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Isorhamnetin Improves Oocyte Maturation by Activating the Pi3k/Akt Signaling Pathway 异鼠李素通过激活 Pi3k/Akt 信号通路促进卵母细胞成熟
IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Pub Date : 2024-07-09 DOI: 10.1002/mnfr.202300904
Xiaoya Li, Jianyong Cheng, Qichun Yao, Jiaxin Duan, Huali Chen, Zelin Zhang, Li Yang, Rongmao Hua, Qingwang Li

Scope

Isorhamnetin is a natural flavonoid with various pharmacological activities, which can be widely and continuously ingested by humans and animals through their daily diet. The aim of this study is to explore the benefits and molecular mechanisms of isorhamnetin on oocyte maturation.

Methods and results

Oocytes are incubated with isorhamnetin (5, 10, 20, and 30 µM) for 44 h. Isorhamnetin (10 µM) increases the polar body extrusion rate of oocytes. Furthermore, isorhamnetin alleviates oxidative stress by inhibiting reactive oxygen species levels and stimulating SOD2 protein expression. The changes in intracellular mitochondrial autophagy and apoptosis-related proteins (Bcl-2, Bax/Bcl-2, and C-Casp3) indicate that isorhamnetin inhibits oocyte apoptosis. Isorhamnetin inhibits endoplasmic reticulum stress by reducing the protein expression of CHOP and GRP78 and improving the normal distribution rate of endoplasmic reticulum. Mechanistic studies show that isorhamnetin activates the PI3K/Akt signaling pathway.

Conclusion

Isorhamnetin promotes oocyte maturation by inhibiting oxidative stress, mitochondrial dysregulation, apoptosis, and endoplasmic reticulum stress, which have important potential for improving oocyte quality and treating female infertility.

研究范围异鼠李素是一种具有多种药理活性的天然黄酮类化合物,可被人类和动物通过日常饮食广泛、持续地摄入。本研究旨在探讨异鼠李素对卵母细胞成熟的益处和分子机制:用异鼠李素(5、10、20 和 30 µM)培养卵母细胞 44 小时。此外,异鼠李素还能通过抑制活性氧水平和刺激 SOD2 蛋白表达来减轻氧化应激。细胞内线粒体自噬和凋亡相关蛋白(Bcl-2、Bax/Bcl-2 和 C-Casp3)的变化表明,异鼠李素能抑制卵母细胞凋亡。异鼠李素通过降低 CHOP 和 GRP78 的蛋白表达以及提高内质网的正常分布率来抑制内质网应激。机理研究表明,异鼠李素能激活 PI3K/Akt 信号通路:结论:异鼠李素通过抑制氧化应激、线粒体失调、细胞凋亡和内质网应激来促进卵母细胞成熟,这对提高卵母细胞质量和治疗女性不孕症具有重要潜力。
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引用次数: 0
The Relationship between Diet, Depression, and Alzheimer's Disease: A Narrative Review 饮食、抑郁和阿尔茨海默病之间的关系:叙述性综述。
IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Pub Date : 2024-07-07 DOI: 10.1002/mnfr.202300419
Hilal Salim Said Al Shamsi, Stephanie R. Rainey-Smith, Samantha L. Gardener, Hamid R. Sohrabi, Rodrigo Canovas, Ralph N. Martins, Warnakulasuriya Mary Ann Dipika Binosha Fernando

Purpose of Review

This narrative review evaluates the role of diet in the relationship between depression and Alzheimer's disease (AD).

Recent Findings

AD and depression are often comorbid, and depression appears to independently increase the future risk of AD. Evidence suggests diet influences the risk of both conditions directly and indirectly. Diet impacts neurochemical and biological processes that may affect the development and progression of depression and cognitive dysfunction. The dietary components offering the greatest protection against depression and AD are yet to be determined. Current evidence highlights the importance of polyphenolic compounds, folate, B vitamins, and polyunsaturated fatty acids, along with adherence to dietary patterns like the Mediterranean diet, which includes multiple beneficial dietary factors.

Summary

The investigation of dietary factors in the prevention of depression and AD is a comparatively young field of research. Comprehensive highly characterised longitudinal datasets and advanced analytical approaches are required to further examine the complex relationship between diet, depression, and AD. There is a critical need for more research in this area to develop effective preventive strategies aimed at maintaining mental and physical health with advancing age.

