acid mainly alleviates hyperlipidemia by enhancing antioxidant and anti-inflammatory defense through the gut–liver axis–mediated SCFAs–glycerophospholipid pathway. These findings support the use of royal jelly acid as a promising MUFA-based therapeutic strategy for hyperlipidemia and provide a scientific basis for its application.
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高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
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2024
·Vol. 22
·期 1
·1-17
·
IF 10.6
Li Nannan,Niu Lili,Liu Yao,Wang Yang,Su Xiaomin,Xu Ce,Sun Zanya,Guo Huishu,Gong Jingru,Shen Shun
Background Colorectal cancer (CRC) incidence is increasing in recent years due to intestinal flora imbalance, making oral probiotics a hotspot for research. However, numerous studies related to intestinal flora regulation ignore its internal mechanisms without in-depth research.Results Here, we developed a probiotic microgel delivery system (L.r@(SA-CS)2) through the layer-by-layer encapsulation technology of alginate (SA) and chitosan (CS) to improve gut microbiota dysbiosis and enhance anti-tumor therapeutic effect. Short chain fatty acids (SCFAs) produced by L.r have direct anti-tumor effects. Additionally, it reduces harmful bacteria such as Proteobacteria and Fusobacteriota, and through bacteria mutualophy increases beneficial bacteria such as Bacteroidota and Firmicutes which produce butyric acid. By binding to the G protein-coupled receptor 109A (GPR109A) on the surface of colonic epithelial cells, butyric acid can induce apoptosis in abnormal cells. Due to the low expression of GPR109A in colon cancer cells, MK-6892 (MK) can be used to stimulate GPR109A. With increased production of butyrate, activated GPR109A is able to bind more butyrate, which further promotes apoptosis of cancer cells and triggers an antitumor response.Conclusion It appears that the oral administration of L.r@(SA-CS)2 microgels may provide a treatment option for CRC by modifying the gut microbiota.
研究领域:
肿瘤学
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微生物学
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药学
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生物技术
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DOI
PubMed
高影响因子
npj Biofilms and Microbiomes
·
2026
·
IF 11.4
Liangliang Guo,Xiaoqi Pei,Jiajian Tan,Haiqing Sun,Siwen Jiang,Hongkui Wei,Jian Peng
The gut microbiota plays a vital role in host reproduction, yet its contribution to semen quality in boars remains unclear. In this study, we analyzed 556 boars from three commercial breeds and identified Muribaculaceae as a key microbial taxon positively associated with sperm quality, with the effect mediated by short-chain fatty acids (SCFAs). This association was validated in Yorkshire boars with extreme semen phenotypes. Fecal microbiota transplantation in mice confirmed that enrichment of Muribaculaceae improved semen quality, likely through enhanced SCFA production and reduced inflammation in the gut and reproductive tract. Furthermore, in vitro fermentation and mouse experiments demonstrated that a designed functional fiber selectively promoted Muribaculaceae , increased SCFA levels, and improved sperm quality. These findings suggest a functionally supported and potentially translational association between gut microbiota and boar fertility, suggesting that targeted dietary modulation of Muribaculaceae may represent a novel strategy to enhance reproductive performance in livestock.
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DOI
PubMed
高影响因子
Frontiers in Microbiology
·
2019
·
IF 4.259
Zhang Jian-Mei,Sun Yin-Shuang,Zhao Li-Qin,Chen Tian-Tian,Fan Mei-Na,Jiao Hong-Chao,Zhao Jing-Peng,Wang Xiao-Juan,Li Fu-Chang,Li Hai-Fang,Lin Hai
The impact of gut microbiota and its metabolites on fat metabolism have been widely reported in human and animals. However, the critical mediators and the signal transductions are not well demonstrated. As ovipara, chicken represents a specific case in lipid metabolism that liver is the main site of lipid synthesis. The aim of this study is to elucidate the linkage of gut microbiota and fat synthesis in broiler chickens. The broilers were subjected to dietary treatments of combined probiotics (Animal bifidobacterium: 4 × 108 cfu/kg; Lactobacillus plantarum: 2 × 108 cfu/kg; Enterococcus faecalis: 2 × 108 cfu/kg; Clostridium butyrate: 2 × 108 cfu/kg, PB) and guar gum (1 g/kg, GG), respectively. Results showed that dietary supplementation of PB and GG changed the cecal microbiota diversity, altered short chain fatty acids (SCFAs) contents, and suppressed lipogenesis. In intestinal epithelial cells (IECs), SCFAs (acetate, propionate, and butyrate) up-regulated the expression of glucagon-like peptide-1 (GLP-1) via mitogen-activated protein kinase (MAPK) pathways, mainly via the phospho - extracellular regulated protein kinase (ERK) and phospho-p38 mitogen activated protein kinase (p38 MAPK) pathways. GLP-1 suppressed lipid accumulation in primary hepatocytes with the involvement of (AMP)-activated protein kinase/Acetyl CoA carboxylase (AMPK/ACC) signaling. In conclusion, the result suggests that SCFAs-induced GLP-1 secretion via MAPK pathway, which links the regulation of gut microbiota on hepatic lipogenesis in chickens.
