JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2025
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IF 6.2
Zhouya Bai,Yunhui Zhang,Xiaojun Huang,Denglin Luo,Shaobin Gu,Kangyi Zhang,Shaoping Nie
The gut microbiota is vital in regulating glycolipid metabolism through bile acid pathways, while pectin maintains gut flora balance. Polysaccharides from red kidney beans (RKPs), particularly pectic types, lower blood sugar and lipids, although the mechanism is unclear. Our findings showed that RKP intervention significantly affects primary bile acid synthesis, especially conjugated bile acids, notably taurocholic acid (TCA). Correspondingly, FXR and TGR5 were identified as key receptors in glucolipid metabolism. Further, Akkermansia was proven to be a vital strain and to effectively improve glycolipid metabolism associated with regulating the activity of bile salt hydrolases (BSHs) and bile acid composition, especially for TCA in diabetic mice. Our results provide an antidiabetic mechanism of RKP and suggest that enriched Akkermansia via regulating the vitality of BSH is altered in response to the composition of bile acid, especially for TCA, thereby alleviating glycolipid metabolism through the TCA-FXR/TGR5 axis.
研究领域:
微生物组学
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代谢生物学
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内分泌学
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营养科学
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分子药理学
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胆汁酸代谢
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肠道菌群与宿主互作
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PubMed
高影响因子
Drug Design Development and Therapy
·
2025
·
IF 5.1
Xuehui Deng,Bingfeng Lin,Wenlong Xiao,Fang Wang,Pingcui Xu,Nani Wang
Background Specnuezhenide (SPN) is an iridoid glycoside isolated from Fructus Ligustri Lucidi, an herb prescribed for the treatment of senile osteoporosis. However, the direct role of SPN on bone metabolism remains unclear. In this study, the effects of SPN on d-galactose (d-gal)-induced mice, bone marrow mesenchymal stem cells (BMSCs), and nuclear factor-κB ligand-induced osteoclasts were examined.Methods Micro-computed tomography was used to observe the bone microstructure. Osteogenesis was examined using Western blotting and alkaline phosphatase staining. Osteoclastogenesis was examined using Western blotting and F-actin ring staining. Senescence-associated β-galactosidase was used to detect cell senescence. In addition, the expression of Takeda G protein-coupled receptor 5 (TGR5)/farnesoid X receptor (FXR) signaling pathway-related genes and proteins was determined through quantitative real-time polymerase chain reaction and immunofluorescence.Results Oral administration of SPN improved the bone microstructure in d-gal-induced mice and increased bone mineral density, bone volume, trabecular thickness, and trabecular number. SPN also upregulated the expression of the osteogenesis markers osteocalcin, bone morphogenetic protein 2, and runt-related transcription factor 2 and downregulated the expression of the osteoclasis markers tartrate-resistant acid phosphatase, nuclear factor-κB, and nuclear factor of activated T-cells in the d-gal-induced bone. Furthermore, SPN increased alkaline phosphatase staining, inhibited F-actin ring formation, and reduced the activity of senescence-associated β-galactosidase in vitro. Mechanistically, SPN activated the TGR5/FXR pathway in d-gal-induced BMSCs and osteoclasts. The protective effects of SPN were abolished after addition of the TGR5 inhibitor SBI-115 or FXR inhibitor DY268. Moreover, SPN could elevate the protein and mRNA levels of TGR5, FXR, and the downstream small heterodimer partner in d-gal-induced bone.Conclusion SPN alleviated senile osteoporosis and cell senescence by activating the TGR5/FXR pathway.
