Journal of Nutritional Biochemistry最新文献

{"title":"Untargeted metabolomics reveals the mechanisms of luteolin and exercise combination treatment against cognitive impairments in AD mice through modulating autophagy","authors":"Xue Tao ,&nbsp;Liguo Wang ,&nbsp;Weijun Gong","doi":"10.1016/j.jnutbio.2025.110011","DOIUrl":"10.1016/j.jnutbio.2025.110011","url":null,"abstract":"<div><div>Alzheimer's disease (AD) yields a dramatic burden on patients and their families, with no complete cure yet. Our group has previously found that AD-related cognitive impairment (ARCI) could be alleviated after luteolin and exercise combination treatment (Lut + Exe), but the potential mechanisms require further exploration. This work used untargeted metabolomics to uncover the mechanisms Lut + Exe protects against ARCI. Utilizing an Aβ_1-42-oligomers-induced AD model, the Morris water maze (MWM) test was performed. Metabolomics of plasma was performed to identify differential metabolites. KEGG and MetaboAnalyst were used to enrich the metabolic pathways. Then, the autophagy inhibitor chloroquine (CQ) was utilized to verify the potential role of autophagy in the Lut+ Exe efficacy against ARCI. The results showed that Lut + Exe alleviated the ARCI in mice. The in-depth analysis showed that Lut + Exe could significantly affect purine metabolism, retinol metabolism, thiamine metabolism, histidine metabolism, and cysteine and methionine metabolism, indicating that the energy metabolism disorder was alleviated. Based on the close relationship between autophagy and energy metabolism, further study found that Lut + Exe could reverse the significant reduction of key autophagy proteins of AD model mice, while the effects of it on the MWM performance and neurogenesis of AD model mice could be blocked by CQ. This study reveals the crucial role of autophagy in the mechanisms of Lut + Exe against ARCI using untargeted metabolomics. Our work provides a novel paradigm to promote the use of combination treatment in curing AD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110011"},"PeriodicalIF":4.8,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AMPK-mediated energy metabolism disorders are associated with impaired type IIB muscle fiber regeneration in broiler chickens with wooden breast myopathy","authors":"Qin-Jian Niu ,&nbsp;Jia-Cheng Yang ,&nbsp;Rong-Hui Huang,&nbsp;Zhi-Yuan Xia,&nbsp;Alainaa Refaie,&nbsp;Lv-Hui Sun","doi":"10.1016/j.jnutbio.2025.110009","DOIUrl":"10.1016/j.jnutbio.2025.110009","url":null,"abstract":"<div><div>Wooden breast (WB) myopathy is a myodegenerative muscle disease, in which muscle regeneration is also commonly observed, and has been increasingly reported in fast-growing broilers in recent years. This study aims to investigate the underlying mechanism of energy metabolism abnormalities on muscle regeneration in WB. A total of 300 male Ross 308 broilers were evaluated at 42 days of age based on physical and biochemical examinations to classify the severity of WB. From these, 16 broilers were selected for each of three groups: the normal group (CON), the moderate WB group (WB-M), and the severe WB group (WB-S). Compared to CON, WB were heavier, thicker, harder and had lower meat quality. Additionally, WB exhibited disturbance of energy metabolism, with increased cholesterol and triglycerides and decreased glycogen and lactate contents. Meanwhile, WB exhibited muscle regeneration as illustrated by the increased central nuclei and inflammation cells in muscle and higher creatine kinase activity in serum and muscle. WB exhibited inhibition of AMPK activity, with lower phosphorylation at Thr172 and higher phosphorylation at Ser496. Consistently, WB dysregulated the downstream pathways of AMPK, such as protein synthesis activity, glycolysis activity, lipid metabolism activity, and inflammatory response. Furthermore, in primary myoblasts, AMPK activation suppressed type II B myofiber hypertrophy, while its inhibition enhanced hypertrophy. In conclusion, this study provides evidence that abnormal ⅡB myofiber regeneration associated with imbalance in AMPK-mediated energy homeostasis, plays a crucial role in the pathogenesis of WB. These finding may provide new insights into mitigating the onset of WB.