Salinity is a significant environmental component that affects the physiological state of aquatic species. This study aimed to investigate whether water salinity had an impact on the biochemical properties and meat quality of adult Aplodinotus grunniens during temporary rearing of 7 days. Salinity caused increased osmotic pressure and antioxidant enzyme activities of Aplodinotus grunniens, which were attributed to the increase in the content of alanine and glutamate. It raised the hardness and shear force with an increase in salinity, leading to an increase in water-holding capacity. Salinity enhanced the DHA ratio with a decrease in the atherosclerotic index and thrombosis index. Combined with the increase in flavor amino acids and nucleotides, salinity enhanced the umami taste of Aplodinotus grunniens. These findings suggest that temporary rearing in salinity might be a practical approach to improving the meat quality of adult Aplodinotus grunniens.
盐度是影响水生物种生理状态的重要环境因素。本研究旨在探讨盐度对暂养 7 天的草鱼成鱼的生化特性和肉质是否有影响。盐度导致草鱼的渗透压和抗氧化酶活性升高,这与丙氨酸和谷氨酸含量增加有关。盐度增加会提高硬度和剪切力,导致持水能力增加。盐度提高了 DHA 比率,降低了动脉粥样硬化指数和血栓形成指数。结合风味氨基酸和核苷酸的增加,盐度提高了草鱼的鲜味。这些研究结果表明,在盐度条件下临时饲养可能是改善成年草鱼肉质的一种实用方法。
{"title":"Effect of Different Salinities on the Biochemical Properties and Meat Quality of Adult Freshwater Drum (<i>Aplodinotus grunniens</i>) During Temporary Rearing.","authors":"Wanwen Chen, Sharifa Mohamed Miraji, Yu Tian, Xueyan Ma, Wu Jin, Haibo Wen, Gangchun Xu, Pao Xu, Hao Cheng","doi":"10.3390/antiox13101273","DOIUrl":"10.3390/antiox13101273","url":null,"abstract":"<p><p>Salinity is a significant environmental component that affects the physiological state of aquatic species. This study aimed to investigate whether water salinity had an impact on the biochemical properties and meat quality of adult <i>Aplodinotus grunniens</i> during temporary rearing of 7 days. Salinity caused increased osmotic pressure and antioxidant enzyme activities of <i>Aplodinotus grunniens</i>, which were attributed to the increase in the content of alanine and glutamate. It raised the hardness and shear force with an increase in salinity, leading to an increase in water-holding capacity. Salinity enhanced the DHA ratio with a decrease in the atherosclerotic index and thrombosis index. Combined with the increase in flavor amino acids and nucleotides, salinity enhanced the umami taste of <i>Aplodinotus grunniens</i>. These findings suggest that temporary rearing in salinity might be a practical approach to improving the meat quality of adult <i>Aplodinotus grunniens</i>.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"13 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11504243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: T-006, a novel neuroprotective derivative of tetramethylpyrazine (TMP), exhibits multifunctional neuroprotective properties. T-006 has been shown to improve neurological and behavioral functions in animal models of ischemic stroke and neurodegenerative diseases. The present study aims to further elucidate the mechanisms underlying the protective effects of T-006 against oxidative injuries induced by glutamate or hypoxia.
Methods: Mouse hippocampal HT22 cells were used to evaluate the neuroprotective effects of T-006 against glutamate-induced injuries, while mouse brain endothelial bEnd.3 cells were used to evaluate the cerebrovascular protective effects of T-006 against oxygen-glucose deprivation followed by reperfusion (OGD/R)-induced injuries. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry were used to measure cell viability and oxidative stress. Western blot and immunofluorescence analyses of protein expression were used to study cell signaling pathways.
Results: T-006 exhibited significant protective effects in both oxidative injury models. In HT22 cells, T-006 reduced cell death and enhanced antioxidant capacity by upregulating mTOR and nuclear factor erythroid 2-related factor 2/Heme oxygenase-1 (Nrf2/HO-1) signaling. Similarly, in bEnd.3 cells, T-006 reduced oxidative injuries and preserved tight junction integrity through Nrf2/HO-1 upregulation. These effects were inhibited by LY294002, a Phosphoinositide 3-kinase (PI3K) inhibitor.
