Mediators of Inflammation最新文献

{"title":"Selenium Nanoparticles Decorated With Stevioside Potentially Attenuate Fructose Palmitate Induced Lipid Accumulation in HepG2 Cells.","authors":"Shuai Li, Hui Yang, Wenjun Zhou, Ruoting Wang, Likang Li, Changfa Zhang, Jingyi Zhang, Yingxin Liu, Zhi Huang, Guowei Li","doi":"10.1155/mi/7942947","DOIUrl":"10.1155/mi/7942947","url":null,"abstract":"<p><p>The excessive accumulation of lipid droplets within hepatocytes stands as a hallmark characteristic of metabolic-associated fatty liver disease (MAFLD). Selenium (Se) nanoparticles (NPs) have garnered considerable attention for their notable bioavailability, minimal toxicity, and exceptional antioxidant properties. However, a critical limitation lies in the propensity of SeNPs to aggregate into the biologically inactive elemental Se, thereby constraining their utility. Here, we utilized <i>Stevioside</i> (<i>SV</i>), a natural sweetener, to modify SeNPs and obtained the SV-SeNPs with a size of about 187 ± 7 nm. We aimed to investigate the effect of SV-SeNPs on high fructose-palmitate (HFP) induced lipid accumulation in HepG2 cells. Noteworthy is the absence of overt cytotoxicity attributed to SV-SeNPs on normal HepG2 cells. Of significance, our findings delineate the profound inhibitory effects of SV-SeNPs on the expression of key genes implicated in de novo lipogenesis, such as fatty-acid synthase (FASN), acetyl-CoA-carboxylase 1 (ACC1), and stearoyl-CoA desaturase-1 (SCD1) within HFP-induced HepG2 cells. Furthermore, our investigation reveals that SV-SeNPs mediate a significant reduction in lipid accumulation by activating the PI3K/AKT/Nrf2 signaling cascades. Additionally, the antioxidative properties of SV-SeNPs are underscored by their ability to counteract oxidative stress via the upregulation of two pivotal antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GSHPx). In conclusion, our study unveils the potential beneficial effects of SV-SeNPs on the prevention and treatment of MAFLD by effectively suppressing lipid accumulation and ameliorating oxidative stress.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"7942947"},"PeriodicalIF":4.4,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842145/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468499","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":"Herbal Medicine Extracts Improve Motor Function by Anti-Inflammatory Activity in hSOD1^G93A Animal Model.","authors":"Eun Jin Yang, Sun Hwa Lee","doi":"10.1155/mi/1999953","DOIUrl":"10.1155/mi/1999953","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is a multicomplex neurodegenerative disorder characterized by motor neuron death, muscle atrophy, and respiratory failure. Owing to its multicomplex mechanisms and multifactorial nature in the skeletal muscle and spinal cord (SC), no effective therapy has been developed. However, herbal medicines, known for their multitarget properties, have demonstrated promising efficacy with limited side effects in treating various diseases. Specifically, <i>Paeonia lactiflora</i> Pallas has been demonstrated to exhibit analgesic, antidepressant, anti-inflammatory, and neuroprotective effects. However, the pharmacological mechanisms underlying the beneficial effects of <i>P. lactiflora</i> in hSOD1^G93A animal models remain unexplored. Therefore, this study was conducted to investigate the multitarget effects of <i>P. lactiflora</i> in hSOD1^G93A transgenic mice, an ALS model. Footprint tests, western blot assays, and immunohistochemical analysis were used to assess the effect of <i>P. lactiflora</i> on the tibia anterior (TA), gastrocnemius (GC), and SC. The results revealed that <i>P. lactiflora</i> augmented motor function and decreased motor neuron loss in hSOD1^G93A mice. Furthermore, <i>P. lactiflora</i> significantly lowered the expression of proteins associated with inflammation and oxidative stress in the skeletal muscle (TA and GC) and SC. <i>P. lactiflora</i> also regulated autophagy function by reducing the levels of key markers, such as P62/sequestosome 1 (SQSTM1), microtubule-associated proteins 1A/1B light chain 3B, and SMAD family member 2, in the muscle and SC. Overall, <i>P. lactiflora</i> treatment improved motor function, prevented motor neuron death, and exhibited anti-inflammatory and antioxidative effects in the skeletal muscle and SC of ALS mouse models. These results suggest that <i>P. lactiflora</i> could serve as a promising multitarget therapeutic agent for systemic and multipathological diseases.