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Rosmarinic Acid Attenuates Salmonella enteritidis-Induced Inflammation via Regulating TLR9/NF-κB Signaling Pathway and Intestinal Microbiota. 迷迭香酸通过调节TLR9/NF-κB信号通路和肠道微生物群减轻肠炎沙门氏菌诱发的炎症
IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-18 DOI: 10.3390/antiox13101265
Dandan Yi, Menghui Wang, Xia Liu, Lanqian Qin, Yu Liu, Linyi Zhao, Ying Peng, Zhengmin Liang, Jiakang He

Salmonella enteritidis (SE) infection disrupts the homeostasis of the intestinal microbiota, causing an intestinal inflammatory response and posing a great threat to human and animal health. The unreasonable use of antibiotics has led to an increase in the prevalence of drug-resistant SE, increasing the difficulty of controlling SE. Therefore, new drug strategies and research are urgently needed to control SE. Rosmarinic acid (RA) is a natural phenolic acid with various pharmacological activities, including antioxidant, anti-inflammatory and antibacterial properties. However, the protective effects and mechanism of RA on intestinal inflammation and the gut microbial disorders caused by SE have not been fully elucidated. In this study, RAW264.7 cells, MCECs and BALB/c mice were challenged with SE to assess the protective effects and mechanisms of RA. The results showed that RA enhanced the phagocytic ability of RAW264.7 cells, reduced the invasion and adhesion ability of SE in MCECs, and inhibited SE-induced inflammation in cells. Moreover, RA inhibited the activation of the NF-κB signaling pathway by upregulating TLR9 expression. Importantly, we found that RA provided protection against SE and increased the diversity and abundance of the intestinal microbiota in mice. Compared with infection control, RA significantly increased the abundance of Firmicutes and Acidibacteria and decreased the abundance of Proteobacteria, Epsilonbacteraeota and Bacteroidota. However, RA failed to alleviate SE-induced inflammation and lost its regulatory effects on the TLR9/NF-κB signaling pathway after destroying the gut microbiota with broad-spectrum antibiotics. These results indicated that RA attenuated SE-induced inflammation by regulating the TLR9/NF-κB signaling pathway and maintaining the homeostasis of the gut microbiota. Our study provides a new strategy for preventing SE-induced intestinal inflammation.

肠炎沙门氏菌(SE)感染会破坏肠道微生物群的平衡,引起肠道炎症反应,对人类和动物的健康构成巨大威胁。抗生素的不合理使用导致耐药 SE 的流行率上升,增加了控制 SE 的难度。因此,迫切需要新的药物策略和研究来控制 SE。迷迭香酸(RA)是一种天然酚酸,具有多种药理活性,包括抗氧化、抗炎和抗菌特性。然而,RA 对 SE 引起的肠道炎症和肠道微生物紊乱的保护作用和机制尚未完全阐明。在本研究中,RAW264.7 细胞、MCECs 和 BALB/c 小鼠受到 SE 的挑战,以评估 RA 的保护作用和机制。结果显示,RA能增强RAW264.7细胞的吞噬能力,降低SE对MCECs的侵袭和粘附能力,抑制SE诱导的细胞炎症。此外,RA 还能通过上调 TLR9 的表达来抑制 NF-κB 信号通路的激活。重要的是,我们发现 RA 能保护小鼠免受 SE 的感染,并能增加小鼠肠道微生物群的多样性和丰度。与感染对照组相比,RA能明显增加固缩菌和酸性杆菌的丰度,降低蛋白杆菌、epsilonbacteraeota和类杆菌的丰度。然而,在使用广谱抗生素破坏肠道微生物群后,RA 未能缓解 SE 诱导的炎症,也失去了对 TLR9/NF-κB 信号通路的调节作用。这些结果表明,RA通过调节TLR9/NF-κB信号通路和维持肠道微生物群的平衡来减轻SE诱导的炎症。我们的研究为预防SE诱导的肠道炎症提供了一种新策略。
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引用次数: 0
Microplastic-Enhanced Cadmium Toxicity: A Growing Threat to the Sea Grape, Caulerpa lentillifera. 微塑料增强的镉毒性:海葡萄(Caulerpa lentillifera)面临的日益严重的威胁。
IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-18 DOI: 10.3390/antiox13101268
Weilong Zhou, Haolong Zheng, Yingyin Wu, Junyi Lin, Xiaofei Ma, Yixuan Xing, Huilong Ou, Hebert Ely Vasquez, Xing Zheng, Feng Yu, Zhifeng Gu