Conclusions: T-006 may exert its neuroprotective and cerebrovascular protective effects via the regulation of PI3K/AKT-mediated pathways, which facilitate downstream mTOR and Nrf2 signaling, leading to improved cell survival and antioxidant defenses.
背景:T-006是四甲基吡嗪(TMP)的一种新型神经保护衍生物,具有多功能神经保护特性。研究表明,T-006 可改善缺血性中风和神经退行性疾病动物模型的神经和行为功能。本研究旨在进一步阐明T-006对谷氨酸或缺氧诱导的氧化损伤具有保护作用的机制:方法:用小鼠海马HT22细胞评估T-006对谷氨酸诱导的损伤的神经保护作用,用小鼠脑内皮细胞bEnd.3评估T-006对氧-葡萄糖剥夺后再灌注(OGD/R)诱导的损伤的脑血管保护作用。3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四氮唑(MTT)测定法和流式细胞术用于测量细胞活力和氧化应激。蛋白表达的 Western 印迹和免疫荧光分析用于研究细胞信号通路:结果:T-006在两种氧化损伤模型中都表现出明显的保护作用。在HT22细胞中,T-006通过上调mTOR和核因子红细胞2相关因子2/血氧合酶-1(Nrf2/HO-1)信号转导,减少了细胞死亡并增强了抗氧化能力。同样,在bEnd.3细胞中,T-006通过上调Nrf2/HO-1减少了氧化损伤并保护了紧密连接的完整性。这些作用受到磷酸肌醇3-激酶(PI3K)抑制剂LY294002的抑制:结论:T-006可能通过调节PI3K/AKT介导的通路,促进下游mTOR和Nrf2信号转导,从而提高细胞存活率和抗氧化防御能力,发挥其神经保护和脑血管保护作用。
{"title":"Tetramethylpyrazine Analogue T-006 Protects Neuronal and Endothelial Cells Against Oxidative Stress via PI3K/AKT/mTOR and Nrf2 Signaling.","authors":"Guiliang Zhang, Zirong Liang, Yuqiang Wang, Zaijun Zhang, Pui-Man Hoi","doi":"10.3390/antiox13101272","DOIUrl":"10.3390/antiox13101272","url":null,"abstract":"<p><strong>Background: </strong>T-006, a novel neuroprotective derivative of tetramethylpyrazine (TMP), exhibits multifunctional neuroprotective properties. T-006 has been shown to improve neurological and behavioral functions in animal models of ischemic stroke and neurodegenerative diseases. The present study aims to further elucidate the mechanisms underlying the protective effects of T-006 against oxidative injuries induced by glutamate or hypoxia.</p><p><strong>Methods: </strong>Mouse hippocampal HT22 cells were used to evaluate the neuroprotective effects of T-006 against glutamate-induced injuries, while mouse brain endothelial bEnd.3 cells were used to evaluate the cerebrovascular protective effects of T-006 against oxygen-glucose deprivation followed by reperfusion (OGD/R)-induced injuries. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry were used to measure cell viability and oxidative stress. Western blot and immunofluorescence analyses of protein expression were used to study cell signaling pathways.</p><p><strong>Results: </strong>T-006 exhibited significant protective effects in both oxidative injury models. In HT22 cells, T-006 reduced cell death and enhanced antioxidant capacity by upregulating mTOR and nuclear factor erythroid 2-related factor 2/Heme oxygenase-1 (Nrf2/HO-1) signaling. Similarly, in bEnd.3 cells, T-006 reduced oxidative injuries and preserved tight junction integrity through Nrf2/HO-1 upregulation. These effects were inhibited by LY294002, a Phosphoinositide 3-kinase (PI3K) inhibitor.</p><p><strong>Conclusions: </strong>T-006 may exert its neuroprotective and cerebrovascular protective effects via the regulation of PI3K/AKT-mediated pathways, which facilitate downstream mTOR and Nrf2 signaling, leading to improved cell survival and antioxidant defenses.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"13 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11505549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lianmeng Ye, Jiazheng Zhao, Zhengpan Xiao, Wenyu Gu, Xiaoxuan Liu, Nuela Manka'a Che Ajuyo, Yi Min, Yechun Pei, Dayong Wang
Alzheimer's disease (AD) is an intractable and progressive neurodegenerative disease. Amyloid beta (Aβ) aggregation is the hallmark of AD. Aβ induces neurotoxicity through a variety of mechanisms, including interacting with membrane receptors to alter downstream signaling, damaging cellular or organelle membranes, interfering with protein degradation and synthesis, and inducing an excessive immune-inflammatory response, all of which lead to neuronal death and other pathological changes associated with AD. In this study, we extracted gene expression profiles from the GSE5281 and GSE97760 microarray datasets in the GEO (Gene Expression Omnibus) database, as well as from the Human Gene Database. We identified differentially expressed genes in the brain tissues of AD patients and healthy persons. Through