Mediators of Inflammation最新文献

{"title":"Glutathione: A Key Regulator of Extracellular Matrix and Cell Death in Intervertebral Disc Degeneration.","authors":"Fudong Li, Shaofei Li, Yangyang Shi, Feng Lin, Lining Rui, Jiangang Shi, Kaiqiang Sun","doi":"10.1155/2024/4482642","DOIUrl":"https://doi.org/10.1155/2024/4482642","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IVDD) is a degenerative disease accompanied by the loss of nucleus pulposus cells and the degradation of extracellular matrix (ECM), which tends to be associated with lower back pain. The ECM and various types of cell death in IVDD are regulated by multiple factors, such as inflammatory responses and oxidative stress. The glutathione (GSH) redox system is the most important antioxidant defense system in cells. GSH is one of the most abundant thiol antioxidants in mammalian cells, which functions directly and indirectly by scavenging peroxides through the GSH redox system. In these reactions, GSH is oxidized by electrophilic substances, such as reactive oxygen species and free radicals, to form glutathione disulfide to exert antioxidative effects. It has been reported that GSH can protect cells against the damage of oxidative stress and various pathophysiological stimulus that can lead to different types of cell death. In addition, it was reported that the level of GSH widely participates in apoptosis, autophagy, ferroptosis, and oxidative stress in many diseases including osteoarthritis and IVDD. Therefore, we summarized the effects of GSH on ECM metabolism and cells' functions during IVDD. In addition, we summarized the regulatory effects of small molecule compounds on GSH to explore potential ways to regulate the level of GSH. Better understanding the underlying role of GSH in regulating IVDD will facilitate the goal of preventing and retarding the progress of IVDD in the future.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"4482642"},"PeriodicalIF":4.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11473174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aloperine Ameliorates Acetaminophen-Induced Acute Liver Injury through HMGB1/TLR4/NF-<i>κ</i>B and NLRP3/Inflammasome Pathway.","authors":"Hui Chen, Shu Wang, Qiuyue Chen, Wen Yu, Hao Nie, Lian Liu, Bing Zheng, Quan Gong","doi":"10.1155/2024/3938136","DOIUrl":"https://doi.org/10.1155/2024/3938136","url":null,"abstract":"<p><strong>Purpose: </strong>Aloperine (ALO), an alkaloid isolated from <i>Sophora alopecuroides</i> L., possesses multiple pharmacological activities and holds a promise potential for the treatment of various clinical conditions, including skin hypersensitivity, cancer, and inflammatory disorders. The purpose of this study was to investigate the role of ALO in acetaminophen (N-acetyl-para-aminophenol (APAP))-induced acute liver injury and its underlying mechanisms.</p><p><strong>Materials and methods: </strong>An animal model of acute liver injury was induced by intraperitoneal injection of APAP (150 mg/kg). Prior to APAP injection, ALO (40 mg/kg) was administered daily for 7 consecutive days. Serum alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase levels were then measured using an automated chemical analyzer. Histopathological changes were evaluated using hematoxylin and eosin staining. Oxidative stress levels were measured by detecting superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA). Pro-inflammatory cytokines were detected in serum and liver tissues using ELISA and quantitative real-time polymerase chain reaction (q-PCR). The expression of members of the HMGB1/TLR4/NF-<i>κ</i>B signaling pathway and NLRP3 inflammasome were determined by Western blot and/or q-PCR. In addition, the expression and location of NLRP3, cleaved caspase-1, high-mobility group box 1 (HMGB1), and phosphorylated p65 (p-p65) were detected by immunofluorescence.</p><p><strong>Results: </strong>Pretreatment with ALO significantly protected mice from APAP-induced acute liver injury, with decreased MDA content, and significantly increased GSH and SOD activities. Furthermore, ALO pretreatment reduced the release of pro-inflammatory cytokines (IL-1<i>β</i> and TNF-<i>α</i>) and decreased the expression of caspase-1, cleaved caspase-1, and NLRP3. In addition, ALO pretreatment also inhibited the activation of the HMGB1/TLR4/NF-<i>κ</i>B signaling pathway.