综述的目的:这篇叙述性综述评估了饮食在抑郁症和阿尔茨海默病(AD)之间关系中的作用:最近的研究结果:阿氏痴呆症和抑郁症通常是并发症,抑郁症似乎会单独增加未来患阿氏痴呆症的风险。有证据表明,饮食会直接或间接地影响这两种疾病的风险。饮食会影响神经化学和生物过程,而这些过程可能会影响抑郁症和认知功能障碍的发生和发展。对抑郁症和注意力缺失症具有最大保护作用的饮食成分尚未确定。目前的证据强调了多酚化合物、叶酸、B 族维生素和多不饱和脂肪酸的重要性,以及坚持地中海饮食等饮食模式的重要性,其中包括多种有益的饮食因素。要进一步研究膳食、抑郁症和注意力缺失症之间的复杂关系,需要全面、高度特征化的纵向数据集和先进的分析方法。亟需在这一领域开展更多的研究,以制定有效的预防策略,随着年龄的增长保持身心健康。
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引用次数: 0
Gubra Amylin-NASH Diet Induced Nonalcoholic Fatty Liver Disease Associated with Histological Damage, Oxidative Stress, Immune Disorders, Gut Microbiota, and Its Metabolic Dysbiosis in Colon Gubra Amylin-NASH 饮食诱发的非酒精性脂肪肝与结肠组织学损伤、氧化应激、免疫紊乱、肠道微生物群及其代谢紊乱有关。
IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Pub Date : 2024-07-05 DOI: 10.1002/mnfr.202300845
Zhimin Zhang, Xinyi Qin, Tao Yi, Yamei Li, Chengfeng Li, Min Zeng, Hongshan Luo, Xiulian Lin, Jingchen Xie, Bohou Xia, Yan Lin, Limei Lin

Scope

The overall changes of colon under nonalcoholic fatty liver disease (NAFLD) remain to be further elucidated.

Methods and Results

This study establishes a mouse model of NAFLD through a long-term Gubra Amylin-nonalcoholic steatohepatitis (NASH) diet (GAN diet). The results show that GAN diet significantly induces weight gain, liver steatosis, colonic oxidative stress, and lipid accumulation in blood, liver, and adipose tissue in mice. GAN feeding reduces the diversity of the gut microbiota, alters the composition and abundance of the gut microbiota, and leads to an increase in microbial metabolites such as long-chain fatty acids (LCFAs) and secondary bile acids (BAs), as well as a decrease in short-chain fatty acids (SCFAs). The RNA-seq and immunofluorescence results reveal that the GAN diet alters the expression of proteins and their coding genes involved in oxidative stress, immune response, and barrier function in colon tissue, such as lipocalin-2 (Lcn2, p < 0.05), heme oxygenase-1 (HO-1/Hmox1, p < 0.05), interferon-gamma (IFN-γ), and claudin-3/7. In addition, correlation analysis indicates a strong correlation between the changes in gut microbiota and lipid biomarkers. Additionally, the expression of immune related genes in colon tissue is related to the LCFAs produced by microbial metabolism.

Conclusion

GAN-induced NAFLD is related to microbiota and its metabolic imbalance, oxidative stress, immune disorders, and impaired barrier function in colon.

范围:非酒精性脂肪肝(NAFLD)下结肠的整体变化仍有待进一步阐明:本研究通过长期Gubra Amylin-非酒精性脂肪性肝炎(NASH)饮食(GAN饮食)建立了非酒精性脂肪性肝炎小鼠模型。结果表明,GAN饮食能显著诱导小鼠体重增加、肝脏脂肪变性、结肠氧化应激以及血液、肝脏和脂肪组织中的脂质积累。GAN喂养降低了肠道微生物群的多样性,改变了肠道微生物群的组成和丰度,导致长链脂肪酸(LCFAs)和次级胆汁酸(BAs)等微生物代谢产物的增加,以及短链脂肪酸(SCFAs)的减少。RNA-seq和免疫荧光结果显示,GAN饮食改变了结肠组织中参与氧化应激、免疫反应和屏障功能的蛋白质及其编码基因的表达,如脂钙蛋白-2(Lcn2,p 结论):GAN诱导的非酒精性脂肪肝与微生物群及其代谢失衡、氧化应激、免疫紊乱和结肠屏障功能受损有关。
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引用次数: 0
Cocoa and Polyphenol-Rich Cocoa Fractions Fail to Improve Acute Colonic Inflammation in Dextran Sulfate Sodium-Treated Mice 可可和富含多酚的可可提取物无法改善右旋糖酐硫酸钠处理小鼠的急性结肠炎症
IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Pub Date : 2024-07-04 DOI: 10.1002/mnfr.202400431
Daphne K. Weikart, Kiana M. Coleman, Michael G. Sweet, Ashley M. McAmis, Helene Hopfer, Andrew P. Neilson, Joshua D. Lambert

Scope

A study is conducted to determine the anti-inflammatory effects of cocoa and polyphenol-rich cocoa fractions in the dextran sulfate sodium (DSS)-induced mouse model of acute colonic inflammation.