研究领域:
动物营养学
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微生物学
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分子生物学
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生理学
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DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2025
·
IF 8.5
Yanhui Zhang,Fangmin Chen,Jin Feng,Fang Wang,Ling Xiong,Luanfeng Wang,Xinchun Shen,Haizhao Song
Polysaccharides, particularly those with prebiotic functions, have profound effects on human health. This study aimed to elucidate the stability and prebiotic potential of a polysaccharide derived from Momordica charantia L. (MCPS-3) through a comprehensive analysis of its behavior during simulated digestion and fermentation. Our findings indicated that MCPS-3 maintained its structural integrity during oral, gastric, and intestinal digestion. This was evidenced by the consistent reducing sugar content, molecular weight, and monosaccharide composition. This stability confirmed that the glycosidic bonds of MCPS-3 remained intact throughout digestion. Then, MCPS-3 underwent fermentation by gut microbiota, resulting in significant production of short-chain fatty acids (SCFAs) and a notable change in microbiota composition. Specifically, the fermentation of MCPS-3 leads to an increase in beneficial SCFAs-producing genera, while decreasing the presence of harmful bacteria. These changes suggested an improved gut environment, which is conducive to health benefits. The study further demonstrated that the fermentation products of MCPS-3 possessed substantial anti-inflammatory properties. This was indicated by the reduction of pro-inflammatory mediators and the enhancement of anti-inflammatory cytokines in LPS-stimulated RAW 264.7 macrophage cells. These results underscored MCPS-3's promise as a prebiotic candidate with potential applications in gut health promotion and inflammation modulation.
研究领域:
食品科学
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微生物学
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营养学
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免疫学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2026
·
IF 8.7
Qiang-Ming Li,Qiao-Qiao Zhang-Yang,Ya-Yi Tan,Xiang-Ling Wu,Xue-Qiang Zha,Zhen-Zi Shang,Jian-Ping Luo,Feng-Yun Zhang
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. The stem of Dendrobium huoshanense is a traditional medicinal food. This study aimed to investigate the effect of cultivated D. huoshanense stem polysaccharide (cDHPS) on AD and elucidate its mechanisms using an Aβ 1–42 -induced AD mouse model. Results showed that cDHPS significantly improved the cognitive dysfunction and ameliorated the hippocampal neuronal injury of AD mice. Meanwhile, cDHPS effectively alleviated the neuroinflammation of AD mice not only by decreasing the expression of caspase-1, NOD-like receptor family pyrin domain-containing 3 (NLRP3), and apoptosis-associated speck-like protein containing a CARD (ASC), as well as their downstream inflammatory cytokines, but also by inhibiting the activation of microglia and astrocytes. Furthermore, the levels of glucagon-like peptide-1 (GLP-1) in the hippocampus, plasma, and intestine of AD mice were markedly elevated by cDHPS, along with an increase in intestinal short-chain fatty acids (SCFAs) levels. However, the treatment of exendin 9–39, a GLP-1 receptor antagonist, weakened the protective effect of cDHPS against AD, and the depletion of SCFAs reversed the beneficial effects of cDHPS on cognitive dysfunction, hippocampal neuronal injury, neuroinflammation, and GLP-1 secretion in AD mice. These results suggest that cDHPS could protect against AD by modulating the SCFAs/GLP-1 axis-mediated neuroinflammation suppression.