The escalating impact of human activities has led to the accumulation of microplastics (MPs) and heavy metals in marine environments, posing serious threats to marine ecosystems. As essential components of oceanic ecosystems, large seaweeds such as Caulerpa lentillifera play a crucial role in maintaining ecological balance. This study investigated the effects of MPs and cadmium (Cd) on the growth, physiology, biochemistry, and Cd accumulation in C. lentillifera while elucidating the underlying molecular regulatory mechanisms. The results demonstrated that exposure to MPs alone significantly promoted the growth. In contrast, exposure to Cd either alone or in combination with MPs significantly suppressed growth by reducing stem and stolon length, bud count, weight gain, and specific growth rates. Combined exposure to MPs and Cd exhibited the most pronounced inhibitory effect on growth. MPs had negligible impact while Cd exposure either alone or combined with MPs impaired antioxidant defenses and exacerbated oxidative damage; with combined exposure being the most detrimental. Analysis of Cd content revealed that MPs significantly increased Cd accumulation in algae intensifying its toxic effects. Gene expression analysis revealed that Cd exposure down-regulated key genes involved in photosynthesis, impairing both photosynthetic efficiency and energy conversion. The combined exposure of MPs and Cd further exacerbated these effects. In contrast, MPs alone activated the ribosome pathway, supporting ribosomal stability and protein synthesis. Additionally, both Cd exposure alone or in combination with MPs significantly reduced chlorophyll B and soluble sugar content, negatively impacting photosynthesis and nutrient accumulation. In summary, low concentrations of MPs promoted C. lentillifera growth, but the presence of Cd hindered it by disrupting photosynthesis and antioxidant mechanisms. Furthermore, the coexistence of MPs intensified the toxic effects of Cd. These findings enhance our understanding of how both MPs and Cd impact large seaweed ecosystems and provide crucial insights for assessing their ecological risks.

人类活动的影响不断升级,导致海洋环境中的微塑料(MPs)和重金属不断积累,对海洋生态系统构成严重威胁。作为海洋生态系统的重要组成部分,大型海藻(如Caulerpa lentillifera)在维持生态平衡方面发挥着至关重要的作用。本研究调查了 MPs 和镉(Cd)对 C. lentillifera 的生长、生理、生化和镉积累的影响,同时阐明了潜在的分子调控机制。结果表明,单独接触 MPs 能显著促进生长。相比之下,单独接触镉或与多羟基化合物一起接触镉会显著抑制生长,因为镉会减少茎和匍匐茎的长度、芽数、增重和特定生长率。同时接触多溴联苯醚和镉对生长的抑制作用最为明显。MPs 的影响可以忽略不计,而单独接触或与 MPs 结合接触镉会损害抗氧化防御能力,加剧氧化损伤;结合接触镉的危害最大。镉含量分析表明,多溴联苯醚显著增加了藻类体内的镉积累,加剧了镉的毒性作用。基因表达分析表明,镉暴露会下调参与光合作用的关键基因,从而影响光合效率和能量转换。MPs 和镉的联合暴露进一步加剧了这些影响。相反,MPs 单独激活了核糖体途径,支持核糖体的稳定性和蛋白质的合成。此外,单独接触镉或同时接触 MPs 都会显著降低叶绿素 B 和可溶性糖含量,从而对光合作用和养分积累产生负面影响。总之,低浓度的 MPs 能促进 C. lentillifera 的生长,但镉的存在会破坏光合作用和抗氧化机制,从而阻碍其生长。此外,MPs 的共存加剧了镉的毒性效应。这些发现加深了我们对 MPs 和镉如何影响大型海藻生态系统的理解,并为评估它们的生态风险提供了重要的启示。
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引用次数: 0
Radical Scavenging Capacity and In Vitro Cytoprotective Effects of Great Salt Lake-Derived Processed Mineral Water. 大盐湖加工矿泉水的自由基清除能力和体外细胞保护作用
IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-18 DOI: 10.3390/antiox13101266
Takayuki Mokudai, Seiko Nakagawa, Hiroyasu Kanetaka, Kazuo Oda, Hiroya Abe, Yoshimi Niwano

