Food & Function最新文献

{"title":"Protective effects of Katsuwonus pelamis hydrolysates against renal injury: Val-Lys as a potent renoprotective peptide†","authors":"Ying Cheng, Mingjie Zhou, Zishan Hong, Lin Zheng and Mouming Zhao","doi":"10.1039/D5FO01092F","DOIUrl":"10.1039/D5FO01092F","url":null,"abstract":"<p >Elevated serum uric acid (UA), a hallmark of diet-induced metabolic dysregulation, induces renal inflammation and oxidative stress, progressively leading to irreversible kidney injury (KI). Although <em>Katsuwonus pelamis</em> hydrolysates (KPHs) exhibit UA-lowering activity, their potential renoprotective effects remain unknown. In this work, KPHs ameliorating UA-induced HK-2 cell injury <em>in vitro</em> were first obtained by controlled enzymatic hydrolysis. Among them, KPHs with a high degree of hydrolysis (DH) showed relatively better activity in enhancing antioxidant enzyme activities and inhibiting the release of cytokines. Utilizing a sophisticated amalgamation of peptidomics, multivariate statistical analysis, and the random forest model, we successfully screened 13 potential renoprotective peptides, among which VK (Val-Lys) had the highest abundance in Pap-H (prepared using Papain with a high DH). <em>In vitro</em> results revealed that VK protected UA-induced HK-2 cells from injury through antioxidant defense. <em>In vivo</em> results demonstrated that VK effectively ameliorated pathological renal injury in KI rats, partially restoring kidney function, as evidenced by significant reductions in serum UA and creatinine levels. Network pharmacology analysis of the underlying mechanisms further indicated that VK might exert renoprotective effects by regulating IL-17 and TNF signaling pathways. Remarkably, our study reveals that VK functions as a potent renoprotective peptide, which may partially account for the superior renoprotective efficacy observed in KPHs.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 13","pages":" 5616-5631"},"PeriodicalIF":5.1,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive analysis of yak milk residue peptides for anti-hypoxic functional foods: targeting neuroinflammation and apoptosis in hypoxic mice†","authors":"Feiyan Yang, Zhang Luo, Zhongxing Chu, Zeyu He, Zuomin Hu, Guangfan Qu, Yaping Zhou, Yiping Tang, Shuguo Sun and Feijun Luo","doi":"10.1039/D5FO01223F","DOIUrl":"10.1039/D5FO01223F","url":null,"abstract":"<p >The hypoxia-induced stress response constitutes a physiological disorder that poses a significant, life-threatening risk. This study aims to investigate the anti-hypoxic brain injury effects of peptides derived from yak milk residue and elucidate their underlying mechanisms. Peptidomic analysis identified three bioactive peptides (YPFPGPIPN, PVVPPFLQPEVMGVSK, and T3-LVYPFPGPIPN (T3)) associated with anti-hypoxic activity. <em>In vitro</em> blood–brain barrier (BBB) modeling demonstrated that T3 exhibited significant time- and concentration-dependent permeability. Under hypoxic stress, T3 effectively inhibited neuronal inflammation and apoptosis. Integrated metabolomics and transcriptomics analyses revealed that T3 mitigates hypoxia-induced neuroinflammation by regulating <small>L</small>-glutamine metabolism through the RAS/TNF-α/MAPK signaling pathway. These findings underscore the potential of yak milk residue-derived peptide (T3) as a neuroprotective agent against hypoxic injury. The insights gained from this research are instrumental in utilizing yak milk byproducts and developing functional foods with anti-hypoxia properties, thereby addressing the market needs of specific demographic groups.