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110009"},"PeriodicalIF":4.8,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferulic acid ethyl ester modulates electrical remodeling in cardiomyocytes exposed to TNF-α-stimulated adipocyte secretome via Nrf2/HO-1 pathway","authors":"Hsiang-Yu Yang ,&nbsp;Kwok-Keung Lam ,&nbsp;Chien-Ju Chou ,&nbsp;Bo-Yao Wen ,&nbsp;Chung-Bai Wang ,&nbsp;Yen-Mei Lee ,&nbsp;Chih-Yuan Lin ,&nbsp;Pao-Yun Cheng","doi":"10.1016/j.jnutbio.2025.110005","DOIUrl":"10.1016/j.jnutbio.2025.110005","url":null,"abstract":"<div><div>Inflammatory epicardial adipose tissue impacts cardiomyocytes, creating an arrhythmogenic substrate. This study examines the effects of tumor necrosis factor-α (TNF-α)-stimulated adipocytes on atrial cardiomyocytes and the protective role of ferulic acid ethyl ester (FAEE). TNF-α-stimulated 3T3-L1-derived adipocytes were utilized and analyzed. Conditioned media from TNF-α-stimulated and TNF-α/FAEE-cotreated adipocytes were examined. Biochemical and electrophysiological studies were performed on HL-1 myocytes exposed to these media. TNF-α stimulation increased the levels of the proinflammatory proteins monocyte chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6) in the adipocytes and conditioned media. The ratio of phosphorylated-NF-κB (pNF-κB) to NF-κB was higher in TNF-α-stimulated adipocytes than in the control group. While the levels of IL-6, MCP-1, and pNF-κB induced by TNF-α stimulation in the adipocytes remained unchanged with FAEE cotreatment, FAEE increased the protein levels of adiponectin in the adipocytes and the conditioned medium. FAEE also upregulated the protein levels of heme-oxygenase 1 (HO-1) and nuclear translocation of nuclear factor-erythroid 2-related factor-2 (Nrf2). The elevated adiponectin levels observed in FAEE-cotreated adipocytes were abolished following treatment with SnPP, a HO-1 inhibitor. The elevated levels of Ca²⁺/calmodulin-dependent protein kinase II and connexin 43, and the enhanced reverse mode Na⁺–Ca²⁺ exchanger current observed in HL-1 myocytes cultured in TNF-α-conditioned medium were abolished when these cardiomyocytes were cultured in TNF-α/FAEE-conditioned medium. FAEE modulates the electrical remodeling of HL-1 cardiomyocytes induced by the secretome of TNF-α-stimulated adipocytes, possibly through Nrf2/HO-1 signaling and adiponectin expression. These findings demonstrate FAEE's cardioprotective mechanisms and therapeutic potential.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110005"},"PeriodicalIF":4.8,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of supplement myo-inositol on meat quality, antioxidant capacity, and gene expression in Procambarus clarkii","authors":"Changchang Pu ,&nbsp;Yuanyi Liu ,&nbsp;Ruyi Sun ,&nbsp;Bingke Wang ,&nbsp;Aimin Wang ,&nbsp;Chunnuan Zhang","doi":"10.1016/j.jnutbio.2025.110003","DOIUrl":"10.1016/j.jnutbio.2025.110003","url":null,"abstract":"<div><div>This study aimed to explore how dietary myo-inositol (MI) affects the meat quality, antioxidant capacity, and muscle development of <em>Procambarus clarkii</em>. A total of 360 young <em>P. clarkii</em> were fed six diets containing graded levels of MI (0 (control), 500, 1,000, 2,000, 3,000, and 4,000 mg/kg diet) for 6 weeks. After the experiment, the abdominal muscle samples were collected from six groups of <em>P. clarkii</em>. Supplementing MI can increase the abdomen meat content and the content of free MI and phosphatidylinositol (PI) in the muscle tissue of <em>P. clarkii</em>. When an appropriate amount of MI is added to the feed, muscle meat