The Great Salt Lake, located in Utah, USA, is a saltwater lake with no outlet and is surrounded by vast mountains and salt deserts. We aimed to use Great Salt Lake-derived processed mineral water (hereafter termed as GSL-MW) for maintaining oral health. Therefore, we examined its radical scavenging activity as an antioxidant and its cytoprotective effect on human gingival fibroblasts (hGFs). The scavenging activity against O2•- radicals was determined by an electron spin resonance (ESR)-spin trapping technique using two kinds of O2•- generation systems; however, we could not reach any concrete conclusion because of the interference caused by GSL-MW in both systems. Detection of ·OH radicals using the ESR-spin trapping technique and kinetic analyses using double-reciprocal plots (corresponding to Lineweaver-Burk plots that are used to represent enzyme kinetics) revealed that GSL-MW has the ability to scavenge ·OH radicals. GSL-MW also showed a weak 2,2-diphenyl-1-picrylhydrazyl (DPPH; a stable radical)-scavenging activity. Regarding the cytoprotective effects, subconfluent hGFs pretreated with 10× and 100× dilutions of GSL-MW for 3 min and then exposed to harsh environmental conditions, such as pure water or 100 μM H2O2 for 3 min, showed enhanced cell viability rate. Moreover, 10× and 100× dilutions of GSL-MW reduced oxidative damage in confluent hGFs exposed to 12.5 and 25 mM H2O2. Our findings show that GSL-MW has antioxidant potential and cytoprotective effects on hGFs, suggesting that GSL-MW can be used to maintain oral health.

大盐湖位于美国犹他州,是一个没有出海口的咸水湖,周围环绕着广袤的山脉和盐漠。我们的目的是利用大盐湖加工矿泉水(以下简称大盐湖矿泉水)来维护口腔健康。因此,我们研究了其作为抗氧化剂的自由基清除活性及其对人牙龈成纤维细胞(hGFs)的细胞保护作用。我们使用电子自旋共振(ESR)--自旋捕获技术,在两种 O2--生成系统中测定了它对 O2--自由基的清除活性;但是,由于 GSL-MW 在两种系统中都造成了干扰,我们无法得出任何具体结论。利用 ESR-自旋捕获技术检测 -OH 自由基,并利用双倒数图(相当于用于表示酶动力学的 Lineweaver-Burk 图)进行动力学分析,结果表明 GSL-MW 具有清除 -OH 自由基的能力。GSL-MW 还显示出微弱的 2,2-二苯基-1-苦基肼(DPPH,一种稳定自由基)清除活性。在细胞保护作用方面,用 10 倍和 100 倍稀释的 GSL-MW 预处理亚融合 hGFs 3 分钟,然后将其暴露在苛刻的环境条件下(如纯水或 100 μM H2O2)3 分钟,结果显示细胞存活率提高。此外,10 倍和 100 倍稀释的 GSL-MW 还能减少暴露于 12.5 和 25 mM H2O2 的汇合 hGF 的氧化损伤。我们的研究结果表明,GSL-MW 具有抗氧化潜力和对 hGFs 的细胞保护作用,这表明 GSL-MW 可用于维护口腔健康。
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引用次数: 0
Association Between NOX2-Mediated Oxidative Stress, Low-Grade Endotoxemia, Hypoalbuminemia, and Clotting Activation in COVID-19. COVID-19中NOX2介导的氧化应激、低度内毒素血症、低白蛋白血症和凝血活化之间的关系
IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-17 DOI: 10.3390/antiox13101260
Roberto Carnevale, Cristina Nocella, Raffaella Marocco, Paola Zuccalà, Anna Carraro, Vittorio Picchio, Alessandra Oliva, Roberto Cangemi, Maria Claudia Miele, Massimiliano De Angelis, Francesca Cancelli, Giovanni Enrico Casciaro, Luca Cristiano, Pasquale Pignatelli, Giacomo Frati, Mario Venditti, Francesco Pugliese, Claudio Maria Mastroianni, Francesco Violi, Lorenzo Ridola, Cosmo Del Borgo, Silvia Palmerio, Emiliano Valenzi, Rita Carnevale, Domenico Alvaro, Miriam Lichtner, Vincenzo Cardinale

Low-grade endotoxemia by lipopolysaccharide (LPS) has been detected in COVID-19 and could favor thrombosis via eliciting a pro-inflammatory and pro-coagulant state. The aim of this study was to analyze the mechanism accounting for low-grade endotoxemia and its relationship with oxidative stress and clotting activation thrombosis in COVID-19. We measured serum levels of sNOX2-dp, zonulin, LPS, D-dimer, and albumin in 175 patients with COVID-19, classified as having or not acute respiratory distress syndrome (ARDS), and 50 healthy subjects. Baseline levels of sNOX2-dp, LPS, zonulin, D-dimer, albumin, and hs-CRP were significantly higher in COVID-19 compared to controls. In COVID-19 patients with ARDS, sNOX2-dp, LPS, zonulin, D-dimer, and hs-CRP were significantly higher compared to COVID-19 patients without ARDS. Conversely, concentration of albumin was lower in patients with ARDS compared with those without ARDS and inversely associated with LPS. In the COVID-19 cohort, the number of patients with ARDS progressively increased according to sNOX2-dp and LPS quartiles; a significant correlation between LPS and sNOX2-dp and LPS and D-dimer was detected in COVID-19. In a multivariable logistic regression model, LPS/albumin levels and D-dimer predicted thrombotic events. In COVID-19 patients, LPS is significantly associated with a hypercoagulation state and disease severity. In vitro, LPS can increase endothelial oxidative stress and coagulation biomarkers that were reduced by the treatment with albumin. In conclusion, impaired gut barrier permeability, increased NOX2 activation, and low serum albumin may account for low-grade endotoxemia and may be implicated in thrombotic events in COVID-19.