Methods and results

Male C57BL/6J mice are treated with dietary cocoa powder, an extractable cocoa polyphenol fraction, or a non-extractable cocoa polyphenol fraction for 2 weeks prior to treatment with 2.5% DSS in the drinking water for 7 days to induce colonic inflammation. Cocoa treatment continues during the DSS period. Cocoa and/or cocoa fractions exacerbate DSS-induced weight loss and fail to mitigate DSS-induced colon shortening but do improve splenomegaly. Cocoa/cocoa fraction treatment fails to mitigate DSS-induced mRNA and protein markers of inflammation. Principal component analysis shows overlap between cocoa or cocoa fraction-treated mice and DSS-induced controls, but separation from mice not treated with DSS.

Conclusion

The results suggest cocoa and cocoa polyphenols may not be useful in mitigating acute colonic inflammation.

研究范围本研究旨在确定可可和富含多酚的可可组分在葡聚糖硫酸钠(DSS)诱导的急性结肠炎小鼠模型中的抗炎作用:雄性 C57BL/6J 小鼠在饮用水中添加 2.5% 的右旋糖酐钠(DSS)诱导结肠发炎 7 天之前,先用可可粉、可提取的可可多酚组分或不可提取的可可多酚组分进行为期 2 周的饮食治疗。在DSS期间继续进行可可处理。可可和/或可可馏分会加剧DSS诱导的体重减轻,无法缓解DSS诱导的结肠缩短,但可改善脾肿大。可可和/或可可成分治疗不能减轻DSS诱导的炎症mRNA和蛋白质标记物。主成分分析表明,可可或可可粉处理的小鼠与DSS诱导的对照组之间存在重叠,但与未用DSS处理的小鼠之间存在分离:结论:研究结果表明,可可和可可多酚可能无助于减轻急性结肠炎。
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引用次数: 0
Lactococcus lactis KF140 Ameliorates Nonalcoholic Fatty Liver Disease Induced by Nε-Carboxymethyl-Lysine and High-Fat Diet 乳酸乳球菌 KF140 可改善 Nε-Carboxymethyl-Lysine 和高脂饮食诱发的非酒精性脂肪肝。
IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Pub Date : 2024-07-04 DOI: 10.1002/mnfr.202400260
Hye-Bin Lee, Miri Park, So-Young Lee, Sang Keun Ha, Yoonsook Kim, Kwang-Won Lee, Ho-Young Park

Scope

Long-term consumption of excessive dietary advanced glycation end-products such as Nε-carboxymethyl-lysine (CML), which are produced by the Maillard reaction during food thermal processing, leads to nonalcoholic fatty liver disease (NAFLD) along with high fat consumption. The study previously finds that administration of Lactococcus lactis KF140 (LL-KF140) detoxifies CML by decreasing CML absorption both in a rat model and clinical trial.

Methods and results

The present study evaluates the ameliorative effect of LL-KF140 on NAFLD and fatty liver-related biomarkers in a mouse model induced by CML and high fat. LL-KF140 is orally administered to mice at a concentration of 1 × 107 or 1 × 108 colony-forming unit (CFU) per mouse for 8 weeks. LL-KF140 administration ameliorates the NAFLD-related symptoms by reducing body weight and fat mass gain along with levels of serum aspartate transaminase, alanine transferase, and lipids as well as glucose intolerance and insulin resistance in CML-treated mice. In addition, histological analysis including staining and western blotting shows that LL-KF140 suppresses the lipogenesis pathway and CML absorption, thereby suppressing CML-induced NAFLD.

Conclusion

These findings suggest that LL-KF140 attenuates dietary CML-induced NAFLD by suppressing the de novo lipogenesis pathway, and it may be used as a probiotic strain.