</p><p><strong>Conclusion: </strong>Taken together, ALO can ameliorate APAP-induced acute liver injury by inhibiting oxidative stress, inflammation by inhibiting the HMGB1/TLR4/NF-<i>κ</i>B, and NLRP3/inflammasome pathway.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"3938136"},"PeriodicalIF":4.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11461077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142391676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophages Promote Atherosclerosis Development by Inhibiting CD8T Cell Apoptosis.","authors":"Xiaoming Xu, Yuteng Wu, Yifei Xu, Wei Mao, Yanyun Pan","doi":"10.1155/2024/1929766","DOIUrl":"https://doi.org/10.1155/2024/1929766","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis is an inflammatory cardiovascular disease. However, whether the association of immune cells in plaques promotes the progression of this disease has not yet been completely elucidated.</p><p><strong>Materials and methods: </strong>Thus, this study aimed to investigate the relationship between C1q+ macrophages and CD8T cells through scRNA-seq data reanalysis, quantitative real-time PCR, and flow cytometry. Chromatin immunoprecipitation-quantitative polymerase chain reaction, western blot, and antibody-blocking experiments were performed to investigate the role of macrophage-CD8T interaction in atherosclerosis. An atherosclerotic mouse model was developed to confirm our findings.</p><p><strong>Results: </strong>Mechanistically, Spi1 expression induced by granulocyte-macrophage colony-stimulating factor promoted C1q expression in the macrophages. Moreover, C1q+ macrophages suppressed CD8T cell apoptosis by upregulating Slc7a7 expression to enhance the L-arginine uptake of CD8T cells. CD8T-derived interferon-<i>γ</i> promoted macrophage activation to induce atherosclerosis. Blockade of the C1q-C1qbp axis attenuated atherosclerosis.</p><p><strong>Conclusion: </strong>In conclusion, macrophages interacting with CD8T promote atherosclerosis development via the C1q-C1qbp axis.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"1929766"},"PeriodicalIF":4.4,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11438514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142349573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LIPS and PaO₂/FiO₂ Combined Plasma Biomarkers Predict Onset of Acute Respiratory Distress Syndrome in Patients of High Risks in SICU: A Prospective Exploratory Study.","authors":"Ziyuan Shen, Zhongnan Yin, Senhao Wei, Zhukai Cong, Feng Zhao, Hua Zhang, Xi Zhu","doi":"10.1155/2024/4936265","DOIUrl":"10.1155/2024/4936265","url":null,"abstract":"<p><strong>Objective: </strong>To explore and validate the value of clinical parameters combined with plasma biomarkers for predicting acute respiratory distress syndrome (ARDS) in patients of high risks in the surgical intensive care unit (SICU).</p><p><strong>Materials and methods: </strong>We conducted a prospective, observational study from January 2020 to December 2023, which enrolled 263 patients of high risks in the SICU of Peking University Third Hospital consecutively; they were classified as ARDS and non-ARDS according to whether ARDS occurred after enrollment. Collected clinical characteristics and blood samples within 24 hr of admission to SICU. Blood samples from the first day to the seventh day of SICU were collected from patients without ARDS, and patients with ARDS were collected until 1 day after ARDS onset, forming data based on time series. ELISA and CBA were used to measure plasma biomarkers. Endpoint of the study was the onset of ARDS. Cox proportional hazard regression analysis was used to find independent risk factors of the onset of ARDS, then constructed a nomogram and tested its goodness-of-fit.</p><p><strong>Results: </strong>About 84 of 263 patients ended with ARDS. Univariate analysis found 15 risk factors showed differences between ARDS and non-ARDS, namely, interleukin 6, interleukin 8 (IL-8), angiopoietin Ⅱ, LIPS, APACHEⅡ, SOFA, PaO₂/FiO₂, age, sex, shock, sepsis, acute abdomen, pulmonary contusion, pneumonia, hepatic dysfunction. We included factors with <i>p</i>  < 0.2 in multivariate analysis and showed LIPS, PaO₂/FiO₂, IL-8, and receptor for advanced glycation end-products (RAGE) of the first day were independent risk factors for ARDS in SICU, a model combining them was good in predicting ARDS (C-index was 0.864 in total patients of high risks). The median of the C-index was 0.865, showed by fivefold cross-validation in the train cohort or validation cohort. The calibration curve shows an agreement between the probability of predicting ARDS and the actual probability of occurrence. Decision curve analysis indicated that the model had clinical use value. We constructed a nomogram that had the ability to predict ARDS in patients of high risks in SICU.