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高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2026
·
IF 6.7
Zhang Qile,Zhou Zhengming,Cheung Yiu Ming,Yeung Hoi Wa,Li Minghui,He Chufeng,Huang Shouhe,Li Cheng,Chen Zhen-Yu,Wong Wing Tak
Exploring alternative staple foods
supports food security,
yet
fresh potatoes have storage and palatability limitations. Potato turned
rice (PTR), a processed potato product to overcome these drawbacks,
may benefit gut health, but its anticolitis effects and underlying
mechanisms remain unclear. This study investigated PTR’s physicochemical
properties, gut microbiota modulation, and protection against dextran
sulfate sodium (DSS)-induced colitis. PTR retained a stable postcooking
V-type crystalline structure of type 5 resistant starch (RS5), distinct
from normal rice (NRC). Long-term PTR intake elevated gut microbial
α diversity and enriched beneficial genera. In colitis mice,
PTR alleviated symptoms, preserved intestinal barrier, promoted short-chain
fatty acids (SCFAs), and restored bile acid metabolism via farnesoid
X receptor (FXR) upregulation. Antibiotic-induced microbiota depletion
abolished PTR’s benefits, while fecal microbiota transplantation
(FMT) from PTR-fed donors transferred colitis protection. Collectively,
PTR alleviates colitis through the gut microbiota–SCFAs–bile
acid axis, showing potential as a gut-beneficial functional staple.
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DOI
高影响因子
PHYTOMEDICINE
·
2024
·
IF 6.7
Ying-Jie Dong,Yi-Piao Zhang,Xiao-Feng Jiang,Zhi-Yi Xie,Bo Li,Ning-Hua Jiang,Su-Hong Chen,Gui-Yuan Lv
s Background The development of gut-liver axis metabolic immune crosstalk is intimately associated with intestinal barrier disorder, intestinal SCFAs-Th17/Treg immunological imbalance, and disorders of the gut microbiota. Prior research has discovered that Dendrobium officinale National Herbal Drink (NHD), a traditional Chinese medicine drink with enhanced immunity, may enhance the immunological response in animals with impaired immune systems brought on by cyclophosphamide by repairing intestinal barrier function and controlling turbulence in the gut microbiota. However, whether NHD can further improve the gut-liver axis metabolic immune crosstalk and its related mechanisms need to be systematically studied. Objectives The purpose of this study is to clarify the function and mechanism of NHD in enhancing the gut-liver axis metabolic immunological crosstalk brought on by excessive alcohol intake. Methods In this work, we set up a mouse model to analyze the metabolic and immunological crosstalk involving the gut-liver axis across 7 weeks of continuous, excessive drinking. At the same time, high and low doses (20,10 mL/kg) of NHD were given by gavage. The effect of NHD on improving the metabolism of gut-liver axis was evaluated by blood lipid, liver lipid deposition, liver function and intestinal pathophysiology. By measuring serum immunological indices, intestinal barrier, and intestinal immune barrier, the impact of NHD on enhancing immune and intestinal barrier function was assessed. Furthermore, immunohistochemistry, immunofluorescence, 16s RNA, Western blot, q-PCR and other methods were used to detect gut microbiota, SCFAs-GPR41/43 pathway, intestinal Th17/Treg immune cells and PPAR-α-NPC1L1/SREBP1 pathway to elucidate the mechanism by which NHD enhances the gut-liver axis' metabolic immune crosstalk. Results Our study demonstrated that NHD has the potential to improve the pathophysiological damage caused by gut-liver axis in model mice. NHD also ameliorated the disorder of lipid metabolism. In addition, it regulated the levels of peripheral blood T cell immunity and serum immune factors. And NHD can restore intestinal mechanical and immune barrier damage. NHD has a favorable impact on the quantity of beneficial bacteria, including uncultured_bacterium_g__norank_f__muribaculacea and uncultured_bacterium_g__Turicibacter . Additionally, it raised the model mice's levels of SCFAs (n-butyric acid, isovaleric acid, etc.). This resulted in the promotion of intestinal GPR41/43-ERK1/2 expression and the reshaping of intestinal CD4 + T cell Th17/Treg homeostasis. As a consequence, colon IL-22 and IL-10 levels increased, while colon IL-17A levels decreased. Lastly, NHD raised the amount of intestinal IAP/LPS, regulated the development of PPAR-α-NPC1L1/SREBP1 pathway in gut-liver axis, and improve lipid metabolism disorder. Conclusions Our study found that NHD can improve the gut-liver axis metabolic immune crosstalk in model mice caused by excessive drinking. The mechanism might be connected to how NHD controls gut microbiota disorders in model mice, the activation of intestinal SCFAs-GPR41/43 pathway, the remodeling of Th17/Treg immune homeostasis of intestinal CD4 + T cells, the improvement of IAP/LPS abnormality, and further mediating the PPAR-α-NPC1L1/SREBP1 pathway of lipid metabolism in gut-liver axis.