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"1999953"},"PeriodicalIF":4.4,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468495","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":"Systematic Review of Interleukin-35 in Endothelial Dysfunction: A New Target for Therapeutic Intervention.","authors":"Kai Li, Jie Feng, Meng Li, Leilei Han, Yanqing Wu","doi":"10.1155/mi/2003124","DOIUrl":"10.1155/mi/2003124","url":null,"abstract":"<p><p>Endothelial dysfunction is a significant factor in the pathogenesis of various diseases. In pathological states, endothelial cells (ECs) undergo activation, resulting in dysfunction characterized by the stimulation of inflammatory responses, oxidative stress, cell proliferation, blood coagulation, and vascular adhesions. Interleukin-35 (IL-35), a novel member of the IL-12 family, is primarily secreted by regulatory T cells (Tregs) and regulatory B cells (Bregs). The role of IL-35 in immunomodulation, antioxidative stress, resistance to apoptosis, control of EC activation, adhesion, and angiogenesis in ECs remains incompletely understood, as the specific mechanisms of IL-35 action and its regulation have yet to be fully elucidated. Therefore, this systematic review aims to comprehensively investigate the impact of IL-35 on ECs and their physiological roles in a range of conditions, including cardiovascular diseases, tumors, sepsis, and rheumatoid arthritis (RA), with the objective of elucidating the potential of IL-35 as a therapeutic target for these ailments.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"2003124"},"PeriodicalIF":4.4,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11839265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458661","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":"Inhibition of SIK1 Alleviates the Pathologies of Psoriasis by Disrupting IL-17 Signaling.","authors":"Dongxuan Huang, Huimin Sun, Lianhui Su, Fan Yang, Dongsheng Huang, Hanchao Gao, Mengtao Cao","doi":"10.1155/mi/3540219","DOIUrl":"10.1155/mi/3540219","url":null,"abstract":"<p><p>Psoriasis is an inflammatory skin disease mediated by multiple immune cells, including T cells, macrophages, and dendritic cells, which exhibit complex pathologies and limited clinical treatment. Here, we found that salt-inducible kinase 1 (SIK1) was upregulated in the imiquimod (IMQ)-induced psoriasis mouse model. This increment may be due to a higher level of interleukin-17, which promoted the expression of SIK1 in keratinocytes. Inhibition of SIK1 kinase activity using a small molecular inhibitor (HG-9-91-01 or YKL-06-062) dramatically alleviated IMQ-induced psoriasis, showing reduced epidermal thickness, inflammation, and hyperproliferative epidermal keratinocytes. Our data demonstrated that SIK1 inhibitors HG-9-91-01 or YKL-06-062 blocked the expression of IL-17-induced proinflammatory cytokines and chemokines, including <i>Il6</i>, <i>Kc</i>, and <i>Ccl20</i>. Mechanistically, we found that SIK1 inhibitor HG-9-91-01 or YKL-06-062 suppressed the phosphorylation of I<i>κ</i>b<i>α</i> and P38. Consistently, SIK1 overexpression in keratinocytes promoted the activation of I<i>κ</i>b<i>α</i> and P38. Collectively, our results reveal that SIK1 participates to promote IL17-induced signaling through enhancing activation of NF-<i>κ</i>B and MAPKs and exacerbates psoriasis-like skin inflammation. Thus, inhibition of SIK1 presents a potential new therapeutic target for psoriasis.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"3540219"},"PeriodicalIF":4.4,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11828648/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433475","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":"NLRP3 Inflammasome Activation Is Involved in Geniposide-Induced Hepatotoxicity.","authors":"Yixuan Liu, Baoyue Liu, Mingzhu Shi, Tianxiang Ye, Huifang Li","doi":"10.1155/mi/4112856","DOIUrl":"10.1155/mi/4112856","url":null,"abstract":"<p><p><b>Background:</b> Geniposide, a prominent iridoid glycoside derived from <i>Gardenia jasminoides J</i>. Ellis, has garnered attention due to its association with hepatotoxicity despite its well-documented pharmacological efficacy in preclinical and clinical contexts. The NOD-like receptor protein 3 (NLRP3) inflammasome is implicated in numerous pathological conditions, including drug-induced liver injury. This study aims to explore the involvement of the NLRP3 inflammasome in geniposide-induced liver toxicity. <b>Methods:</b> Rats were administered geniposide for 5 days, concurrently treated with or without glibenclamide (GLY), an in vivo inhibitor of NLRP3. In vitro, HL-7702 cells were exposed to genipin (a metabolite of geniposide via hepatointestinal circulation), with or without GLY supplement. Liver tissue was examined through pathological sections. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), γ-glutamyl transpeptidase (γ-GT), and total bilirubin (T-Bil) levels were determined using the enzyme plate method. IL-1<i>β</i> and IL-18 levels in the supernatant and serum were quantified through ELISA. Apoptosis-associated speck-like protein (ASC), NLRP3, caspase-1, pro-IL-1<i>β</i>, and pro-IL-18 mRNA levels in cells or the liver were assessed by RT-PCR. Protein levels of ASC, NLRP3, caspase-1, pro-IL-1<i>β</i>, and pro-IL-18 in cells or the liver were analyzed by Western blot. <b>Results:</b> Rats treated with geniposide displayed notable liver damage characterized by inflammatory infiltration, elevated serum transaminases, and heightened levels of inflammatory factors IL-1<i>β</i> and IL-18. This liver damage was concomitant with NLRP3 inflammasome activation within the liver. Furthermore, genipin induction led to reduced cell viability, increased transaminases in the cell supernatant, and an upsurge in inflammatory factors, resulting in heightened NLRP3 inflammasome expression within the cells. However, GLY effectively curtailed excessive NLRP3 activation, dampened the production of inflammatory factors IL-1<i>β</i> and IL-18, and ameliorated liver damage caused by geniposide. <b>Conclusions:</b> Our findings collectively elucidate that geniposide induces hepatotoxicity by triggering NLRP3 inflammasome signaling. Inhibition of the inflammasome presents a promising novel therapeutic target for mitigating geniposide-induced hepatotoxicity.