</p><p><strong>Conclusions: </strong>LIPS, PaO₂/FiO₂, plasma IL-8, and RAGE of the first day were independent risk factors of the onset of ARDS. The predictive ability for ARDS can be greatly improved when combining clinical parameters and plasma biomarkers.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"4936265"},"PeriodicalIF":4.4,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11421942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142349572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nuclear Factor Erythroid 2-Related Factor 2 Intervenes the Release of Neutrophil Extracellular Traps during Lipopolysaccharide-Induced Acute Lung Injury in Mice.","authors":"Junying Lu, Guilan Xiong, Hongxiang Li, Dong Zhang, Xiaohao Zhang","doi":"10.1155/2024/8847492","DOIUrl":"10.1155/2024/8847492","url":null,"abstract":"<p><p>The pathogenesis of acute lung injury is complex. Studies have demonstrated the role of neutrophil extracellular traps (NETs) in the process of lipopolysaccharide (LPS)-induced acute lung injury (ALI). However, the underlying mechanism remains unclear. In this study, the regulation of Nrf2 in the formation of NETs, which was pathogenic in LPS-induced ALI, was identified by analyzing the levels of Cit-H3, lung function, lung tissue pathology, lung wet/dry ratio, the inflammatory cells, cytokines and proteins in the bronchoalveolar lavage fluid (BALF) and in addition, the activity of lung myeloperoxidase (MPO) was also measured. Results showed that the levels of Cit-H3 measured by western blot in Nrf2-knockout (KO) mice were higher compared with the WT mice after LPS stimulation. To further investigate the NETs formation was pathogenic during LPS-induced ALI, the Nrf2-KO mice were treated with DNase I. Results showed that DNase I improved lung function and lung tissue pathology and significantly reduced lung wet/dry ratio and proteins in the BALF. Besides, DNase I also attenuated the infiltration of inflammatory cells and the cytokines (TNF-<i>α</i>, IL-1<i>β</i>) production in the BALF and the activity of lung MPO. Therefore, these results together indicate that Nrf2 may intervene in the release of NETs during LPS-induced ALI in mice.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"8847492"},"PeriodicalIF":4.4,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11377114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring Unique Extracellular Vesicles Associated Signatures: Prognostic Insights, Immune Microenvironment Dynamics, and Therapeutic Responses in Pancreatic Adenocarcinoma.","authors":"Kai Nan, Ming Zhang, Zilong Geng, Yuankai Zhang, Lin Liu, Zhi Yang, Peng Xu","doi":"10.1155/2024/2825971","DOIUrl":"10.1155/2024/2825971","url":null,"abstract":"<p><p>Extracellular vesicles play an important role in the progression of pancreatic adenocarcinoma (PAAD) through the transfer of proteins, mRNAs, and long noncoding RNAs (lncRNAs). However, the intricate interplay between extracellular vesicles-related lncRNAs and the tumor microenvironment (TME) remains poorly elucidated. Consequently, our investigation aimed to delineate the association between extracellular vesicles-related lncRNAs and the PAAD microenvironment. Initially, we identified differentially expressed lncRNAs (DELs) from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) project datasets. Subsequently, we validated the expression of these DELs within extracellular vesicles and assessed their prognostic implications in PAAD using the GSE133684 and TCGA datasets. Multiomics data were analyzed comprehensively, including genomic landscape, functional annotation, immune profiles, and therapeutic responses. Differential expression of selected lncRNAs in both cellular and exosomal fractions of PAAD was further confirmed through quantitative polymerase chain reaction (qPCR). Eight DELs were identified from TCGA and GTEx datasets, and two exosomal lncRNAs exhibited a significant correlation with overall survival, warranting further investigation. Specifically, elevated expression of LINC00996 correlated positively with immune infiltration and enhanced response to immunotherapy. Conversely, heightened expression of TRHED-AS1 was associated with compromised immune cell infiltration and diminished responsiveness to immunotherapy. Our study establishes a compelling link between two extracellular vesicles-related gene signatures, prognosis, and immune infiltration in PAAD. Notably, these signatures serve as robust prognostic indicators for PAAD patients, offering valuable insights for the strategic selection of immunotherapeutic interventions.