GO, KEGG, and ROC analyses, annexin A2 (AnxA2) was identified as a putative target gene. Notably, accumulating evidence suggests that intracellular AnxA2 is a key regulator in various biological processes, including endocytosis, transmembrane transport, neuroinflammation, and apoptosis. Thus, we conducted a series of cell biology experiments to explore the biological function of AnxA2 in AD. The results indicate that AnxA2 gene knockdown primarily affects oxidative phosphorylation, cell cycle, AD, protein processing in the endoplasmic reticulum, SNARE interactions in vesicular transport, and autophagy. In SH-SY5Y cells secreting Aβ42, AnxA2 gene knockdown exacerbated Aβ42-induced cytotoxicity, including cell death, intracellular ROS levels, and neuronal senescence, altered cell cycle, and reduced ATP levels, suggesting its critical role in mitochondrial function maintenance. AnxA2 gene knockdown also exacerbated the inhibitory effect of Aβ42 on cell migration. AnxA2 overexpression reduced the inflammatory response induced by Aβ42, while its absence increased pro-inflammatory and decreased anti-inflammatory responses. Furthermore, AnxA2 gene knockdown facilitated apoptosis and decreased autophagy. These results indicated potential pathophysiological roles of AnxA2 in AD.
{"title":"Integrative Human Genetic and Cellular Analysis of the Pathophysiological Roles of AnxA2 in Alzheimer's Disease.","authors":"Lianmeng Ye, Jiazheng Zhao, Zhengpan Xiao, Wenyu Gu, Xiaoxuan Liu, Nuela Manka'a Che Ajuyo, Yi Min, Yechun Pei, Dayong Wang","doi":"10.3390/antiox13101274","DOIUrl":"10.3390/antiox13101274","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is an intractable and progressive neurodegenerative disease. Amyloid beta (Aβ) aggregation is the hallmark of AD. Aβ induces neurotoxicity through a variety of mechanisms, including interacting with membrane receptors to alter downstream signaling, damaging cellular or organelle membranes, interfering with protein degradation and synthesis, and inducing an excessive immune-inflammatory response, all of which lead to neuronal death and other pathological changes associated with AD. In this study, we extracted gene expression profiles from the GSE5281 and GSE97760 microarray datasets in the GEO (Gene Expression Omnibus) database, as well as from the Human Gene Database. We identified differentially expressed genes in the brain tissues of AD patients and healthy persons. Through GO, KEGG, and ROC analyses, annexin A2 (AnxA2) was identified as a putative target gene. Notably, accumulating evidence suggests that intracellular AnxA2 is a key regulator in various biological processes, including endocytosis, transmembrane transport, neuroinflammation, and apoptosis. Thus, we conducted a series of cell biology experiments to explore the biological function of AnxA2 in AD. The results indicate that AnxA2 gene knockdown primarily affects oxidative phosphorylation, cell cycle, AD, protein processing in the endoplasmic reticulum, SNARE interactions in vesicular transport, and autophagy. In SH-SY5Y cells secreting Aβ42, AnxA2 gene knockdown exacerbated Aβ42-induced cytotoxicity, including cell death, intracellular ROS levels, and neuronal senescence, altered cell cycle, and reduced ATP levels, suggesting its critical role in mitochondrial function maintenance. AnxA2 gene knockdown also exacerbated the inhibitory effect of Aβ42 on cell migration. AnxA2 overexpression reduced the inflammatory response induced by Aβ42, while its absence increased pro-inflammatory and decreased anti-inflammatory responses. Furthermore, AnxA2 gene knockdown facilitated apoptosis and decreased autophagy. These results indicated potential pathophysiological roles of AnxA2 in AD.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"13 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11504888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kyung-Mi Jung, Ga-Ram Yu, Da-Hoon Kim, Dong-Woo Lim, Won-Hwan Park