在COVID-19中检测到了由脂多糖(LPS)引起的低度内毒素血症,这种血症可通过激发促炎症和促凝血状态而有利于血栓形成。本研究旨在分析低度内毒素血症的机制及其与 COVID-19 中氧化应激和凝血活化血栓形成的关系。我们测量了 175 例 COVID-19 患者(分为急性呼吸窘迫综合征(ARDS)与否)和 50 例健康受试者血清中 sNOX2-dp、zonulin、LPS、D-二聚体和白蛋白的水平。与对照组相比,COVID-19 患者的 sNOX2-dp、LPS、zonulin、D-二聚体、白蛋白和 hs-CRP 基线水平明显较高。在患有 ARDS 的 COVID-19 患者中,sNOX2-dp、LPS、zonulin、D-二聚体和 hs-CRP 与未患有 ARDS 的 COVID-19 患者相比明显升高。相反,与无 ARDS 患者相比,ARDS 患者的白蛋白浓度较低,且与 LPS 成反比。在COVID-19队列中,根据sNOX2-dp和LPS四分位数的不同,ARDS患者人数逐渐增加;在COVID-19中,LPS与sNOX2-dp、LPS与D-二聚体之间存在显著相关性。在多变量逻辑回归模型中,LPS/白蛋白水平和 D-二聚体可预测血栓事件。在 COVID-19 患者中,LPS 与高凝状态和疾病严重程度明显相关。在体外,LPS 可增加内皮氧化应激和凝血生物标志物,而用白蛋白治疗可降低这些生物标志物。总之,肠道屏障通透性受损、NOX2 激活增加和血清白蛋白低可能是低度内毒素血症的原因,也可能与 COVID-19 中的血栓事件有关。
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引用次数: 0
AIBP Protects Müller Glial Cells Against Oxidative Stress-Induced Mitochondrial Dysfunction and Reduces Retinal Neuroinflammation. AIBP 可保护缪勒神经胶质细胞免受氧化应激诱导的线粒体功能障碍的影响,并减轻视网膜神经炎症。
IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-17 DOI: 10.3390/antiox13101252
Seunghwan Choi, Soo-Ho Choi, Tonking Bastola, Keun-Young Kim, Sungsik Park, Robert N Weinreb, Yury I Miller, Won-Kyu Ju

Glaucoma, an optic neuropathy with the loss of retinal ganglion cells (RGCs), is a leading cause of irreversible vision loss. Oxidative stress and mitochondrial dysfunction have a significant role in triggering glia-driven neuroinflammation and subsequent glaucomatous RGC degeneration in the context of glaucoma. It has previously been shown that apolipoprotein A-I binding protein (APOA1BP or AIBP) has an anti-inflammatory function. Moreover, Apoa1bp-/- mice are characterized by retinal neuroinflammation and RGC loss. In this study, we found that AIBP deficiency exacerbated the oxidative stress-induced disruption of mitochondrial dynamics and function in the retina, leading to a further decline in visual function. Mechanistically, AIBP deficiency-induced oxidative stress triggered a reduction in glycogen synthase kinase 3β and dynamin-related protein 1 phosphorylation, optic atrophy type 1 and mitofusin 1 and 2 expression, and oxidative phosphorylation, as well as the activation of mitogen-activated protein kinase (MAPK) in Müller glia dysfunction, leading to cell death and inflammatory responses. In vivo, the administration of recombinant AIBP (rAIBP) effectively protected the structural and functional integrity of retinal mitochondria under oxidative stress conditions and prevented vision loss. In vitro, incubation with rAIBP safeguarded the structural integrity and bioenergetic performance of mitochondria and concurrently suppressed MAPK activation, apoptotic cell death, and inflammatory response in Müller glia. These findings support the possibility that AIBP promotes RGC survival and restores visual function in glaucomatous mice by ameliorating glia-driven mitochondrial dysfunction and neuroinflammation.