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 13","pages":" 5632-5651"},"PeriodicalIF":5.1,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"d-Tagatose attenuates DSS-induced ulcerative colitis by inhibiting inflammation, reducing intestinal barrier damage and modulating the intestinal flora composition†","authors":"Le Wang, Houzhen Lu, Haitao Gui, Zifu Ni, Zhongke Sun, Zihua Wang, Zhihua Wang, Xuanyan Liu and Qipeng Yuan","doi":"10.1039/D4FO06475E","DOIUrl":"10.1039/D4FO06475E","url":null,"abstract":"<p >Ulcerative colitis (UC) is a prevalent inflammatory bowel disease (IBD) posing a significant health threat. This study explored the protective effects of <small>D</small>-tagatose against DSS-induced colitis in mice and its underlying mechanisms using H&amp;E staining, AB-PAS staining, immunofluorescence, immunohistochemistry, ELISA, qPCR, western blotting, and other assays. <small>D</small>-Tagatose improved colitis by increasing body weight and colon length, with decreased DAI (disease activity index) and histopathological scores. The results showed that <small>D</small>-tagatose inhibited the secretion of myeloperoxidase (MPO), inflammatory enzymes (iNOS and COX-2) and pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) as well as increased the content of anti-inflammatory cytokines (IL-10) <em>in vitro</em>. In addition, <small>D</small>-tagatose enhanced the expression of tight junction proteins (ZO-1 and Occludin) and mucin (MUC-2). Furthermore, <small>D</small>-tagatose was able to modulate the gut microbiota dysbiosis caused by DSS-induced UC and increased the content of short-chain fatty acids (SCFAs). This study indicated that <small>D</small>-tagatose attenuated DSS-induced UC by modulating inflammatory cytokines, restoring intestinal barrier function, maintaining gut microbiota homeostasis, and enhancing SCFA production. These findings provide <small>D</small>-tagatose as a safe and effective novel functional food strategy for the prevention and treatment of UC.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 13","pages":" 5556-5572"},"PeriodicalIF":5.1,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2′-Fucosyllactose evokes colonization of Alloprevotella and alleviates renal injury in hyperuricemia mice†","authors":"Yifan Lei, Shuyan Sun, Liping Chen and Yongzhong Wang","doi":"10.1039/D5FO00580A","DOIUrl":"10.1039/D5FO00580A","url":null,"abstract":"<p >Hyperuricemia (HUA) is a metabolic disease characterized by the overproduction of uric acid (UA) in the blood, with an increasing prevalence of associated renal injury. Intestinal microbiota and its associated metabolites are important mediators in the gut–kidney axis that can induce renal impairment. This study investigated the effect of 2′-fucosyllactose (2′FL) on HUA and its underlying mechanisms. In a hyperuricemic <em>Caenorhabditis elegans</em> model, 2′FL reduced the xanthine-induced UA levels and oxidative stress. In a HUA mice model induced with potassium oxonate and UA, 2′FL intervention (200 mg per kg body weight per d) improved UA metabolism and decreased the serum UA concentration, xanthine oxidase activity, blood urea nitrogen, and creatinine levels. 2′FL also alleviated renal injury, inflammatory response and oxidative stress, as evidenced by the reduced lipopolysaccharide, interleukin-6, and malondialdehyde levels and myeloperoxidase activity and increased interleukin-10 level and total antioxidant capacity. 2′FL enhanced renal UA excretion by upregulating ATP-binding cassette subfamily G member 2 (ABCG2) expression and downregulating urate transporter 1 (URAT1) expression. It inhibited renal ferroptosis by restoring the nuclear factor erythroid 2-related factor 2 (Nrf2)/glutathione peroxidase 4 (GPX4) pathway and alleviated renal injury. In the gut, 2′FL protected the intestinal barrier, increased fecal short-chain fatty acids, and modulated intestinal microbiota composition. In particular, it reversed the HUA-induced changes in the <em>Firmicutes</em>/<em>Bacteroidetes</em> ratio and affected the abundance of certain genera correlated with UA metabolism. These findings suggest that 2′FL is a potential natural agent for HUA treatment with multiple beneficial effects on metabolism, renal function, and gut microbiota.