quality will be beneficially improved, mainly reflected in water-holding capacity (WHC), elasticity, meat color, etc. Compared with the control group, adding 1,000 mg/kg of MI to the feed can significantly increase muscle L* value (<em>P</em>&lt;.05) and reduce muscle centrifugal loss (<em>P</em>&lt;.05). Moreover, when 1,000 mg/kg of MI was added to the feed, the total essential amino acid (TEAA) and hydroxyproline (HYP) content of muscles were significantly higher than the control group (<em>P</em>&lt;.05). Supplementing MI reduced muscle oxidative metabolite content (ROS, MDA, and LA), and increased antioxidant enzyme activity and related gene expression. These results suggest that dietary MI can activate the Nrf2/Keap1 signaling pathways, increasing muscle antioxidant enzyme activity. In addition, supplementing MI can activate the expression of crayfish GH-IGF axis-related genes. When 1,000 mg/kg MI was added, the <em>Mef2a, Mef2b</em>, and <em>IGF-1</em> genes expression levels were significantly higher than the control group (<em>P</em>&lt;.05). In summary, supplementing 1,000 mg/kg MI can regulate muscle amino acid metabolism by regulating the Nrf2/Keap1 signaling pathway to promote muscle development and improve meat quality.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110003"},"PeriodicalIF":4.9,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of pasture-fed versus total mixed ration derived whole milk powder (WMP) on circulating fatty acid concentrations and cardiometabolic health in healthy adults: Results from a randomized controlled crossover trial","authors":"Martina Rooney ,&nbsp;Aileen O’Connor ,&nbsp;Clare Gollogly ,&nbsp;Andrea Mills ,&nbsp;Simone Dunne ,&nbsp;Clíona Ní Chonnacháin ,&nbsp;Mark Timlin ,&nbsp;André Brodkorb ,&nbsp;Tom F. O’Callaghan ,&nbsp;Jonathan B. Magan ,&nbsp;John Tobin ,&nbsp;Michael O’Donovan ,&nbsp;Deirdre Hennessy ,&nbsp;Niamh Harbourne ,&nbsp;Karina M. Pierce ,&nbsp;Emma L. Feeney ,&nbsp;Eileen R. Gibney","doi":"10.1016/j.jnutbio.2025.110004","DOIUrl":"10.1016/j.jnutbio.2025.110004","url":null,"abstract":"<div><div>Whole milk powder (WMP) produced from pasture-fed dairy herds has been shown to have increased concentrations of unsaturated fatty acids (FA), including, but not limited to, ALA (C18:3 n-3) and oleic acid (C18:1 <em>cis</em>-9), compared to WMP derived from indoor herds consuming total mixed ration (TMR). Dairy products have been shown to have neutral or beneficial effects on cardiometabolic health, however, evidence on WMP in this area is lacking. Given the global market for WMP as a food ingredient, an investigation into the effect of TMR-fed vs pasture-fed WMP on human health is warranted. Therefore, the aim of this study was to test the effect of WMP derived from TMR-fed and pasture-fed herds on circulating FA concentrations and other markers of cardiometabolic health in adults. Healthy subjects were randomized to receive up to 200 g WMP/day as part of a 6-week crossover trial, with a 4-week washout period. WMP was produced from milks of TMR-fed and pasture-fed cows. WMPs were isocaloric and macro-nutrient matched. The primary outcome was difference in circulating FA between weeks 0 and 6. Changes in cholesterol concentrations, glycemic control, blood pressure and anthropometry were secondary outcomes. Dietary intake was also analyzed. A total of <em>n</em> 29 participants, 58.6% male, with a mean±SE age of 39.8±2.3 years and BMI of 26.12±1.39 kg/m² completed the study protocol. No time × treatment interactions were observed for cholesterol concentrations, markers of glycemic control, blood pressure or anthropometry. There was no time × treatment interaction for classes of FA, however, the very long-chain saturated FA, lignoceric acid (C24:0), decreased in response to pasture-fed WMP consumption (−0.05±0.04 %TFA) with no change observed in response to the TMR WMP consumption (0.00±0.04 %TFA, <em>P</em>=.041), although this was not significant after Bonferroni correction for Type 2 error. Chronic, high-dose consumption of TMR and pasture-fed WMP had no effect on cardiometabolic health in healthy adults, despite different fatty acid composition. Comparison of foods with a proven dairy matrix effect, <em>e.g.