青光眼是一种视网膜神经节细胞(RGC)丧失的视神经病变,是造成不可逆视力丧失的主要原因。氧化应激和线粒体功能障碍在引发神经胶质细胞驱动的神经炎症和随后的青光眼 RGC 退化中起着重要作用。此前已有研究表明,载脂蛋白 A-I 结合蛋白(APOA1BP 或 AIBP)具有抗炎功能。此外,Apoa1bp-/-小鼠具有视网膜神经炎症和 RGC 丢失的特征。在这项研究中,我们发现 AIBP 缺乏会加剧氧化应激引起的视网膜线粒体动力学和功能的破坏,从而导致视功能进一步下降。从机理上讲,AIBP 缺乏诱导的氧化应激引发了糖原合酶激酶 3β 和动态相关蛋白 1 磷酸化、视神经萎缩 1 型和丝裂蛋白 1 和 2 表达、氧化磷酸化的减少,以及 Müller 胶质功能障碍中丝裂原活化蛋白激酶(MAPK)的激活,从而导致细胞死亡和炎症反应。在体内,服用重组 AIBP(rAIBP)可有效保护氧化应激条件下视网膜线粒体结构和功能的完整性,防止视力丧失。在体外,用 rAIBP 培养可保护线粒体的结构完整性和生物能,同时抑制 MAPK 激活、细胞凋亡和 Müller 胶质的炎症反应。这些发现支持了AIBP通过改善胶质细胞驱动的线粒体功能障碍和神经炎症来促进RGC存活和恢复青光眼小鼠视觉功能的可能性。
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引用次数: 0
Metabolome and Metagenome Integration Unveiled Synthesis Pathways of Novel Antioxidant Peptides in Fermented Lignocellulosic Biomass of Palm Kernel Meal. 代谢组和元基因组整合揭示了发酵棕榈仁粕木质纤维素生物质中新型抗氧化肽的合成途径。
IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-17 DOI: 10.3390/antiox13101253
Hammad Qamar, Rong He, Yuanfei Li, Min Song, Dun Deng, Yiyan Cui, Miao Yu, Xianyong Ma

Approximately one-third of the entire world's food resources are deemed to be wasted. Palm kernel meal (PKM), a product that is extensively generated by the palm oil industry, exhibits a unique nutrient-rich composition. However, its recycling is seldom prioritized due to numerous factors. To evaluate the impact of enzymatic pretreatment and Lactobacillus plantarum and Lactobacillus reuteri fermentation upon the antioxidant activity of PKM, we implemented integrated metagenomics and metabolomics approaches. The substantially enhanced (p < 0.05) property of free radicals scavenging, as well as total flavonoids and polyphenols, demonstrated that the biotreated PKM exhibited superior antioxidant capacity. Non-targeted metabolomics disclosed that the Lactobacillus fermentation resulted in substantial (p < 0.05) biosynthesis of 25 unique antioxidant biopeptides, along with the increased (p < 0.05) enrichment ratio of the isoflavonoids and secondary metabolites biosynthesis pathways. The 16sRNA sequencing and correlation analysis revealed that Limosilactobacillus reuteri, Pediococcus acidilactici, Lacticaseibacillus paracasei, Pediococcus pentosaceus, Lactiplantibacillus plantarum, Limosilactobacillus fermentum, and polysaccharide lyases had significantly dominated (p < 0.05) proportions in PMEL, and these bacterial species were strongly (p < 0.05) positively interrelated with antioxidants peptides. Fermented PKM improves nutritional value by enhancing beneficial probiotics, enzymes, and antioxidants and minimizing anti-nutritional factors, rendering it an invaluable feed ingredient and gut health promoter for animals, multifunctional food elements, or as an ingredient in sustainable plant-based diets for human utilization, and functioning as a culture substrate in the food sector.