范围:长期摄入过量的膳食高级糖化终产物(如在食品热加工过程中通过马氏反应产生的Nε-羧甲基赖氨酸(CML))会导致非酒精性脂肪肝(NAFLD),同时还会消耗大量脂肪。之前的研究发现,在大鼠模型和临床试验中,服用乳球菌 KF140(LL-KF140)可通过减少 CML 的吸收来解毒:本研究评估了 LL-KF140 在 CML 和高脂肪诱导的小鼠模型中对非酒精性脂肪肝和脂肪肝相关生物标志物的改善作用。小鼠口服 LL-KF140 的浓度为每只小鼠 1 × 107 或 1 × 108 菌落总数形成单位(CFU),连续服用 8 周。服用 LL-KF140 可改善非酒精性脂肪肝相关症状,减轻 CML 治疗小鼠的体重和脂肪量增加,降低血清天冬氨酸转氨酶、丙氨酸转氨酶和血脂水平,以及糖耐量减低和胰岛素抵抗。此外,包括染色和 Western 印迹在内的组织学分析表明,LL-KF140 可抑制脂肪生成途径和 CML 吸收,从而抑制 CML 诱导的非酒精性脂肪肝:这些研究结果表明,LL-KF140可通过抑制新生脂肪生成途径来减轻饮食CML诱导的非酒精性脂肪肝,可用作益生菌株。
{"title":"Lactococcus lactis KF140 Ameliorates Nonalcoholic Fatty Liver Disease Induced by Nε-Carboxymethyl-Lysine and High-Fat Diet","authors":"Hye-Bin Lee,&nbsp;Miri Park,&nbsp;So-Young Lee,&nbsp;Sang Keun Ha,&nbsp;Yoonsook Kim,&nbsp;Kwang-Won Lee,&nbsp;Ho-Young Park","doi":"10.1002/mnfr.202400260","DOIUrl":"10.1002/mnfr.202400260","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Scope</h3>\u0000 \u0000 <p>Long-term consumption of excessive dietary advanced glycation end-products such as <i>N</i><sup>ε</sup>-carboxymethyl-lysine (CML), which are produced by the Maillard reaction during food thermal processing, leads to nonalcoholic fatty liver disease (NAFLD) along with high fat consumption. The study previously finds that administration of <i>Lactococcus lactis</i> KF140 (LL-KF140) detoxifies CML by decreasing CML absorption both in a rat model and clinical trial.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and results</h3>\u0000 \u0000 <p>The present study evaluates the ameliorative effect of LL-KF140 on NAFLD and fatty liver-related biomarkers in a mouse model induced by CML and high fat. LL-KF140 is orally administered to mice at a concentration of 1 × 10<sup>7</sup> or 1 × 10<sup>8</sup> colony-forming unit (CFU) per mouse for 8 weeks. LL-KF140 administration ameliorates the NAFLD-related symptoms by reducing body weight and fat mass gain along with levels of serum aspartate transaminase, alanine transferase, and lipids as well as glucose intolerance and insulin resistance in CML-treated mice. In addition, histological analysis including staining and western blotting shows that LL-KF140 suppresses the lipogenesis pathway and CML absorption, thereby suppressing CML-induced NAFLD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings suggest that LL-KF140 attenuates dietary CML-induced NAFLD by suppressing the de novo lipogenesis pathway, and it may be used as a probiotic strain.</p>\u0000 </section>\u0000 </div>","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"68 16","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mnfr.202400260","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141496524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Unabsorbed Fecal Fat Content Correlates with a Reduction of Immunoglobulin a Coating of Gut Bacteria in High-Lard Diet-Fed Mice 未吸收的粪便脂肪含量与高猪油饮食小鼠肠道细菌免疫球蛋白 a 涂层的减少有关。
IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Pub Date : 2024-07-04 DOI: 10.1002/mnfr.202400078
Emiko Katsumata, Takeshi Tsuruta, Kei Sonoyama, Takashi Yoshida, Mio Sasaki, Mao Teraoka, Tianyang Wang, Naoki Nishino

Scope

Immunoglobulin A (IgA) selectively coats gut bacteria and contributes to regulatory functions in gastrointestinal inflammation and glucose metabolism. Excess intake of lard leads to decrease in the IgA coating of gut bacteria, although the underlying mechanisms remain unknown. This study validates how unabsorbed fat derived from a high-lard diet in the gut affects the IgA coating of bacteria, as assessed in mouse models using three types of dietary fat (lard, medium-, and long-chain triglycerides [MLCTs], and medium-chain triglycerides [MCTs]) exhibiting different digestibilities.