研究领域:
药理学
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骨生物学
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分子生物学
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PubMed
高影响因子
MOLECULAR MEDICINE
·
2025
·Vol. 31
·期 1
·1-11
·
IF 6.4
Liu Miao,Xie Wen-jie,Zhang Xu,Wu Wei,Li Guang,Wang Lu
Background Macrophages play an important role in the pathogenesis of ulcerative colitis (UC). We will explore the effects of sodium butyrate (SB) on macrophage function.Methods The targets of butyric acid were identified using SwissTargetPrediction database and surface plasmon resonance (SPR). Limited proteolysis mass spectrometry (Lip-MS) was used to further investigate the binding sites of butyric acid with its targets and molecular docking was employed to simulate their binding modes. Macrophage polarization model was established with lipopolysaccharide (LPS) in vitro. Takeda G protein-coupled receptor 5 (TGR5) and β-arrestin2 expression and macrophage polarization markers were detected with or without SB.Results TGR5 was identified as the target of butyric acid. Moreover, the amino acid regions 275–286 and 321–330 of TGR5 (GPBAR1 [275–286] and GPBAR1 [321–330]) were the potential binding regions for butyric acid. Based on molecular docking analysis, butyric acid formed effective hydrogen-bonding interactions with ASP-284 and TYR-287 of TGR5. In cell experiments, LPS inhibited the expression of TGR5, β-arrestin2, IL-10, ARG1, and CD206 and increased the expression of IL-1β, iNOS, and CD86, while SB reversed the effect of LPS. SBI-115, a TGR5 antagonist, and knockdown of β-arrestin2 inhibited the effect of sodium butyrate. INT-777, a TGR5 agonist, reversed the inhibitory effect of knockdown of β-arrestin2.Conclusion SB inhibited M1-like polarization and promoted M2-like polarization induced by LPS via TGR5/β-arrestin2 in RAW264.7 cells and TGR5 was the target of SB.
研究领域:
免疫学
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药理学
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胃肠病学
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细胞生物学
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PubMed
高影响因子
BIOORGANIC CHEMISTRY
·
2025
·
IF 4.7
Xinyan Shen,Xuemei Shao,Bowei Dong,Yuting Gu,Jingjing Sun,Yujie Zhang,Yan Li,Shuai Zhao,Yanan Hou,Xin Chen,Mingcheng Qian
In this study, we designed and synthesized 12 novel non-steroidal cholic acid (CA) analogues as potential Takeda G protein coupled receptor 5 (TGR5) allosteric agonists based on scaffold hopping strategy. Biological results showed that all final compounds were able to activate the receptor both in human TGR5 (hTGR5) and mouse TGR5 (mTGR5) by Glosensor cAMP accumulation assay. Remarkably, lactone A1 and lactam A10 displayed 48- and 24-fold higher potencies than that of CA in hTGR5 cAMP accumulation, respectively. Furthermore, target compounds exhibited higher selectivity for cAMP formation compared to β-arrestin2 recruitment. Interestingly, target compounds A1–10 positively modulated the functional activity and potency of lithocholic acid (LCA) in TGR5, indicating that A1–10 are TGR5 allosteric agonists. Molecular docking study displayed that both lactone in A5 and lactam in A10 formed H-bonds with the key amino acid residue Thr131, which are critical for TGR5 allosteric effect. Unexpectedly, none of target compounds A1–10 could activate farnesoid X receptor (FXR), indicating that final compounds are potent and selective TGR5 allosteric agonists. More importantly, both A1 and A10 exhibited significant glucose-lowering effects in the oral glucose tolerance test (OGTT) in mice. Taken together, we discovered two potent and selective TGR5 allosteric agonists A1 and A10 , which could be employed as lead compounds to further study TGR5 allostery with potential antidiabetic effects.