全世界约有三分之一的粮食资源被浪费。棕榈仁粕(PKM)是棕榈油行业广泛生产的一种产品,具有独特的营养成分。然而,由于诸多因素,其回收利用很少被优先考虑。为了评估酶预处理、植物乳杆菌和吕特氏乳杆菌发酵对 PKM 抗氧化活性的影响,我们采用了元基因组学和代谢组学的综合方法。经生物处理的 PKM 的自由基清除能力、总黄酮类化合物和多酚类物质的含量均大幅提高(p < 0.05),这表明经生物处理的 PKM 具有卓越的抗氧化能力。非靶向代谢组学显示,乳酸菌发酵导致 25 种独特的抗氧化生物肽的大量生物合成(p < 0.05),同时异黄酮和次生代谢物生物合成途径的富集比例也有所提高(p < 0.05)。16sRNA 测序和相关分析表明,Limosilactobacillus reuteri、Pediococcus acidilactici、Lacticaseibacillus paracasei、Pediococcus pentosaceus、Lactiplantibacillus plantarum、Limosilactobacillus fermentum 和多糖裂解酶在 PME 中的比例明显占优势(p < 0.05),而且这些细菌种类与抗氧化剂肽呈强烈的正相关(p < 0.05)。发酵 PKM 可提高有益益生菌、酶和抗氧化剂的含量,减少抗营养因子,从而提高营养价值,使其成为宝贵的饲料配料和动物肠道健康促进剂、多功能食品元素,或作为可持续植物膳食的配料供人类使用,并可作为食品行业的培养基。
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引用次数: 0
Recovery of Selenium-Enriched Polysaccharides from Cardamine violifolia Residues: Comparison on Structure and Antioxidant Activity by Different Extraction Methods. 从 Cardamine violifolia 残留物中回收富硒多糖:比较不同提取方法的结构和抗氧化活性
IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-17 DOI: 10.3390/antiox13101251
Yong Liang, Jiali Yu, Lulu Wu, Xin Cong, Haiyuan Liu, Xu Chen, Shuyi Li, Zhenzhou Zhu

The residues from selenium-enriched Cardamine violifolia after the extraction of protein were still rich in polysaccharides. Thus, the recovery of selenium polysaccharides (SePSs) was compared using hot water extraction and ultrasonic-assisted extraction techniques. The yield, extraction rate, purity, specific energy consumption, and content of total and organic selenium from different SePS extracts were determined. The results indicated that at conditions of 250 W (ultrasonic power), 30 °C, and a liquid-to-material ratio of 30:1 extracted for 60 min, the yield of SePSs was 3.97 ± 0.07%, the extraction rate was 22.76 ± 0.40%, and the purity was 65.56 ± 0.35%, while the total and organic selenium content was 749.16 ± 6.91 mg/kg and 628.37 ± 5.93 mg/kg, respectively. Compared to traditional hot water extraction, ultrasonic-assisted extraction significantly improves efficiency, reduces energy use, and boosts both total and organic selenium content in the extract. Measurements of particle size, molecular weight, and monosaccharide composition, along with infrared and ultraviolet spectroscopy, revealed that ultrasonic-assisted extraction breaks down long-chain structures, decreases particle size, and changes monosaccharide composition in SePSs, leading to lower molecular weight and reduced dispersity. The unique structure of SePSs, which integrates selenium with polysaccharide groups, results in markedly improved antioxidant activity and reducing power, even at low concentrations, due to the synergistic effects of selenium and polysaccharides. This study establishes a basis for using SePSs in functional foods.

富硒红豆杉提取蛋白质后的残留物中仍含有丰富的多糖。因此,采用热水提取和超声波辅助提取技术比较了硒多糖(SePSs)的回收率。测定了不同 SePS 提取物的产率、提取率、纯度、比能量消耗以及总硒和有机硒的含量。结果表明,在 250 W(超声波功率)、30 °C、液料比为 30:1 的条件下萃取 60 分钟,SePS 的产率为 3.97 ± 0.07%,萃取率为 22.76 ± 0.40%,纯度为 65.56 ± 0.35%,总硒和有机硒的含量分别为 749.16 ± 6.91 mg/kg 和 628.37 ± 5.93 mg/kg。与传统的热水萃取相比,超声波辅助萃取显著提高了效率,降低了能耗,并提高了提取物中的总硒和有机硒含量。粒度、分子量和单糖组成的测量以及红外光谱和紫外光谱的分析表明,超声波辅助萃取能破坏 SePSs 中的长链结构,减小粒度,改变单糖组成,从而降低分子量和分散性。SePSs 的独特结构将硒与多糖基团结合在一起,由于硒和多糖的协同作用,即使在低浓度下,SePSs 的抗氧化活性和还原力也明显提高。这项研究为在功能食品中使用 SePSs 奠定了基础。
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引用次数: 0
Aged Gut Microbiome Induces Metabolic Impairment and Hallmarks of Vascular and Intestinal Aging in Young Mice. 衰老的肠道微生物组诱发年轻小鼠的代谢损伤以及血管和肠道衰老的特征
IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-17 DOI: 10.3390/antiox13101250
Chak-Kwong Cheng, Lianwei Ye, Yuanyuan Zuo, Yaling Wang, Li Wang, Fuyong Li, Sheng Chen, Yu Huang