Methods and results

C57BL/6J mice are maintained on diets containing lard, MLCTs, or MCTs at 7% or 30% w/w for 10 weeks (n = 6 per group). The fecal fatty acid concentration is measured to quantify unabsorbed fat content. The ratio of IgA-coated bacteria to total bacteria (IgA coating ratio) in the feces is measured by flow cytometry. Compared to lard-fed mice, MLCT- and MCT-fed mice exhibit lower fecal concentrations of palmitic acid, stearic acid, and oleic acid and higher IgA coating ratios at both 7% and 30% dietary fat, and these parameters exhibit significant negative correlations.

Conclusion

Unabsorbed fat content in the gut may result in attenuated IgA coating of bacteria in high-lard diet-fed mice.

范围免疫球蛋白 A (IgA) 可选择性地包裹肠道细菌,并在胃肠道炎症和葡萄糖代谢中发挥调节功能。过量摄入猪油会导致肠道细菌的 IgA 涂层减少,但其潜在机制仍不清楚。本研究验证了肠道中来自高猪油饮食的未吸收脂肪如何影响细菌的 IgA 涂层,并在小鼠模型中使用三种具有不同消化率的饮食脂肪(猪油、中长链甘油三酯 [MLCTs] 和中链甘油三酯 [MCTs])进行了评估:C57BL/6J 小鼠连续 10 周食用含 7% 或 30% w/w 猪油、中长链甘油三酯或中链甘油三酯的食物(每组 6 只)。测量粪便中的脂肪酸浓度,以量化未吸收的脂肪含量。通过流式细胞术测量粪便中 IgA 包被细菌与细菌总数的比率(IgA 包被比率)。与饲喂猪油的小鼠相比,饲喂 MLCT 和 MCT 的小鼠在膳食脂肪含量为 7% 和 30% 时,粪便中棕榈酸、硬脂酸和油酸的浓度较低,IgA 包被率较高,而且这些参数呈现显著的负相关:结论:肠道中未被吸收的脂肪含量可能会导致高猪油饮食喂养的小鼠体内细菌的 IgA 包被率降低。
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引用次数: 0
Issue Information: Mol. Nutr. Food Res. 12'24 发行信息:Mol.Nutr.12'24
IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Pub Date : 2024-07-03 DOI: 10.1002/mnfr.202470023
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引用次数: 0
Front Cover: Nobiletin Protects Against Alcoholic Liver Disease in Mice via the BMAL1-AKT-Lipogenesis Pathway 封面:金没药通过 BMAL1-AKT-Lipogenesis 通路保护小鼠免受酒精性肝病的侵害
IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Pub Date : 2024-07-03 DOI: 10.1002/mnfr.202470022
Xudong Li, Runxuan Zhuang, Ke Zhang, Yuchun Zhang, Zhitian Lu, Fan Wu, Xiaoli Wu, Wenxue Li, Zheqing Zhang, Huijie Zhang, Wei Zhu, Bo Zhang

Mol. Nutr. Food Res. 2024, 68, 2300833

DOI: 10.1002/mnfr.202300833

The cover image is based on the Research Article Nobiletin Protects Against Alcoholic Liver Disease in Mice via the BMAL1-AKT-Lipogenesis Pathway by Xudong Li et al., https://doi.org/10.1002/mnfr.202300833

Mol.Nutr.2024, 68, 2300833
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引用次数: 0
In Vitro Protective Effect of Pea-Derived Peptides (PPs) via the Keap1/Nrf2 Signaling Pathway on Alpha-Gliadin-Sensitizing Peptide Induced Cacao-2 Cells 豌豆衍生肽 (PP) 通过 Keap1/Nrf2 信号通路对 Alpha-Gliadin 致敏肽诱导的 Cacao-2 细胞的体外保护作用。
IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Pub Date : 2024-07-03 DOI: 10.1002/mnfr.202400010
Bing Gao, Chenxu Cui, Fang Yan, Ning Li, Xuefeng Sun, Fangyu Wang, Chunfeng Wang

Scope

Celiac disease (CD) is an allergic intestinal disease caused mainly by gliadin in wheat, which is widespread in the population and currently lacks effective treatment. α-Gliadin peptides cause cellular damage by substantially increasing cellular reactive oxygen species (ROS) levels.