</em>, cheese made from TMR-fed and pasture-fed milks, may have more promising effects on human health. This trial was registered as ISRCTN10490434 (<span><span>https://doi.org/10.1186/ISRCTN10490434</span><svg><path></path></svg></span>).</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110004"},"PeriodicalIF":4.8,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of vitamin D and omega 3 fatty acids in improving HDL biogenesis among multiple sclerosis patients via orchestrating CHROME/APOA1-AS/ABCA1/APOA1 milieu","authors":"Mai A. Abd-Elmawla ,&nbsp;Heba R. Ghaiad ,&nbsp;Mohammed M. Nooh ,&nbsp;Mai A. Amer ,&nbsp;Lobna Talaat El-Ghoneimy ,&nbsp;Noha A. Mehana","doi":"10.1016/j.jnutbio.2025.110007","DOIUrl":"10.1016/j.jnutbio.2025.110007","url":null,"abstract":"<div><div>Clinical approaches that could correct the disturbed lipid profile may improve neurological disturbances in multiple sclerosis (MS) patients. However, the underlying mechanisms are still not well understood. The study aimed to characterize the performance of vitamin D (Vit.D) and omega 3 fatty acid (ω3) in adjusting the lipid profile of MS patients via modulating CHROME/APOA1-AS/ABCA1/APOA1 along with sphingosine kinase (SPHK)-1/2, and sphingosine 1-phosphate receptors (S1PR)-1/5. 72 MS patients were recruited for this study; 25 received Vit.D, 21 received ω3, and 26 didn’t receive any supplementation. Blood samples were collected and then plasma were separated for further biochemical and molecular investigations. Both vit.D or ω3 improved the lipid profile in the studied groups as well as elevated the expression of the lncRNA CHROME, the concentrations of ABCA1 and ApoA1 along with lowering APOA1-AS relative to MS patients without supplementation. Vit.D supplementation group revealed higher levels of SPHK1 and lower levels of SPHK2, whereas ω3 supplementation reduced both S1PR1 and S1PR5 relative to the MS control group. This study demonstrated the beneficial role of Vit.D and ω3 supplementation in adjusting the lipid profile of MS patients via modulating ABCA1 and ApoA1 and their upstream regulators CHROME and APOA1-AS. The administration of Vit.D upregulated SPHK1 and downregulated SPHK2 gene expression. On the other hand, ω3 supplements downregulated S1PR1 and S1PR5 gene expression in MS patients.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110007"},"PeriodicalIF":4.8,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbial–purine metabolic crosstalk regulates colitis-related intestinal fibrosis: A multiomics and cohort analysis approach","authors":"Xiaoxuan Mai ,&nbsp;Jinzhen Wu ,&nbsp;Zhenyi Tian ,&nbsp;Le Liu ,&nbsp;Xiaoduan Zhuang ,&nbsp;Zhipeng Liu ,&nbsp;Ruiming Wan ,&nbsp;Bang Li ,&nbsp;Yuting Shi ,&nbsp;Bingsheng Li ,&nbsp;Xinying Wang","doi":"10.1016/j.jnutbio.2025.109984","DOIUrl":"10.1016/j.jnutbio.2025.109984","url":null,"abstract":"<div><div>Intestinal fibrosis (IF) is a severe complication of inflammatory bowel disease (IBD), often requiring surgical interventions. The modulating role of the microbial-metabolic link in IF remains unclear. We aimed to identify disturbances in microbiome–metabolome interactions during IF progression and recognize potential metabolic biomarkers. Compositional and functional signatures, along with murine IF progression, were determined through 16S rRNA sequencing and widely targeted metabolomics. Overall, 109 patients with IBD and 111 healthy controls (HCs) were enrolled and clinically evaluated. Correlations analyses were performed to reveal the relationship between microbial–purine metabolic alterations and disease markers. Gut