Aging, an independent risk factor for cardiometabolic diseases, refers to a progressive deterioration in physiological function, characterized by 12 established hallmarks. Vascular aging is driven by endothelial dysfunction, telomere dysfunction, oxidative stress, and vascular inflammation. This study investigated whether aged gut microbiome promotes vascular aging and metabolic impairment. Fecal microbiome transfer (FMT) was conducted from aged (>75 weeks old) to young C57BL/6 mice (8 weeks old) for 6 weeks. Wire myography was used to evaluate endothelial function in aortas and mesenteric arteries. ROS levels were measured by dihydroethidium (DHE) staining and lucigenin-enhanced chemiluminescence. Vascular and intestinal telomere function, in terms of relative telomere length, telomerase reverse transcriptase expression and telomerase activity, were measured. Systemic inflammation, endotoxemia and intestinal integrity of mice were assessed. Gut microbiome profiles were studied by 16S rRNA sequencing. Some middle-aged mice (40-42 weeks old) were subjected to chronic metformin treatment and exercise training for 4 weeks to evaluate their anti-aging benefits. Six-week FMT impaired glucose homeostasis and caused vascular dysfunction in aortas and mesenteric arteries in young mice. FMT triggered vascular inflammation and oxidative stress, along with declined telomerase activity and shorter telomere length in aortas. Additionally, FMT impaired intestinal integrity, and triggered AMPK inactivation and telomere dysfunction in intestines, potentially attributed to the altered gut microbial profiles. Metformin treatment and moderate exercise improved integrity, AMPK activation and telomere function in mouse intestines. Our data highlight aged microbiome as a mechanism that accelerates intestinal and vascular aging, suggesting the gut-vascular connection as a potential intervention target against cardiovascular aging and complications.

衰老是心血管代谢疾病的一个独立风险因素,是指生理功能的逐渐退化,有 12 个既定的特征。血管老化是由内皮功能障碍、端粒功能障碍、氧化应激和血管炎症驱动的。本研究调查了老年肠道微生物组是否会促进血管老化和代谢损伤。研究人员将老龄小鼠(>75 周龄)的粪便微生物组转移到年轻的 C57BL/6 小鼠(8 周龄)体内,为期 6 周。用线肌电图评估主动脉和肠系膜动脉的内皮功能。ROS水平通过二氢乙锭(DHE)染色和荧光素增强化学发光进行测量。通过端粒相对长度、端粒酶逆转录酶表达和端粒酶活性测量了血管和肠道端粒功能。对小鼠的全身炎症、内毒素血症和肠道完整性进行了评估。通过 16S rRNA 测序研究了肠道微生物组概况。对一些中年小鼠(40-42 周大)进行了为期 4 周的慢性二甲双胍治疗和运动训练,以评估它们的抗衰老功效。为期六周的FMT损害了葡萄糖稳态,并导致年轻小鼠主动脉和肠系膜动脉血管功能障碍。FMT引发血管炎症和氧化应激,同时导致端粒酶活性下降和主动脉端粒长度缩短。此外,FMT还会损害肠道完整性,引发肠道中AMPK失活和端粒功能障碍,这可能是由于肠道微生物谱发生了改变。二甲双胍治疗和适度运动改善了小鼠肠道的完整性、AMPK活化和端粒功能。我们的数据强调了老化的微生物组是加速肠道和血管老化的机制,这表明肠道与血管的联系是防止心血管老化和并发症的潜在干预目标。
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引用次数: 0
Biological Response of Treatment with Saffron Petal Extract on Cytokine-Induced Oxidative Stress and Inflammation in the Caco-2/Human Leukemia Monocytic Co-Culture Model. 藏红花花瓣提取物对 Caco-2/ 人白血病单核细胞共培养模型中细胞因子诱导的氧化应激和炎症的生物反应
IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-17 DOI: 10.3390/antiox13101257
Federica De Cecco, Sara Franceschelli, Valeria Panella, Maria Anna Maggi, Silvia Bisti, Arturo Bravo Nuevo, Damiano D'Ardes, Francesco Cipollone, Lorenza Speranza

The pathogenesis of Inflammatory Bowel Disease (IBD) involves complex mechanisms, including immune dysregulation, gut microbiota imbalances, oxidative stress, and defects in the gastrointestinal mucosal barrier. Current treatments for IBD often have significant limitations and adverse side effects, prompting a search for alternative therapeutic strategies. Natural products with anti-inflammatory and antioxidant properties have demonstrated potential for IBD management. There is increasing interest in exploring food industry waste as a source of bioactive molecules with healthcare applications. In this study, a co-culture system of Caco-2 cells and PMA-differentiated THP-1 macrophages was used to simulate the human intestinal microenvironment. Inflammation was induced using TNF-α and IFN-γ, followed by treatment with Saffron Petal Extract (SPE). The results demonstrated that SPE significantly attenuated oxidative stress and inflammation by downregulating the expression of pro-inflammatory mediators such as iNOS, COX-2, IL-1β, and IL-6 via modulation of the NF-κB pathway. Given that NF-κB is a key regulator of macrophage-driven inflammation, our findings support further investigation of SPE as a potential complementary therapeutic agent for IBD treatment.