Methods and results

This study investigates the protective effect of 11 pea-derived peptides (PPs) on ɑ-gliadin peptide (P31-43) treated Caco-2 cells. Results show that cells treated with PP2, PP5, and PP6 peptides significantly reduce the cell mortality caused by P31-43. Three PPs significantly reduce the P31-43-induced decrease in ROS levels to control levels, and there is no difference between them and the vitamin C (Vc) group. The results in terms of antioxidant-related enzymes show that PPs significantly decrease superoxide dismutase activity (SOD), glutathione reductases (GR), and glutathione (GSH)/oxidized glutathione (GSSG) levels, thus significantly enhancing the antioxidant level of cells. By studying the key proteins of the Kelch-like ECH-associated protein 1 (Keap1)/NF-E2-related factor 2 (Nrf2) pathway, it is found that PPs activate the Keap1/Nrf2 signaling pathway.

Conclusion

The study finds that peptides from peas can effectively alleviate ɑ-gliadin peptide-induced cell damage. The discovery of these food-derived peptides provides novel potential solutions for the prevention and treatment of CD.

范围:乳糜泻(CD)是一种过敏性肠道疾病,主要由小麦中的麦胶蛋白引起,在人群中广泛存在,目前缺乏有效的治疗方法。α-麦胶蛋白肽通过大幅提高细胞活性氧(ROS)水平造成细胞损伤:本研究调查了 11 种豌豆衍生肽(PPs)对经ɑ-麸质肽(P31-43)处理的 Caco-2 细胞的保护作用。结果表明,用 PP2、PP5 和 PP6 肽处理的细胞能显著降低 P31-43 导致的细胞死亡率。三种多肽能明显降低 P31-43 诱导的 ROS 水平,使其降至控制水平,且与维生素 C(Vc)组无差异。抗氧化相关酶的研究结果表明,PPs能明显降低超氧化物歧化酶(SOD)活性、谷胱甘肽还原酶(GR)和谷胱甘肽(GSH)/氧化谷胱甘肽(GSSG)水平,从而显著提高细胞的抗氧化水平。通过研究 Kelch-like ECH-associated protein 1 (Keap1)/NF-E2-related factor 2 (Nrf2)通路的关键蛋白,发现 PPs 可激活 Keap1/Nrf2 信号通路:研究发现,豌豆肽能有效缓解ɑ-麸质肽诱导的细胞损伤。这些食物肽的发现为预防和治疗 CD 提供了新的潜在解决方案。
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引用次数: 0
Effects of Anthocyanins on Cognition and Vascular Function: A Systematic Review 花青素对认知和血管功能的影响:系统综述。
IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY Pub Date : 2024-07-03 DOI: 10.1002/mnfr.202300502
Lucy R. Ellis, Christine Boesch, Louise Dye

Scope

Good vascular function is crucial for cerebral blood flow and cognitive performance. Diets high in anthocyanins have been shown to improve vascular function and are associated with improvements in cognition. This systematic review investigates randomized controlled trials examining the impact of anthocyanin intake on both cognition and vascular function.

Methods and results

Of the 1486 studies identified through searching Ovid Medline and AMED, PsychInfo, Web of Science, and Scopus, 20 studies are selected which measured cognitive and vascular function. Overall, positive effects on verbal and working memory are observed, which are supported by studies using functional magnetic resonance imaging to demonstrate increased blood flow in brain regions related to these cognitive domains. However, effects of anthocyanins on blood pressure and markers of endothelial function are inconsistent.

Conclusion

This systematic review provides evidence for a positive effect of anthocyanins on cognition and insight into the relevance of endothelial function. Anthocyanins are widely available and can be easily consumed in a range of different fruits, vegetables, and other products. Further studies should establish the optimal daily intake of anthocyanins for cardiovascular and cognitive health.

范围良好的血管功能对脑血流量和认知能力至关重要。花青素含量高的饮食可改善血管功能,并与认知能力的改善相关。本系统综述调查了研究花青素摄入量对认知和血管功能影响的随机对照试验:通过检索 Ovid Medline 和 AMED、PsychInfo、Web of Science 和 Scopus,在 1486 项研究中选出了 20 项测量认知和血管功能的研究。总体而言,这些研究观察到了花青素对言语记忆和工作记忆的积极影响,使用功能性磁共振成像技术进行的研究也证实了这一点,该技术显示与这些认知领域相关的大脑区域的血流量有所增加。然而,花青素对血压和内皮功能指标的影响并不一致:本系统综述提供了花青素对认知产生积极影响的证据,并深入分析了内皮功能的相关性。花青素的来源广泛,可以从各种不同的水果、蔬菜和其他产品中轻松摄取。进一步的研究应确定花青素对心血管和认知健康的最佳日摄入量。
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引用次数: 0
期刊
Molecular Nutrition & Food Research
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