研究领域:
免疫学
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胃肠病学
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药理学
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微生物学
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代谢组学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Xinglishang He,Wanfeng Xu,Linzi Li,Xiaofeng Jiang,Yingjie Dong,Kun Liu,Xiaojie Feng,Jie Su,Bo Li,Guiyuan Lv,Suhong Chen
Ethnopharmacological relevance Polygonatum Rhizoma Ginseng Formula (HJRS) is a traditional Chinese medicine preparation commonly used to enhance immunity. Traditionally, it is believed to “moisten dryness and nourish yin, tonify the spleen, and benefit qi.” However, a systematic evaluation of its efficacy and mechanism of action is still lacking. Aim of the study To explore the pharmacodynamic effects and underlying mechanisms of HJRS in cyclophosphamide (CTX)-induced immunocompromised model mice. Method To explore the immunomodulatory effects of HJRS, we used cyberpharmacology combined with in vivo experiments. An immunocompromised mouse model was established using CTX, and different doses of HJRS were administered by gavage during the modeling period. The efficacy of HJRS was evaluated by assessing immune-related parameters, including body weight, heat pain threshold, and behavioral activity. Biochemical markers (acid phosphatase, total nitric oxide synthase, and lactate dehydrogenase), immune function indicators (C3, C4, secretory immunoglobulin A [sIgA]), and immune organ indices (spleen and thymus coefficients) were measured. Additionally, intestinal mucosal immunity (Peyer’s patches, sIgA, and IgM), cellular immunity (delayed-type hypersensitivity [DTH]), and humoral immunity (serum hemolysin, hemolysin, and IgM) were analyzed in the model mice. To further investigate the underlying mechanisms, we used 16S RNA sequencing, western blotting, gas chromatography-mass spectrometry, and other techniques to examine the intestinal microbiota, the short-chain fatty acids–G protein-coupled receptor 41 (SCFAs-GPR41) pathway, and the downstream mitogen-activated protein kinase (MAPK) signaling pathway. Result Network pharmacology analysis identified 34 active compounds and predicted 154 potential targets in HJRS that may regulate immune function by interacting with multiple targets (tumor-necrosis factor [TNF], PIK3CG, JUN, AKT1, and MAPK) and immune-related signaling pathways (MAPK and TNF-signaling pathway). Experimental validation demonstrated that HJRS alleviated symptoms of weakness and reduced behavioral activity in the model mice. It significantly enhanced the DTH response, elevated serum hemolysin levels, and restored the balance of white blood cells, lymphocytes, red blood cells, and hemoglobin percentages. HJRS also rebalanced the serum CD3 + CD4 + /CD3 + CD8 + ratio and increased C3 and C4 levels. Furthermore, it improved immune organ function by raising the thymus and spleen coefficients and increasing serum IgA, IgA, and IgM levels. Histopathological examination revealed that HJRS ameliorated CTX-induced pathological damage in the thymus, spleen, and intestines. HJRS regulated gut microbiota composition by enhancing the richness of Bacteroidetes and increasing the Firmicutes/Bacteroidetes ratio, while reducing the abundance of Firmicutes . It decreased the relative abundance of harmful genera, such as Bacteroides and Enterorhabdus , and promoted the growth of beneficial genera, including Muribaculaceae , Clostridia , and Alloprevotella . Additionally, HJRS increased the fecal acetic acid, propionic acid, hexanoic acid, and total SCFA levels in the model mice. It activated the SCFAs-GPR41 pathway and downstream MAPK signaling, thereby enhancing intestinal mucosal immune function. Conclusion HJRS effectively improved immune function in CTX-induced immunocompromised mice. Its mechanism of action may be associated with the regulation of intestinal microbiota dysbiosis, activation of the intestinal “SCFA-GPR41” pathway, and modulation of the downstream MAPK signaling pathway.
研究领域:
民族药理学
·
免疫学
·
分子生物学
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产品关联
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PubMed
高影响因子
危险品化学品经营许可证（带存储）