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高影响因子
PHYTOMEDICINE
·
2025
·
IF 8.3
Bao-xin Zheng,Yan Yi,Xing-wen Wang,Chun-ying Li,Yong Zhao,Jing-zhuo Tian,Lian-mei Wang,Jia-yin Han,Chen Pan,Su-yan Liu,Chen-yue Liu,Sha-sha Qin,Xuan Tang,Mei-ting Liu,Ai-hua Liang
Background Geniposide (GE) has potential efficacy in treating ulcerative colitis (UC). However, its reactivity can be affected by rapid degradation after oral administration. Furthermore, increasing oral doses may lead to hepatotoxicity. Thus, We used enema administration, characterized by smaller dose and higher localized concentration in the lesion, to improve the above situation. Purpose We aimed to confirm that enema administration is a better modality than oral administration for GE against UC and to explore its mechanism. Study design/Method We established UC mouse model, monitoring Disease Activity Index (DAI), inflammatory cytokines levels, and histopathology. Macrogenomics and bile acid (BAs) metabolomics analysed the major intestinal flora and BAs. Simultaneouslly, we conducted quantitative proteomics analysis and screened core proteins and pathway. In vitro validation was taken by qPCR, immunofluorescence and immunoblotting experiments. Results GE via enema alleviate UC by inhibiting inflammatory factor production through downregulating S100A8/S100A9/NF-κB pathway. Analysis of the intestinal flora and BAs revealed that the enhanced abundance of Lachnospiraceae , which improves the ratio of primary to secondary BAs, and the reduced abundance of Provocaceae , which increases intestinal permeability and promotes inflammation, favored the restoration of the intestinal barrier. In addition, in vitro experiments confirmed that the key BA metabolites (mainly UDCA, DCA, and LCA) stimulated TGR5 signal to inhibit the assembly of the NLRP3 inflammasome and alleviated inflammation. Conclusion We firstly confirmed that GE alleviates UC via the enema route in a better manner than the oral route, through enhancing the intestinal barrier, restoring intestinal flora and BAs homeostasis, and inhibiting inflammatory injury. This study initially revealed that GE can alleviate UC through elevating UDCA, DCA, and LCA levels at the colonic site to activate TGR5 receptor for inhibiting the NLRP3 inflammasome, in addition to downregulating the S100A8/S100A9/-TLR4-NF-κB pathway related inflammatory response directly. The evidences offer a promising strategy and profround meaning for UC treatment.
研究领域:
药理学
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免疫学
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微生物学
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代谢组学
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PubMed
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METABOLISM-CLINICAL AND EXPERIMENTAL
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2025
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IF 11.9
Long Xu,Xinyan Wu,Luosha Long,Suchun Li,Meiying Huang,Meng Li,Pinning Feng,Moshe Levi,Wei Chen,Lei Wang,Chunling Li,Weidong Wang
Epithelial sodium channel (ENaC), located in the collecting duct principal cells of the kidney, is responsible for the reabsorption of sodium and plays a critical role in the regulation of extracellular fluid volume and consequently blood pressure. The G protein-coupled bile acid receptor (TGR5) is a membrane receptor mediating effects of bile acid and is implicated in kidney diseases. The current study aims to investigate whether TGR5 activation in the kidney regulated ENaC expression and potential mechanism. Lithocholic acid (LCA), a TGR5 agonist, markedly decreased systolic blood pressure induced by DOCA-salt in mice, which was associated with decreased ENaC expression in the kidney. DOCA-salt treatment increased renal expression of histone H3 lysine 4 trimethylation (H3K4me3) and decreased expression of lysine-specific demethylase 5A (KDM5A), a lysine demethylase, which was markedly reversed by LCA. TGR5 knockout caused further increased systolic blood pressure and ENaC expression in mice with DOCA-salt in association with increased H3K4me3 and decreased KDM5A. In immortalized mouse cortical collecting duct (mpkCCD) cells LCA markedly inhibited aldosterone-induced ENaC-mediated current. LCA treatment or TGR5 overexpression markedly inhibited ENaC and H3K4me3 protein expression in association with decreased KDM5A in mpkCCD cells treated with either aldosterone or angiotensin II. Inhibition or knockdown of KDM5A in mpkCCD cells prevented LCA-induced downregulation of ENaC expression by promoting H3K4me3 on the ENaC transcription start site. LCA upregulated KDM5A expression was likely through JNK/c-Jun signal pathway. In conclusion, LCA decreased blood pressure and ENaC protein expression in the kidney of mice with DOCA-salt, likely through activating TGR5 and upregulating KDM5A-induced H3K4me3 demethylation in ENaC promoter region.