Massa Medicata Fermentata (MMF) is a naturally fermented product used to treat indigestion and increase stomach activity in traditional medicine. This study examined the ability of the hydrothermal extract of MMF to scavenge free radicals corresponding to biological oxidative stresses, further protecting essential biomolecules. The anti-inflammatory effects of MMF were evaluated in LPS-induced RAW264.7 macrophages and zebrafish. In addition, the effects of MMF on the body mass index (BMI) and cholesterol accumulation in adult zebrafish fed a high-cholesterol diet (HCD) for three weeks were examined. MMF prevented the DNA and lipid damage caused by oxidative stress, inhibited LDL oxidation, and reduced the expression of cytokines and related proteins (MAPK and NFκB), with prominent anti-oxidative pathway (NRF2-HO-1) activation properties. LPS-induced NO production was reduced, and the increase in BMI and TC caused by the HCD diet was suppressed by MMF in zebrafish embryos or adult zebrafish. The bioactive aglycone of quercetin may be contributing to the mechanisms of systemic effects. MMF has excellent antioxidant properties and is useful for improving inflammation status and metabolic profile, thus highlighting its potential as a healthy, functional food.
{"title":"Massa Medicata Fermentata, a Functional Food for Improving the Metabolic Profile via Prominent Anti-Oxidative and Anti-Inflammatory Effects.","authors":"Kyung-Mi Jung, Ga-Ram Yu, Da-Hoon Kim, Dong-Woo Lim, Won-Hwan Park","doi":"10.3390/antiox13101271","DOIUrl":"10.3390/antiox13101271","url":null,"abstract":"<p><p>Massa Medicata Fermentata (MMF) is a naturally fermented product used to treat indigestion and increase stomach activity in traditional medicine. This study examined the ability of the hydrothermal extract of MMF to scavenge free radicals corresponding to biological oxidative stresses, further protecting essential biomolecules. The anti-inflammatory effects of MMF were evaluated in LPS-induced RAW264.7 macrophages and zebrafish. In addition, the effects of MMF on the body mass index (BMI) and cholesterol accumulation in adult zebrafish fed a high-cholesterol diet (HCD) for three weeks were examined. MMF prevented the DNA and lipid damage caused by oxidative stress, inhibited LDL oxidation, and reduced the expression of cytokines and related proteins (MAPK and NFκB), with prominent anti-oxidative pathway (NRF2-HO-1) activation properties. LPS-induced NO production was reduced, and the increase in BMI and TC caused by the HCD diet was suppressed by MMF in zebrafish embryos or adult zebrafish. The bioactive aglycone of quercetin may be contributing to the mechanisms of systemic effects. MMF has excellent antioxidant properties and is useful for improving inflammation status and metabolic profile, thus highlighting its potential as a healthy, functional food.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"13 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11504248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Giovanni Tossetta, Sonia Fantone, Lucrezia Togni, Andrea Santarelli, Fabiola Olivieri, Daniela Marzioni, Maria Rita Rippo
Periodontitis affects up to 40% of adults over 60 years old and is a consequence of gingivitis. Periodontitis is characterized by a chronic inflammation, periodontal damage, and alveolar bone resorption. The nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2)/Kelch-like ECH-Associated Protein 1 (KEAP1) (NRF2/KEAP1) signaling pathway plays a key role in periodontitis by modulating redox balance and inflammation of the periodontium. However, NRF2 expression is decreased in gingival tissues of patients with periodontitis while oxidative stress is significantly increased in this pathology. Oxidative stress and lipopolysaccharide (LPS) produced by gram-negative bacteria favor the production of inflammatory causing periodontal inflammation and favoring alveolar bone. In this review, we analyzed the current literature regarding the role of natural and synthetic compounds in modulating the NRF2/KEAP1 pathway in in vitro and in vivo models of periodontitis in order to evaluate new potential treatments of periodontitis that can improve the outcome of this disease.