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"2825971"},"PeriodicalIF":4.4,"publicationDate":"2024-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11366062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"C-Reactive Protein Level as a Novel Serum Biomarker in Sarcopenia.","authors":"Shangjin Lin, Xiuxiu Chen, Ying Cheng, Hou Huang, Fengjian Yang, Zhijun Bao, Yongqian Fan","doi":"10.1155/2024/3362336","DOIUrl":"10.1155/2024/3362336","url":null,"abstract":"<p><strong>Background: </strong>The role of C-reactive protein (CRP), an inflammatory marker, in the development of sarcopenia remains uncertain.</p><p><strong>Methods: </strong>This cross-sectional research involved the enrollment of 207 patients, classified into two groups: 74 patients with sarcopenia and 133 patients without sarcopenia. Clinical data of the participants, including hand grip strength, walking speed, appendicular lean mass (ALM), and calf circumference, were collected and recorded. We evaluated the extent to which CRP levels are associated with the risk of sarcopenia using both univariate and multivariate logistic regression models. Besides, the correlation between CRP levels, hand grip strength, ALM, and walking speed was examined using the Spearman rank correlation test. Moreover, we have employed the Mendelian randomization (MR) analysis technique to explore the causal relationship between CRP levels and the occurrence of sarcopenia.</p><p><strong>Results: </strong>The sarcopenia group showed a higher proportion of older women, with significant differences in anemia prevalence, calf circumference, gait speed, ALM, hand grip strength, and elevated CRP levels compared to the control group. Logistic regression analyses identified CRP as an independent risk factor for sarcopenia (OR: 1.151, 95% CI:1.070-1.238, and <i>P</i> < 0.001). Correlation analysis results revealed a noteworthy inverse association with hand grip strength (<i>R</i> = -0.454 and <i>P</i> < 0.001), ALM (<i>R</i> = -0.426 and <i>P</i> < 0.001), and walking speed (<i>R</i> = -0.431 and <i>P</i> < 0.001). MR analysis provided further evidence of a significant detrimental link between genetically predicted CRP levels and essential sarcopenia characteristics, with consistent results across various statistical models.</p><p><strong>Conclusions: </strong>Our study uncovered strong evidence supporting a noteworthy inverse association and causality between CRP concentrations and sarcopenia, indicating that CRP has the potential to serve as a biomarker for sarcopenia.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"3362336"},"PeriodicalIF":4.4,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11535261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TLR2 Derangements Likely Play a Significant Role in the Inflammatory Response and Thrombosis in Patients with <i>Ph</i>(-) Classical Myeloproliferative Neoplasm.","authors":"Jen Chin Wang, Guanfang Shi, Chi Chen, Ching Wong, Vladimir Gotlieb, Gardith Joseph, Kiron V Nair, Lakshmi Boyapati, Enayati Ladan, James T Symanowski, Lishi Sun","doi":"10.1155/2024/1827127","DOIUrl":"10.1155/2024/1827127","url":null,"abstract":"<p><p>We investigated the role of toll-like receptors (TLRs) in inflammatory pathways in Philadelphia chromosome-negative myeloproliferative neoplasms (<i>Ph</i>(-)MPNs). TLR2 expression was increased in ET, PV, and MPN (grouped as (PV + (ET) + MF)), whereas TLR4 was elevated only in MPN. TLR3, 7, and 9 were not elevated. Cultured monocyte-derived dendritic cells and plasma assays in TLR2-elevated patients were found to secrete more cytokines than those from TLR2-normal patients. These facts suggest that TLR2 is the major inflammatory pathways in MPN. We also measured S100A9 and reactive oxygen species (ROS), revealing increased S100A9 in PV, MF, and MPN, while ROS were only increased in MF. These data suggests that MPNs initially involve TLR2, with minor contributions from TLR4, and with S100A9, leading to ROS formation, JAK2 mutation, and progression to MF or leukemia. Furthermore, patients with JAK2 mutations or leukocytosis exhibited higher TLR2 expression. In leukocyte-platelet interactions, cells from MPN patients displayed a stronger response to a TLR2 agonist than TLR4 agonist. A TLR2 inhibitor (but not a TLR4 inhibitor) attenuated this response. Thrombosis incidence was higher in TLR2-elevated patients (29%) than in TLR2-normal patients (19%). These findings suggest that TLR2 likely contributes to thrombosis in MPN.