研究领域:
肾病学
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分子生物学
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药理学
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PubMed
高影响因子
Frontiers in Pharmacology
·
2024
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IF 4.4
Wang Jiahua,Zang Juan,Yu Yang,Liu Yang,Cao Huimin,Guo Ruibo,Zhang Lu,Liu Mo,Zhang Zixu,Li Xuetao,Kong Liang
Background: The preservation of the Lingguizhugan (LGZG) decoction and patient compliance issue often limit the treatment of metabolic dysfunction-associated steatotic liver disease (MASLD). Hence, herein, an LGZG oral solution was developed for alleviating MASLD. Additionally, the potential mechanisms underlying LGZG-mediated MASLD mitigation were explored.Methods: A MASLD mouse model was constructed using oleic and palmitic acid-induced LO2 cells and a high-fat diet. The apoptosis, lipid deposition, and mouse liver function were analyzed to assess the therapeutic effects of the LGZG oral solution on MASLD. Serum untargeted metabolomics, gut microbiota, bile acid (BA) metabolism, immunohistochemistry, and Western blotting analyses were performed to investigate the potential mechanism of action of LGZG oral solution on MASLD.Results: The LGZG oral solution ameliorated lipid deposition, oxidative stress, inflammation, and pathological damage. Serum untargeted metabolomics results revealed the LGZG-mediated regulation of the primary BA biosynthetic pathway. The 16S ribosomal RNA sequencing of the fecal microbiota showed that LGZG oral solution increased the relative abundance of the BA metabolism-associated Bacteroides, Akkermansia, and decreased that of Lactobacillus. Additionally, the BA metabolism analysis results revealed a decrease in the total taurine-α/β-muricholic acid levels, whereas those of deoxycholic acid were increased, which activated specific receptors in the liver and ileum, including farnesoid X receptor (FXR) and takeda G protein-coupled receptor 5 (TGR5). Activation of FXR resulted in an increase in short heterodimer partner and subsequent inhibition of cholesterol 7α-hydroxylase and sterol regulatory element-binding protein-1c expression, and activation of FXR also results in the upregulation of fibroblast growth factor 15/19 expression, and consequently inhibition of cholesterol 7α-hydroxylase, which correlated with hepatic BA synthesis and lipogenesis, ultimately attenuating lipid deposition and bile acid stasis, thereby improving MASLD.Conclusion: Altogether, the findings of this study suggest that modulating microbiota–BA–FXR/TGR5 signaling pathway may be a potential mechanism of action of LGZG oral solution for the treatment of MASLD.
研究领域:
药理学
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肝病学
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代谢学
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微生物学
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分子生物学
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PubMed
高影响因子
Journal of Pharmaceutical Analysis
·
2024
·
IF 6.1
Huanhuan Xue,Peijie Li,Jing Guo,Tinggui Chen,Shifei Li,Liwei Zhang
Ulcerative colitis (UC) is an idiopathic, relapsing, and etiologically complicated chronic inflammatory bowel disease. Despite substantial progress in the management of UC, the outcomes of mucosal barrier repair are unsatisfactory. In this study, phillygenin (PHI) treatment alleviated the symptoms of chronic colitis in mice, including body weight loss, severe disease activity index scores, colon shortening, splenomegaly, oxidative stress, and inflammatory response. In particular, PHI treatment ameliorated the tight junction proteins (TJs) reduction, fibrosis, apoptosis, and intestinal stem cell activity, indicating that PHI exerted beneficial effects on the intestinal mucosal barrier in mice with chronic colitis. In the NCM460 cells damage model, dextran sulfate sodium triggered the sequential induction of TJs reduction, fibrosis, and apoptosis. Takeda G protein-coupled receptor-5 (TGR5) dysfunction mediated NCM460 cell injury. Moreover, PHI treatment enhanced TJs and suppressed fibrosis and apoptosis to maintain NCM460 cell function, depending on TGR5 activation. PHI promoted TGR5 activation and elevated intracellular cyclic adenosine monophosphate levels in HEK 293T cells transfected with TGR5 expression plasmids. Cellular thermal shift assay and molecular docking studies confirmed that PHI directly binds to TGR5, indicating that PHI is an agonist of TGR5. The process of PERK-eIF2α pathway-mediated endoplasmic reticulum Ca 2+ release was involved in NCM460 cell injury as well, which was associated with TGR5 dysfunction. When NCM460 cells were pretreated with PHI, the PERK-eIF2α pathway and elevated Ca 2+ levels were blocked. In conclusion, our study demonstrated a novel mechanism that PHI inhibited the PERK-eIF2α-Ca 2+ pathway through TGR5 activation to against DSS-induced TJs reduction, fibrosis, and apoptosis.