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 13","pages":" 5586-5600"},"PeriodicalIF":5.1,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144323891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary strategies for appetite regulation: satiety and obesity management","authors":"Pengkui Xia, Bin Li, Yudie Yu, Wanxu Yu, Mahmoud Youssef, Tao Hou and Jing Li","doi":"10.1039/D5FO01349F","DOIUrl":"10.1039/D5FO01349F","url":null,"abstract":"<p >Increased prevalence of diseases associated with obesity has driven research into appetite suppression to reduce high-calorie intake. Dietary modulation of appetite is recognized as one of the most significant and effective ways to reduce the risk of obesity-related diseases. This review evaluates the roles of dietary nutrients and their metabolites in satiety and proposes dietary strategies for appetite regulation. Brain circuits of hunger, hormones and organs that directly control the appetite, and the role of gut microbiota in indirect appetite modulation are discussed in detail. We explored the impact of dietary nutrients and their metabolites on appetite, based on the basic mechanics of hunger. Additionally, based on the impact of different dietary factors on satiety, we outlined three strategies for appetite regulation: systems for controlled nutrient delivery to decelerate digestion, alteration of dietary physicochemical characteristics, and establishment of dietary rhythms. This review presents a theoretical framework for examining the influence of dietary nutrition on appetite regulation.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 13","pages":" 5202-5218"},"PeriodicalIF":5.1,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Untargeted metabolomics reveals the inhibition effect of a high-fat diet on colorectal cancer tumorigenesis in obesity-resistant mice via regulating bile acid, glutathione, and glycerophospholipid metabolisms†","authors":"Qi Cheng, Kun Na, Chunsheng Xu, He Peng, Xiaojian Lin, Jiajun Chen, Yan Li, Die Wu, Menghao Du and Xingya Wang","doi":"10.1039/D4FO06132B","DOIUrl":"10.1039/D4FO06132B","url":null,"abstract":"<p >The interplay between high fat intake and cancer is complex and multifaceted. Contradictory results exist between obesity, high-fat diet (HFD), and colorectal cancer (CRC), necessitating further research. In this study, we investigated the effect of HFD on tumorigenesis in obesity-resistant and obesity-susceptible mouse models. Our results revealed that HFD significantly inhibited CRC HCT116 and HT-29 xenograft tumor growth in obesity-resistant BALB/c nude mice in comparison with a low-fat diet (LFD). HFD feeding did not induce increases in body weight, serum pro-inflammatory cytokines, and lipid accumulation in the liver and white adipose tissue (WAT) in nude mice. However, HFD promoted tumor growth in melanoma B16-F10-bearing C57BL/6J mice, accompanied by obesity and increased pro-inflammatory cytokine levels. Untargeted metabolomics showed that HFD induced significantly changed metabolites in serum, tumor, and liver samples of the HCT116 xenograft model. In all samples, many glycerophospholipids (<em>e.g.</em> LysoPE (0:0/20:1) and LysoPC (16:1)) and bile acids (<em>e.g.</em> glycocholic acid and chenodeoxycholic acid) were significantly reduced by HFD. Enrichment and pathway analyses suggested that bile acid biosynthesis and metabolisms of lipids, amino acids, and organic acids were significantly regulated by HFD. Additionally, the glutathione metabolism was significantly downregulated, while the TCA cycle was upregulated by HFD in tumor samples. Moreover, univariate and multivariate analyses on the differential metabolites in tumors suggested that uracil, chenodeoxycholic acid, glutathione, LysoPE (0:0/20:1), and SM (d18:1/18:0) were the main metabolite biomarkers for discrimination between LFD- and HFD-fed xenograft tumors. These findings suggest that HFD elicits an anti-tumorigenic effect against CRC in obesity-resistant BALB/c nude mice <em>via</em> regulating bile acid, glutathione, and glycerophospholipid metabolisms.