{"title":"Modulation of NRF2/KEAP1 Signaling by Phytotherapeutics in Periodontitis.","authors":"Giovanni Tossetta, Sonia Fantone, Lucrezia Togni, Andrea Santarelli, Fabiola Olivieri, Daniela Marzioni, Maria Rita Rippo","doi":"10.3390/antiox13101270","DOIUrl":"10.3390/antiox13101270","url":null,"abstract":"<p><p>Periodontitis affects up to 40% of adults over 60 years old and is a consequence of gingivitis. Periodontitis is characterized by a chronic inflammation, periodontal damage, and alveolar bone resorption. The nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2)/Kelch-like ECH-Associated Protein 1 (KEAP1) (NRF2/KEAP1) signaling pathway plays a key role in periodontitis by modulating redox balance and inflammation of the periodontium. However, NRF2 expression is decreased in gingival tissues of patients with periodontitis while oxidative stress is significantly increased in this pathology. Oxidative stress and lipopolysaccharide (LPS) produced by gram-negative bacteria favor the production of inflammatory causing periodontal inflammation and favoring alveolar bone. In this review, we analyzed the current literature regarding the role of natural and synthetic compounds in modulating the NRF2/KEAP1 pathway in in vitro and in vivo models of periodontitis in order to evaluate new potential treatments of periodontitis that can improve the outcome of this disease.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"13 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11504014/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Luis Gerardo Ortega-Pérez, José Armando Hernández-Soto, Osvaldo Padilla-Avalos, Luis Alberto Ayala-Ruiz, Oliver Rafid Magaña-Rodríguez, Jonathan Saúl Piñón-Simental, Asdrúbal Aguilera-Méndez, Daniel Godínez-Hernández, Patricia Rios-Chavez
Phytosomes are used as vehicles that carry plant extracts. They exhibit biological activities and possess better bioavailability, bioabsorption, and lower toxicity than drugs. Obesity is an inflammatory state in which oxidative stress is present, which triggers severe effects on the body's organs. This study aimed to evaluate the impact of the extract and phytosomes of Callistemon citrinus on oxidative stress and inflammation in the liver and heart of Wistar rats fed with a high-fat-fructose diet. Phytosomes containing the extract of leaves of C. citrinus were prepared. The antioxidant, pro-inflammatory enzymes, and biomarkers of oxidative stress were evaluated. Among the groups, only the high-fat-fructose group presented an increase in the COX-2, 5-LOX, and MPO inflammatory enzymes, while the XO enzyme exhibited decreased activity. The groups were fed a hypercaloric diet for 15 weeks while orlistat, C. citrinus extract, and phytosomes were administered at three different concentrations, exhibiting enzyme activities similar to those of the control group. It was also observed that the lowest concentration of phytosomes had a comparable effect to the other concentrations. Callistemon citrinus extract can modulate the activities of enzymes involved in the inflammation process. Furthermore, small doses of phytosomes can serve as anti-inflammatory agents.