研究领域:
胃肠病学
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药理学
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细胞生物学
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炎症性肠病
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DOI
PubMed
高影响因子
BIOORGANIC CHEMISTRY
·
2026
·
IF 5.1
Sheng-Li Wu,Xiao-Feng He,Pianchou Gongpan,Xiao-Yan Huang,Chang-An Geng
DCA stimulated GLP-1 secretion in STC-1 and NCI-H716 cells. • DCA decreased fasting blood glucose levels by promoting GLP-1 secretion in db/db mice. • DCA ameliorated glucose intolerance and insulin resistance and lowered serum TC levels. • DCA promoted GLP-1 secretion through specific activation on TGR5/PKA/MEK/ERK pathway. Type 2 diabetes mellitus (T2DM) is a heterogeneous metabolic disorder characterized by insulin resistance and progressive β cell dysfunction. Deoxycalyxin A (DCA), a unique diarylheptanoid-chalcone hybrid isolated from Alpinia katsumadai , was identified as a novel stimulator of GLP 1 secretion in both STC-1 (EC 50 : 10.7 μM) and NCI-H716 (EC 50 : 13.4 μM) cells. Oral administration of DCA (40 and 80 mg/kg) in db/db mice significantly reduced fasting blood glucose, ameliorated glucose intolerance and insulin resistance by enhancing endogenous GLP-1 secretion, and lowered the total serum cholesterol levels. Mechanistic study demonstrated that DCA identify the TGR5 receptor, which induces a significant increase in intracellular cyclic AMP (cAMP) levels, which activates PKA with subsequent sequential phosphorylation of MEK1/2 and ERK activation, ultimately enhancing GLP-1 secretion. Our findings identify DCA as a novel TGR5 agonist to stimulate GLP-1 secretion via the TGR5/PKA/MEK/ERK pathway, which has the potential to be developed as a promising antidiabetic lead with a distinct mechanism of action. DCA, a unique diarylheptanoid-chalcone from Alpinia katsumadai , is a novel TGR5 agonist to stimulate GLP-1 secretion via PKA/MEK/ERK pathway, which has the potential to be developed as a promising antidiabetic candidate. Download: Download high-res image (123KB) Download: Download full-size image
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高影响因子
BRITISH JOURNAL OF PHARMACOLOGY
·
2025
·
IF 7.7
Yu-Chen Jiang,Jia Guo,Sai-Hu Liu,Xu Dai,Chen-Yu Wang,Li-Hua Lian,Zhen-Yu Cui,Ji-Xing Nan,Yan-Ling Wu
Background and Purpose Vincamine has extensive biological and pharmaceutical activity. We examined the hepatoprotective effects and mechanisms by which vincamine suppresses hepatic fibrosis. Experimental Approach Hepatic stellate cells (HSCs), TGF- β stimulated, were cultured with either vincamine, farnesoid X receptor (NR1H4; FXR) agonist or antagonist. Further, C57BL/6 mice were given thioacetamide (TAA) to induce hepatic fibrosis and subsequently treated with vincamine or curcumin. Key Results Vincamine regulated the deposition of extracellular matrix (ECM), inflammatory factors and S100A4, and up-regulated FXR and TGR5 (GPBA receptor) in activated HSCs, by activating FXR. FXR deficiency blocked vincamine effect on FXR, TGR5, α -smooth muscle actin ( α -SMA) and IL1R1 in activated LX-2 cells. Vincamine corrected ECM imbalance, inflammatory secretion and FXR/TGR5 down-regulation in activated LX-2 cells with stimulating medium from LPS-primed THP-1 cells. S100A4 deficiency increased FXR and TGR5, and decreased IL-1β expression in activated THP-1. Further, S100A4 deficiency in activated macrophages could elevate FXR and TGR5 expression in activated LX-2, strengthening the impact of vincamine on α -SMA and IL-1β expression. Further, vincamine reduced serum ALT/AST levels, liver and intestinal histopathological changes, and caused ECM accumulation and protected the intestinal barrier in thioacetamide-induced hepatic fibrosis mice. Vincamine decreased inflammatory factors e.g. caspase 1 and IL-1β, and inhibited the S100A4-mediated FXR-TGR5 pathway. Conclusion and Implications Vincamine significantly reverses hepatic fibrosis via inhibiting S100A4 involved in the crosstalk between macrophages and HSCs, and by activating the FXR-TGR5 pathway. Targeting the S100A4-mediated FXR dependence on modulating the liver environment may be the key target of vincamine in inhibiting hepatic fibrosis. Graphical
研究领域:
药理学
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肝脏病学
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分子生物学
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DOI
PubMed
高影响因子
Frontiers in Immunology
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2025