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 13","pages":" 5526-5542"},"PeriodicalIF":5.1,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperoside promotes autophagy of colonic epithelial cells to protect intestinal barrier function in ulcerative colitis†","authors":"Wenxin Xia, Haochang Lin, Jing Zhang, Yawen Bai, Zhifeng Wei, Huatou Zhao, Yufeng Xia and Yue Dai","doi":"10.1039/D5FO00256G","DOIUrl":"10.1039/D5FO00256G","url":null,"abstract":"<p >Intestinal barrier defects represent a significant contributor to the development and progression of ulcerative colitis (UC). This study examined the protective effect of hyperoside (Hyp), a naturally occurring flavonol glycoside with anti-colitis potential, on intestinal barrier, and explored the underlying mechanisms based on the expression of barrier-related proteins. In mice with dextran sulfate sodium (DSS)-induced colitis, Hyp, orally administered, maintained the intestinal barrier integrity, evidenced by reducing intestinal permeability and elevating expression of the proteins relevant to tight junction (occludin and claudin 1) and adhesion junction (E-cadherin and β-catenin). In human colonic epithelial cells, Hyp diminished lipopolysaccharide (LPS)-induced defects of epithelial barrier function, and increased the expression of tight junction- and adhesion junction-related proteins. Hyp promoted the protein degradation of snail, a co-repressor of tight junction proteins, which was reversed by treatment of chloroquine (the autophagy inhibitor) but not MG132 (the ubiquitin-proteasome inhibitor). Consistently, Hyp rescued LPS-reduced autophagy, restored the formation of autophagosomes and autophagic lysosomes, and increased the expression of Beclin-1, ATG 5, ATG7, and LC3 II/I. Combination with chloroquine significantly attenuated up-regulation of Hyp on transmembrane electrical resistance and down-regulation of epithelial permeability. In mice with colitis, the protection against intestinal barrier and the promotion of expression of tight junction and adhesion junction proteins by Hyp was nearly completely reversed by chloroquine. These findings highlight the protective role of Hyp in the colonic mucosal barrier and provide new insights into the development of innovative strategies for the treatment of UC.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 13","pages":" 5543-5555"},"PeriodicalIF":5.1,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phenethyl isothiocyanate modulates macrophage migration inhibitory factor and suppresses malignant phenotypes of glioblastoma cells†","authors":"Jeng-Rong Lin, Wen-Chieh Liao, Yin-Hung Chu, Yu-Cheng Chou and Chiung-Hui Liu","doi":"10.1039/D5FO00415B","DOIUrl":"10.1039/D5FO00415B","url":null,"abstract":"<p >Phenethyl Isothiocyanate (PEITC) is a well-studied compound within the isothiocyanate family. Accumulating evidence indicates that PEITC induces apoptosis and inhibits the growth of various cancer cells <em>in vitro</em>, including aggressive glioblastoma cells. However, its tumor suppression effects and mechanisms <em>in vivo</em> remain largely unexplored. In this study, we utilized cell culture experiments and an orthotopic transplant brain tumor model in mice to evaluate the impact of PEITC on tumor growth, physiological changes, and immune cell populations. Our results showed that PEITC significantly reduced the viability of glioma cells while having moderate effects on astrocytes. <em>In vitro</em>, PEITC effectively inhibited cell viability, migration, and invasion in GL-261 cells. <em>In vivo</em>, PEITC treatment led to prolonged survival rates and reduced tumor volumes in mice without significant toxicity. Notably, PEITC increased the populations of natural killer (NK) cells and natural killer T (NKT) cells in peripheral blood, indicating an immunomodulatory effect. Migration Inhibitory Factor (MIF) was identified as a potential direct target of PEITC. Our findings revealed that PEITC significantly reduced MIF expression in GL-261 cells, both in culture and in orthotopic tumor tissue, and decreased MIF-induced cellular signaling. These results suggest that PEITC has potential to be a therapeutic agent for glioblastoma by inhibiting tumor growth and modulating the immune response through MIF suppression.