{"title":"Role of <i>Callistemon citrinus</i> Leaf Phytosomes Against Oxidative Stress and Inflammation in Rats Fed with a High-Fat-Fructose Diet.","authors":"Luis Gerardo Ortega-Pérez, José Armando Hernández-Soto, Osvaldo Padilla-Avalos, Luis Alberto Ayala-Ruiz, Oliver Rafid Magaña-Rodríguez, Jonathan Saúl Piñón-Simental, Asdrúbal Aguilera-Méndez, Daniel Godínez-Hernández, Patricia Rios-Chavez","doi":"10.3390/antiox13101263","DOIUrl":"10.3390/antiox13101263","url":null,"abstract":"<p><p>Phytosomes are used as vehicles that carry plant extracts. They exhibit biological activities and possess better bioavailability, bioabsorption, and lower toxicity than drugs. Obesity is an inflammatory state in which oxidative stress is present, which triggers severe effects on the body's organs. This study aimed to evaluate the impact of the extract and phytosomes of <i>Callistemon citrinus</i> on oxidative stress and inflammation in the liver and heart of Wistar rats fed with a high-fat-fructose diet. Phytosomes containing the extract of leaves of <i>C. citrinus</i> were prepared. The antioxidant, pro-inflammatory enzymes, and biomarkers of oxidative stress were evaluated. Among the groups, only the high-fat-fructose group presented an increase in the COX-2, 5-LOX, and MPO inflammatory enzymes, while the XO enzyme exhibited decreased activity. The groups were fed a hypercaloric diet for 15 weeks while orlistat, <i>C. citrinus</i> extract, and phytosomes were administered at three different concentrations, exhibiting enzyme activities similar to those of the control group. It was also observed that the lowest concentration of phytosomes had a comparable effect to the other concentrations. <i>Callistemon citrinus</i> extract can modulate the activities of enzymes involved in the inflammation process. Furthermore, small doses of phytosomes can serve as anti-inflammatory agents.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"13 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11504497/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gastric cancer (GC) is an asymptomatic malignancy in early stages, with an invasive and cost-ineffective diagnostic toolbox that contributes to severe global mortality rates on an annual basis. Ectopic expression of the lineage survival transcription factors (LS-TFs) GATA4 and 6 promotes stomach oncogenesis. However, LS-TFs also govern important physiological roles, hindering their direct therapeutic targeting. Therefore, their downstream target genes are particularly interesting for developing cancer-specific molecular biomarkers or therapeutic agents. In this work, we couple inducible knockdown systems with chromatin immunoprecipitation and RNA-seq to thoroughly detect and characterize direct targets of GATA-mediated transcriptional regulation in gastric cancer cells. Our experimental and computational strategy provides evidence that both factors regulate the expression of several coding and non-coding RNAs that in turn mediate for their cancer-promoting phenotypes, including but not limited to cell cycle, apoptosis, ferroptosis, and oxidative stress response. Finally, the diagnostic and prognostic potential of four metagene signatures consisting of selected GATA4/6 target transcripts is evaluated in a multi-cancer panel of ~7000 biopsies from nineteen tumor types, revealing elevated specificity for gastrointestinal tumors. In conclusion, our integrated strategy uncovers the landscape of GATA-mediated coding and non-coding transcriptional regulation, providing insights regarding their molecular and clinical function in gastric cancer.
{"title":"Deciphering the Landscape of GATA-Mediated Transcriptional Regulation in Gastric Cancer.","authors":"Rodiola Begolli, Anastasia Patouna, Periklis Vardakas, Anastasia Xagara, Kleanthi Apostolou, Demetrios Kouretas, Antonis Giakountis","doi":"10.3390/antiox13101267","DOIUrl":"10.3390/antiox13101267","url":null,"abstract":"<p><p>Gastric cancer (GC) is an asymptomatic malignancy in early stages, with an invasive and cost-ineffective diagnostic toolbox that contributes to severe global mortality rates on an annual basis. Ectopic expression of the lineage survival transcription factors (LS-TFs) GATA4 and 6 promotes stomach oncogenesis. However, LS-TFs also govern important physiological roles, hindering their direct therapeutic targeting. Therefore, their downstream target genes are particularly interesting for developing cancer-specific molecular biomarkers or therapeutic agents. In this work, we couple inducible knockdown systems with chromatin immunoprecipitation and RNA-seq to thoroughly detect and characterize direct targets of GATA-mediated transcriptional regulation in gastric cancer cells. Our experimental and computational strategy provides evidence that both factors regulate the expression of several coding and non-coding RNAs that in turn mediate for their cancer-promoting phenotypes, including but not limited to cell cycle, apoptosis, ferroptosis, and oxidative stress response. Finally, the diagnostic and prognostic potential of four metagene signatures consisting of selected GATA4/6 target transcripts is evaluated in a multi-cancer panel of ~7000 biopsies from nineteen tumor types, revealing elevated specificity for gastrointestinal tumors. In conclusion, our integrated strategy uncovers the landscape of GATA-mediated coding and non-coding transcriptional regulation, providing insights regarding their molecular and clinical function in gastric cancer.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"13 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11504088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eduardo Pena, Samia El Alam, Constanza Gonzalez, Isaac Cortés, Diego Aguilera, Karen Flores, Karem Arriaza
In Chile, individuals are commonly exposed to high altitude due to the work shift system, involving days of exposure to high altitude followed by days at sea level over the long term, which can result in chronic intermittent hypobaric hypoxia (CIHH). CIHH can cause high-altitude pulmonary hypertension (HAPH), the principal manifestation of which is right ventricular hypertrophy (RVH), in some cases leading to heart failure and eventually death. Studies have shown the contribution of oxidative stress and inflammation to RVH development. Recently, it was determined that the pigment astaxanthin has high antioxidant capacity and strong anti-inflammatory and cardioprotective effects. Therefore, the aim of this study was to determine the effects of astaxanthin on RVH development in rats subjected to CIHH.