·
IF 5.9
Yang Yuexiang,Rong Zhiwei,Baitian Li,Wang Qing,Liu Chunzheng,Wang Zetian,Liao Lijun
Introduction Sepsis-related acute liver injury (SALI) is a severe and life-threatening complication in septic patients, for which current therapeutic options are limited. This study aimed to investigate the potential protective role of taurochenodeoxycholic acid (TCDCA) against SALI and to elucidate the underlying mechanisms. Methods A cecal ligation and puncture (CLP) mouse model was employed to induce SALI. The effects of TCDCA treatment were assessed by measuring serum liver injury markers (AST, ALT) and pro-inflammatory cytokines (IL-6, TNF-α, IL-1β). Liver histology, hepatocyte apoptosis, and the macrophage response were evaluated. Molecular docking was used to predict the interaction between TCDCA and the receptor TGR5, which was functionally validated using the TGR5 antagonist SBI-115. Transcriptomic analysis and Western blotting were performed to identify the key signaling pathways involved. Results TCDCA treatment significantly reduced serum levels of AST and ALT, suppressed the production of IL-6, TNF-α, and IL-1β, and alleviated histological liver damage, including lobular disruption, inflammation, and hemorrhage. TCDCA also decreased hepatocyte apoptosis and modulated the liver macrophage response. Molecular docking confirmed a strong interaction between TCDCA and TGR5, and the protective effects of TCDCA were abolished by the TGR5 antagonist SBI-115. Transcriptomic analysis identified 430 differentially expressed genes after TCDCA treatment, with significant enrichment in pyroptosis-related pathways. Accordingly, Western blot analysis demonstrated that TCDCA inhibited the activation of the NLRP3 inflammasome and its downstream pyroptotic proteins, an effect that was also reversed by SBI-115. Discussion Our findings demonstrate that TCDCA confers a protective effect against SALI by suppressing hepatocyte pyroptosis, and this action is mediated through the TGR5 receptor. These results highlight TCDCA as a promising therapeutic candidate for SALI. However, further research, including clinical trials, is necessary to address potential species-specific differences and to fully elucidate its comprehensive mechanisms of action.
研究领域:
肝病学
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免疫学
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分子医学
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炎症研究
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重症医学
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高影响因子
Microbial Biotechnology
·
2025
·Vol. 18
·期 11
·e70257
·
IF 5.2
Hui Chen,Fengjiao Wang,Shengjie Li,Longxian Lv,Hao Xu,Jiafeng Xia,Lvwan Xu,Ding Shi,Lanjuan Li
Pediococcus pentosaceus Li05, a strain of lactic acid bacteria isolated from the faeces of healthy volunteers, exhibited potential protective effects against various diseases. This study performed third-generation sequencing and detailed characterisation of its genome. The Li05 chromosome harboured conserved genes associated with acid resistance ( atp ), bile salt resistance ( bsh ), oxidative stress resistance ( hsl , dltA , and et al.), and adhesion ( nrd , gap , and et al.), whereas the plasmid did not contain antibiotic resistance or virulence genes. Following intervention with Li05 in loperamide-induced constipated mice, constipation symptoms improved. Meanwhile, alterations in gut microbiota, increased BSH activity in faeces, and modifications to the faecal bile acid profile were observed. Additionally, expression levels of TGR5 and TPH1 in the colon of the mice increased, leading to elevated 5-HT levels. When the TGR5 gene was knocked out or the TPH1 inhibitor LX1606 was administered to suppress 5-HT synthesis in constipated mice, the beneficial effects of Li05 on gastrointestinal motility and mucus secretion were reversed. Culturing intestinal organoids demonstrated that increased bile acids such as DCA, Iso-LCA, and EALCA could enhance 5-HT levels through the TGR5/TPH1 axis. Therefore, we concluded that Li05 regulated bile acid metabolism, subsequently increasing 5-HT levels through the TGR5/TPH1 axis, thus alleviating constipation. Graphical The mechanism of Li05 in alleviating constipation. Li05 intervention regulated gut microbiota and bile acid metabolism, increasing 5-HT levels through the TGR5/TPH1 activation to ameliorate constipation.
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高影响因子
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