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 13","pages":" 5573-5585"},"PeriodicalIF":5.1,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potential effect of polyphenols in emerging pharmacological liver targets for glucose regulation and insulin resistance: a review","authors":"Sónia Rocha, Inês Santos, M. Luísa Corvo, Eduarda Fernandes and Marisa Freitas","doi":"10.1039/D4FO06329E","DOIUrl":"10.1039/D4FO06329E","url":null,"abstract":"<p >In type 2 diabetes <em>mellitus</em> (DM), there is a combination of impaired insulin secretion and resistance in the target tissues. In the case of the liver, these events lead to decreased insulin effectiveness and increased glucagon levels, resulting in an imbalance that promotes excessive hepatic gluconeogenesis and glycogenolysis, contributing to hyperglycemia. Effective management of hyperglycemia and insulin resistance is crucial, underscoring the need for innovative liver-specific interventions. Polyphenols, renowned for their diverse biological activities, have emerged as promising candidates to treat type 2 DM. Based on a literature review spanning the last decade, this comprehensive systematic review thoroughly evaluates the effectiveness of polyphenols in targeting hepatic pathways for managing type 2 DM. The focus will be on assessing how polyphenols affect key targets, including protein tyrosine phosphatase 1B (PTP1B), the glucagon receptor, glucokinase, glycogen phosphorylase, and fructose 1,6-bisphosphatase. While there has been considerable attention on polyphenols as PTP1B inhibitors, studies on their impact on other targets have been comparatively limited. Notably, there is a lack of studies exploring polyphenols as glucagon receptor antagonists. Among polyphenols, flavonoids exhibit significant potential across diverse pathways, with hydroxy groups playing a pivotal role in their biological activities. However, further research, especially in cellular and animal models, is warranted to thoroughly validate their efficacy.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 13","pages":" 5231-5277"},"PeriodicalIF":5.1,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.rsc.org/en/content/articlepdf/2025/fo/d4fo06329e?page=search","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary procyanidin B1 attenuates fibrogenesis and inflammation in hepatic fibrosis: research on the possible health benefits of procyanidin B1","authors":"Qi-Yuan Feng, Jiang-Tao Zhong, Hai-Ming Sun, Zheng Luo, Yu-Chen Jiang and Jian Song","doi":"10.1039/D5FO01415H","DOIUrl":"10.1039/D5FO01415H","url":null,"abstract":"<p >Procyanidin B1 (PB1) is a natural polyphenol abundant in whole-grain highland barley as well as in many fruits, vegetables, and medicinal plants. The current study investigated the hepatoprotective effect and potential mechanism of PB1 against hepatic fibrosis. C57BL/6 mice with hepatic fibrosis were induced with thioacetamide (TAA), followed by the administration of PB1 or a positive control, silymarin, or followed by gene silencing of the thyroid hormone-responsive protein (THRSP). Hepatic stellate cells (HSCs) were stimulated with transforming growth factor β (TGF-β) or an isolated mouse peritoneal macrophage (MPM)-primed conditioned medium and cultured with PB1, silymarin or the THRSP agonist. MPMs were cultured in the presence of LPS/ATP and/or PB1. It was found that PB1 decreased the release of inflammatory factors, such as caspase-1 and IL-1β. Moreover, PB1 could activate THRSP and decrease P2X7r-modulated NLRP3 inflammasome activation in the TAA-induced mice. Additionally, PB1 inhibited the expressions of α-SMA, collagen I, the TIMP-1/MMP13 ratio, inflammatory factors, P2X7r, and NLRP3 and increased THRSP expression in activated HSCs and macrophages. THRSP deficiency attenuated the regulatory effect of PB1 on the reverse inflammation of activated HSCs, promoting hepatic fibrosis <em>in vivo</em> and <em>in vitro</em>. PB1 reversed the activation of HSCs by increasing the THRSP-mediated P2X7r/NLRP3 axis, similar in function to THRSP overexpression. PB1 could reverse the activation of HSCs and mitigate hepatic inflammation and fibrogenesis in TAA-induced hepatic fibrosis. Targeting THRSP-mediated P2X7r/NLRP3 is crucial for PB1's action against hepatic fibrosis, underscoring a promising approach and the utility of PB1 for the treatment of hepatic fibrosis.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 13","pages":" 5456-5474"},"PeriodicalIF":5.1,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144256854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}