microbiome analysis identified structural disruptions, including a reduction in uric acid (UA)-decomposed microbes and an increase in hyperuricemia-associated taxa (<em>P</em>&lt;.05), which contributed to impaired purine metabolism (<em>P</em>&lt;.05). Metabolomic profiling further indicated reprogramming of purine metabolism in fibrogenesis, as evidenced by elevated UA levels in fecal, colonic, and serum samples that correlated with inflammatory and fibrotic markers. In IBD patients, compared to HCs, serum UA (342.55±95.69 vs. 294.78±66.58 µmol/L) and UA/creatinine (UA/Cr) levels (5.17±1.57 vs. 4.40±1.28) were greatly increased (<em>P</em>&lt;.001) and positively correlated with the clinical and endoscopic activities, especially in CD patients. Serial measurements demonstrated elevated UA during stenosis formation. UA/Cr may be an independent risk factor (<em>P</em>=.006) for stenosis prognosis. Abnormal purine metabolism may regulate IF, as reflected in purine metabolism-related microbes and metabolites. Elevated serum UA and UA/Cr levels are promising biomarkers for detecting disease activity and predicting stenosis in IBD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"144 ","pages":"Article 109984"},"PeriodicalIF":4.8,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"1,25(OH)2D3 ameliorates DSS-induced intestinal ferroptosis through the SIRT3–SOD2–mtROS pathway","authors":"Hong-Qian Wang ,&nbsp;Ya-Wen Zhu ,&nbsp;Zi-Yue Dou ,&nbsp;Zhuo Chen ,&nbsp;Cheng-Cheng Tong ,&nbsp;Xue He ,&nbsp;Xiao-Han Ma ,&nbsp;Jing Guan ,&nbsp;De-Xiang Xu ,&nbsp;Xi Chen","doi":"10.1016/j.jnutbio.2025.109999","DOIUrl":"10.1016/j.jnutbio.2025.109999","url":null,"abstract":"<div><div>Ferroptosis has been shown to play a significant role in the pathogenesis of ulcerative colitis (UC). This study investigated the effects of 1,25(OH)₂D₃ supplementation on ferroptosis in dextran sulfate sodium (DSS)-evoked colitis. Intestinal VDR was reduced in UC patients. Accordingly, GPX4 was downregulated and ACSL4 was upregulated in the intestine of UC patients. Animal experiments indicated that vitamin D deficiency exacerbated DSS-induced intestinal ferroptosis in mice. Conversely, pretreatment with 1,25(OH)₂D₃ alleviated DSS-induced ferroptosis in mouse intestine. Similarly, 1,25(OH)₂D₃ supplementation inhibited DSS-induced ferroptosis in HT-29 cells. Furthermore, we found decreased intestinal SIRT3 protein and increased acetylated superoxide dismutase 2 (Ac-SOD2) in UC patients. Pretreatment with 1,25(OH)₂D₃ attenuated DSS-induced downregulation of SIRT3 and acetylation of SOD2 in both mouse intestine and HT-29 cells. Moreover, 1,25(OH)₂D₃ pretreatment inhibited mitochondrial reactive oxygen species (mtROS) in DSS-treated HT-29 cells. Finally, transfection with SIRT3 siRNA antagonized the protective effect of 1,25(OH)₂D₃ on ferroptosis in DSS-treated HT-29 cells. Overall, our results suggest that 1,25(OH)₂D₃ alleviates DSS-induced intestinal ferroptosis via the SIRT3-SOD2-mtROS pathway, further supporting the potential use of 1,25(OH)₂D₃ supplementation in UC treatment.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"144 ","pages":"Article 109999"},"PeriodicalIF":4.8,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fucoxanthin ameliorates vascular remodeling via attenuating oxidative stress in hypoxic pulmonary hypertension rats","authors":"Xu Zheng ,&nbsp;Jina Zhao ,&nbsp;Xiaoqin Jia ,&nbsp;Jinjin Pan ,&nbsp;Shuo Xu ,&nbsp;Dingyou Wang ,&nbsp;Junxia Li ,&nbsp;Yuke Ji ,&nbsp;Zhilong Zhu ,&nbsp;Muhammad Hasnain ,&nbsp;Zheng Sui ,&nbsp;Rui Wang ,&nbsp;Yuhui Yuan","doi":"10.1016/j.jnutbio.2025.110002","DOIUrl":"10.1016/j.jnutbio.2025.110002","url":null,"abstract":"<div><div>Hypoxic pulmonary hypertension (HPH) is a fatal cardiopulmonary disease characterized by pulmonary vascular remodeling, primarily resulting from abnormal proliferation of pulmonary artery smooth muscle cells (PASMCs). Fucoxanthin, a natural carotenoid with potent antioxidant activity, was investigated for its therapeutic potential in HPH, given the critical role of oxidative stress in disease pathogenesis. In this study, Sprague–Dawley rats were exposed to intermittent chronic hypoxia for 4 weeks to mimic severe HPH. The results demonstrated that fucoxanthin significantly reduced the elevated right ventricular systolic pressure (RVSP), alleviated right ventricular hypertrophy, and mitigated pulmonary artery remodeling in the HPH rats. Additionally, fucoxanthin enhanced superoxide dismutase (SOD) activity and glutathione (GSH)/glutathione disulfide (GSSG) ratio while decreasing malondialdehyde (MDA) levels in both lung tissues and serum of HPH rats. <em>In vitro,</em> fucoxanthin inhibited cell proliferation and migration, decreased reactive oxygen species (ROS) production in hypoxia-induced PASMCs, and improved cell viability in hypoxia-induced endothelial cells (ECs). Importantly, fucoxanthin reduced hypoxia-inducible factor 1 alpha (HIF-1α) expression in both lung tissues and PASMCs under hypoxia. Notably, fucoxanthin exhibited effects similar to those of 2-methoxyestradiol (2ME2), an inhibitor of HIF-1α, on cell proliferation and ROS production in hypoxia-induced PASMCs. Moreover, fucoxanthin treatment did not significantly alter HIF-1α expression, cell proliferation, or ROS production after 2ME2 blocked HIF-1α. Collectively, fucoxanthin suppressed hypoxia-induced oxidative stress primarily by regulating the HIF-1α-ROS pathway, thereby alleviating pulmonary remodeling in HPH. Our findings represent a promising therapeutic strategy for HPH by improving pulmonary vascular remodeling.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110002"},"PeriodicalIF":4.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of flavan-3-ols on ovariectomy-induced bone loss in mice and the potential mechanisms","authors":"Shanshan Chen ,&nbsp;Jiapeng Huang ,&nbsp;Xuanrui Zhang ,&nbsp;Zhen Hong ,&nbsp;Yanbin Ye ,&nbsp;Xiaoping Lin ,&nbsp;Zheqing Zhang","doi":"10.1016/j.jnutbio.2025.110001","DOIUrl":"10.1016/j.jnutbio.2025.110001","url":null,"abstract":"<div><div>Flavan-3-ols (FLOs) have been reported to confer various health benefits, the majority of which reaching the colon for fermentation by gut microbiota. This study sought to examine the effects of FLOs on bone health and to evaluate the influence of gut microbiota on these effects. Using an ovariectomy-induced bone loss model in mice, the animals were administered either a low or high dose of FLOs, or a combination of FLOs with an antibiotic cocktail (Abs+FLOs). Compared to the control group, serum markers of bone formation, as well as bone quality as determined by micro-CT, were elevated in the groups supplemented with FLOs, particularly when combined with Abs. Furthermore, both FLOs and Abs+FLOs interventions significantly improved the levels of estrogen. However, no additional influence of FLOs on these markers was detected compared to the group supplemented with Abs alone. Analysis of 16S rRNA sequencing data revealed that the abundance of certain operational taxonomic units, such as <em>s__unclassified_Clostridia_UCG_014, s__unclassified_Ruminococcus</em>, and <em>s__unclassified_Lachnospiraceae</em>, was significantly reduced in osteoporotic mice but effectively reversed following the administration of FLOs. Transcriptomic analysis coupled with KEGG enrichment analysis indicated that Adrb3, Gdf10 (BMP3), Fosb, and Cxcl2, along with the PPARα/PGC-1/UCP1 signaling pathway, may potentially mediate the regulation of bone metabolism by flavanols. Collectively, the study uncovers the osteoprotective properties of flavan-3-ols, indicating that these effects may depend on the presence of gut microbiota.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110001"},"PeriodicalIF":4.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}