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"1827127"},"PeriodicalIF":4.4,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11329310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Function of Necroptosis and Its Treatment Target in IBD.","authors":"Francis Atim Akanyibah, Yi Zhu, Tao Jin, Dickson Kofi Wiredu Ocansey, Fei Mao, Wei Qiu","doi":"10.1155/2024/7275309","DOIUrl":"10.1155/2024/7275309","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD), which encompasses Crohn's disease (CD) and ulcerative colitis (UC), is a complicated illness whose exact cause is yet unknown. Necroptosis is associated with IBD pathogenesis, leading to intestinal barrier abnormalities and uncontrolled inflammation. Molecules involved in necroptosis, however, exhibit different expression levels in IBD and its associated colorectal cancer. Multiple studies have shown that inhibiting these molecules alleviates necroptosis-induced IBD. Moreover, due to the severe scarcity of clinical medications for treating IBD caused by necroptosis, we review the various functions of crucial necroptosis molecules in IBD, the stimuli regulating necroptosis, and the current emerging therapeutic strategies for treating IBD-associated necroptosis. Eventually, understanding the pathogenesis of necroptosis in IBD will enable the development of additional therapeutic approaches for the illness.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"7275309"},"PeriodicalIF":4.4,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141908843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-Inflammatory and Antioxidant Properties of a New Mixture of Vitamin C, Collagen Peptides, Resveratrol, and Astaxanthin in Tenocytes: Molecular Basis for Future Applications in Tendinopathies.","authors":"Monica Marzagalli, Stefania Battaglia, Michela Raimondi, Fabrizio Fontana, Marco Cozzi, Francesca R Ranieri, Roberto Sacchi, Valeria Curti, Patrizia Limonta","doi":"10.1155/2024/5273198","DOIUrl":"10.1155/2024/5273198","url":null,"abstract":"<p><p>Tendinopathy is one of the most frequent musculoskeletal disorders characterized by sustained tissue inflammation and oxidative stress, accompanied by extracellular matrix remodeling. Patients suffering from this pathology frequently experience pain, swelling, stiffness, and muscle weakness. Current pharmacological interventions are based on nonsteroidal anti-inflammatory drugs; however, the effectiveness of these strategies remains ambiguous. Accumulating evidence supports that oral supplementation of natural compounds can provide preventive, and possibly curative, effects. Vitamin C (Vit C), collagen peptides (Coll), resveratrol (Res), and astaxanthin (Asx) were reported to be endowed with potential beneficial effects based on their anti-inflammatory and antioxidant activities. Here, we analyzed the efficacy of a novel combination of these compounds (Mix) in counteracting proinflammatory (IL-1<i>β</i>) and prooxidant (H₂O₂) stimuli in human tenocytes. We demonstrated that Mix significantly impairs IL-6-induced IL-1<i>β</i> secretion, NF-<i>κ</i>B nuclear translocation, and MMP-2 production; notably, a synergistic effect of Mix over the single compounds could be observed. Moreover, Mix was able to significantly counteract H₂O₂-triggered ROS production. Together, these results point out that Mix, a novel combination of Vit C, Coll, Resv, and Asx, significantly impairs proinflammatory and prooxidant stimuli in tenocytes, mechanisms that contribute to the onset of tendinopathies.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"5273198"},"PeriodicalIF":4.4,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303056/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141897772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}