Methods: Thirty two male Wistar rats were randomly assigned to the following groups (n = 8 per group): the normoxia with vehicle (NX), normoxia with astaxanthin (NX + AS), chronic intermittent hypobaric hypoxia with vehicle (CIHH), and chronic intermittent hypobaric hypoxia with astaxanthin (CIHH + AS) groups. CIHH was simulated by 2 days in a hypobaric chamber followed by 2 days at sea level for 29 days.
Results: Exposure to CIHH induced RVH and increased lipid peroxidation (MDA), Nox2 expression, and SOD activity, however, it decreased pro-IL-1β expression. Astaxanthin restored oxidative stress markers (Nox2 and MDA), increased GPx activity, and decreased RVH compared to CIHH.
Conclusion: Astaxanthin alleviates RVH and reduces Nox2 and MDA levels while increasing GPx activity in rats subjected to CIHH. These findings provide new insights of astaxanthin as a new nutraceutical against high-altitude effects.
{"title":"Astaxanthin Supplementation Effects in Right Ventricle of Rats Exposed to Chronic Intermittent Hypobaric Hypoxia.","authors":"Eduardo Pena, Samia El Alam, Constanza Gonzalez, Isaac Cortés, Diego Aguilera, Karen Flores, Karem Arriaza","doi":"10.3390/antiox13101269","DOIUrl":"10.3390/antiox13101269","url":null,"abstract":"<p><p>In Chile, individuals are commonly exposed to high altitude due to the work shift system, involving days of exposure to high altitude followed by days at sea level over the long term, which can result in chronic intermittent hypobaric hypoxia (CIHH). CIHH can cause high-altitude pulmonary hypertension (HAPH), the principal manifestation of which is right ventricular hypertrophy (RVH), in some cases leading to heart failure and eventually death. Studies have shown the contribution of oxidative stress and inflammation to RVH development. Recently, it was determined that the pigment astaxanthin has high antioxidant capacity and strong anti-inflammatory and cardioprotective effects. Therefore, the aim of this study was to determine the effects of astaxanthin on RVH development in rats subjected to CIHH.</p><p><strong>Methods: </strong>Thirty two male Wistar rats were randomly assigned to the following groups (n = 8 per group): the normoxia with vehicle (NX), normoxia with astaxanthin (NX + AS), chronic intermittent hypobaric hypoxia with vehicle (CIHH), and chronic intermittent hypobaric hypoxia with astaxanthin (CIHH + AS) groups. CIHH was simulated by 2 days in a hypobaric chamber followed by 2 days at sea level for 29 days.</p><p><strong>Results: </strong>Exposure to CIHH induced RVH and increased lipid peroxidation (MDA), Nox2 expression, and SOD activity, however, it decreased pro-IL-1β expression. Astaxanthin restored oxidative stress markers (Nox2 and MDA), increased GPx activity, and decreased RVH compared to CIHH.</p><p><strong>Conclusion: </strong>Astaxanthin alleviates RVH and reduces Nox2 and MDA levels while increasing GPx activity in rats subjected to CIHH. These findings provide new insights of astaxanthin as a new nutraceutical against high-altitude effects.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"13 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11504862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
He N Xu, Diego Gonzalves, Jonathan H Hoffman, Joseph A Baur, Lin Z Li, Erik A Jensen
In the original publication [...].