炎症性肠病(IBD)的发病机制复杂,包括免疫失调、肠道微生物群失衡、氧化应激和胃肠道粘膜屏障缺陷。目前治疗 IBD 的方法往往有很大的局限性和不良副作用,这促使人们寻找替代治疗策略。具有抗炎和抗氧化特性的天然产品已被证明具有治疗 IBD 的潜力。越来越多的人开始关注将食品工业废弃物作为生物活性分子的来源,并将其应用于医疗保健领域。本研究使用 Caco-2 细胞和 PMA 分化的 THP-1 巨噬细胞共培养系统模拟人类肠道微环境。用 TNF-α 和 IFN-γ 诱导炎症,然后用藏红花花瓣提取物(SPE)处理。结果表明,SPE 通过调节 NF-κB 通路,下调了 iNOS、COX-2、IL-1β 和 IL-6 等促炎介质的表达,从而显著减轻了氧化应激和炎症反应。鉴于NF-κB是巨噬细胞驱动的炎症的关键调节因子,我们的研究结果支持进一步研究SPE,将其作为治疗IBD的潜在辅助治疗药物。
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引用次数: 0
α-Terpineol Induces Shelterin Components TRF1 and TRF2 to Mitigate Senescence and Telomere Integrity Loss via A Telomerase-Independent Pathway. α-松油醇通过端粒酶依赖性途径诱导保护素成分TRF1和TRF2减轻衰老和端粒完整性损失
IF 6 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-17 DOI: 10.3390/antiox13101258
Marianna Kapetanou, Sophia Athanasopoulou, Andreas Goutas, Dimitra Makatsori, Varvara Trachana, Efstathios Gonos

Cellular senescence is a hallmark of aging characterized by irreversible growth arrest and functional decline. Progressive telomeric DNA shortening in dividing somatic cells, programmed during development, leads to critically short telomeres that trigger replicative senescence and thereby contribute to aging. Therefore, protecting telomeres from DNA damage is essential in order to avoid entry into senescence and organismal aging. In several organisms, including mammals, telomeres are protected by a protein complex named shelterin that prevents DNA damage at the chromosome ends through the specific function of its subunits. Here, we reveal that the nuclear protein levels of shelterin components TRF1 and TRF2 decline in fibroblasts reaching senescence. Notably, we identify α-terpineol as an activator that effectively enhances TRF1 and TRF2 levels in a telomerase-independent manner, counteracting the senescence-associated decline in these crucial proteins. Moreover, α-terpineol ameliorates the cells' response to oxidative DNA damage, particularly at the telomeric regions, thus preserving telomere length and delaying senescence. More importantly, our findings reveal the significance of the PI3K/AKT pathway in the regulation of shelterin components responsible for preserving telomere integrity. In conclusion, this study deepens our understanding of the molecular pathways involved in senescence-associated telomere dysfunction and highlights the potential of shelterin components to serve as targets of therapeutic interventions, aimed at promoting healthy aging and combating age-related diseases.

细胞衰老是衰老的一个标志,其特征是不可逆转的生长停滞和功能衰退。在发育过程中,分裂的体细胞中端粒DNA会逐渐缩短,导致端粒极短,引发复制衰老,从而导致衰老。因此,为了避免进入衰老和机体老化,保护端粒免受DNA损伤至关重要。在包括哺乳动物在内的一些生物体中,端粒受到一种名为 "保护蛋白"(shelterin)的蛋白质复合物的保护,该复合物通过其亚基的特定功能防止染色体末端的DNA损伤。在这里,我们揭示了在进入衰老期的成纤维细胞中,保护蛋白成分TRF1和TRF2的核蛋白水平会下降。值得注意的是,我们发现α-松油醇是一种激活剂,能以端粒酶无关的方式有效提高TRF1和TRF2的水平,从而抵消衰老相关的这些关键蛋白水平的下降。此外,α-松油醇还能改善细胞对氧化DNA损伤的反应,尤其是在端粒区域,从而保持端粒长度并延缓衰老。更重要的是,我们的研究结果揭示了 PI3K/AKT 通路在调控负责维护端粒完整性的保护蛋白成分中的重要作用。总之,这项研究加深了我们对参与衰老相关端粒功能障碍的分子途径的理解,并强调了保护蛋白成分作为治疗干预靶点的潜力,旨在促进健康衰老和防治与年龄相关的疾病。
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引用次数: 0
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