在最初的出版物中 [......] 。
{"title":"Correction: Xu et al. Use of Optical Redox Imaging to Quantify Alveolar Macrophage Redox State in Infants: Proof of Concept Experiments in a Murine Model and Human Tracheal Aspirates Samples. <i>Antioxidants</i> 2024, <i>13</i>, 546.","authors":"He N Xu, Diego Gonzalves, Jonathan H Hoffman, Joseph A Baur, Lin Z Li, Erik A Jensen","doi":"10.3390/antiox13101262","DOIUrl":"10.3390/antiox13101262","url":null,"abstract":"<p><p>In the original publication [...].</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"13 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11505320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ahmad Yaman Abdin, Muhammad Jawad Nasim, Claus Jacob
Recent years have witnessed a rather controversial debate on what antioxidants are and how beneficial they may be in the context of human health. Despite a considerable increase in scientific evidence, the matter remains highly divisive as different pieces of new data seem to support both the pro- and the anti-antioxidant perspective. Here, we argue that the matter at the heart of this debate is not necessarily empirical but of semantics. Thus, the controversy cannot be resolved with the traditional tools of natural sciences and by the mere accumulation of new data. In fact, the term "antioxidants" has been part of the scientific language game for a few decades and is nowadays used differently in the context of different scientific disciplines active at different levels of scientific complexity. It, therefore, represents not a single expression but an entire family of words with distinctively different connotations and associations. The transcendent use of this expression from a basic to a more complex discipline, such as going from chemistry to physiology, is problematic as it assigns the term with connotations that are not corroborated empirically. This may lead to false claims and aspirations not warranted by empirical data. Initially, health claims may not even be indented, yet, on occasion, they are welcome for reasons other than scientific ones. To resolve this debate, one may need to refrain from using the term "antioxidants" in disciplines and contexts where its meaning is unclear, limit its use to disciplines where it is essential and beneficial, and, in any case, become more specific in such contexts where its use is warranted, for instance, in the case of "dietary antioxidants".
{"title":"Antioxidants: A Hot Controversy Defused by Cool Semantics.","authors":"Ahmad Yaman Abdin, Muhammad Jawad Nasim, Claus Jacob","doi":"10.3390/antiox13101264","DOIUrl":"10.3390/antiox13101264","url":null,"abstract":"<p><p>Recent years have witnessed a rather controversial debate on what antioxidants are and how beneficial they may be in the context of human health. Despite a considerable increase in scientific evidence, the matter remains highly divisive as different pieces of new data seem to support both the pro- and the anti-antioxidant perspective. Here, we argue that the matter at the heart of this debate is not necessarily empirical but of semantics. Thus, the controversy cannot be resolved with the traditional tools of natural sciences and by the mere accumulation of new data. In fact, the term \"antioxidants\" has been part of the scientific language game for a few decades and is nowadays used differently in the context of different scientific disciplines active at different levels of scientific complexity. It, therefore, represents not a single expression but an entire family of words with distinctively different connotations and associations. The transcendent use of this expression from a basic to a more complex discipline, such as going from chemistry to physiology, is problematic as it assigns the term with connotations that are not corroborated empirically. This may lead to false claims and aspirations not warranted by empirical data. Initially, health claims may not even be indented, yet, on occasion, they are welcome for reasons other than scientific ones. To resolve this debate, one may need to refrain from using the term \"antioxidants\" in disciplines and contexts where its meaning is unclear, limit its use to disciplines where it is essential and beneficial, and, in any case, become more specific in such contexts where its use is warranted, for instance, in the case of \"dietary antioxidants\".</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"13 10","pages":""},"PeriodicalIF":6.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11505030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}