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"4112856"},"PeriodicalIF":4.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11824841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414698","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":"Elevated Type 2 Inflammatory Factors, Th2/Th1 Balanced Status, and Exosomes as a Marker of Severity in Chronic Actinic Dermatitis.","authors":"Tang Jun-Ting, Tu Ying, Nong Xiang, Sun Dong-Jie, He Li","doi":"10.1155/mi/7967853","DOIUrl":"10.1155/mi/7967853","url":null,"abstract":"<p><p><b>Background:</b> Chronic actinic dermatitis (CAD) is a skin inflammation triggered by light exposure, occurring at the exposed site and potentially causing widespread inflammation throughout the body. While we hypothesize that severe CAD could progress to atopic dermatitis, the exact inflammatory mechanisms and pathogenesis remain unclear. <b>Objective:</b> We aimed to investigate the relationships between CAD severity and clinical and immunological parameters. <b>Methods:</b> CAD patients were classified into two groups based on severity: mild CAD and severe CAD. We assessed total IgE levels, eosinophil count in peripheral blood (PB), the ratio of Th2 cell percentage to Th1 cell percentages (Th2/Th1), and cytokine/chemokine levels in both PB and skin lesions. <b>Results:</b> In our study, eosinophil counts in patients with severe CAD and mild CAD were significantly higher than those in the control group (<i>p</i>  < 0.05). It was exhibited a higher Th2/Th1 ratio in severe-CAD patients compared with mild-CAD patients and control group (<i>p</i>  < 0.05). There were significant increases in the levels of IL-4, IL-5, IL-8, IL-31, and IFN-<i>γ</i> in the lesions of severe CAD patients compared to the control group (<i>p</i>  < 0.05). Additionally, the level of CD63 exosomes in the PB of severe-CAD patients was significantly elevated compared to the control group (<i>p</i>  < 0.05). Persistent elevations of CD63 exosomes in severe CAD patients were associated with the Th2/Th1 balance status in PB (<i>p</i>  < 0.05). <b>Conclusion:</b> Severe CAD demonstrates a shift toward Th2 immunity from Th2/Th1, accompanied by elevated with inflammatory factors such as IL-4, IL-5, IL-31, IL-8, and IFN-<i>γ</i> in skin lesions, as well as increased CD63 exosomes in PB. Thus, consequently, exosomes and Th2/Th1 imbalance may contribute to the systemic manifestations observed in CAD patients.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"7967853"},"PeriodicalIF":4.4,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11824299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414691","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":"<i>Trapa natans L</i>. Extract Attenuates Inflammation and Oxidative Damage in Cisplatin-Induced Cardiotoxicity in Rats by Promoting M2 Macrophage Polarization.","authors":"Vesna Matovic, Biljana Ljujic, Ivana Radojevic, Gorica Đelic, Marina Miletic Kovacevic, Suzana Zivanovic, Milos Papic, Nevena Milivojevic, Ivica Petrovic, Marina Gazdic Jankovic","doi":"10.1155/mi/6587305","DOIUrl":"10.1155/mi/6587305","url":null,"abstract":"<p><p><b>Background:</b> <i>Trapa natans</i> L. fruits and leaf extracts have a broad range of immunomodulatory, anti-inflammatory, and antioxidant effects; however, their effects on cardiac protection have not been investigated. <b>Objective:</b> The study aims to test the biological activity of <i>Trapa natans</i> L. extract (TNE) in cisplatin (CDDP)-induced cardiotoxicity. <b>Methods:</b> Wistar albino rats received a single dose of CDDP intraperitoneally and TNE ones per day for 2 weeks orally. Cardiac inflammation, necrosis, and fibrosis were determined by histological and immunohistochemical analyses. Cytokines in rat sera and cardiac tissue were detected by enzyme-linked immunosorbent assay (ELISA) and quantitative real-time (qRT)-PCR. Rat macrophages cultured in the presence of TNE for 48 h were harvested for flow cytometry, while supernatants were collected for cytokine and reactive oxygen species (ROS) measurement. <b>Results:</b> Application of TNE significantly attenuated CDDP induced cardiotoxicity as demonstrated by biochemical and histopathological analysis. Administration of TNE once daily for 14 days decreased level of proinflammatory (TNF-<i>α</i>, IFN-<i>γ</i>, and IL-6) and prooxidative parameters (NO₂, O₂, and H₂O₂), while increased level of immunosuppressive IL-10 and antioxidative glutathione (GSH), catalase (CAT) and uperoxide dismutase (SOD) in the systemic circulation. TNE treatment resulted in attenuated heart inflammation and fibrosis accompanied with the reduced infiltration of macrophages and reduced expression of proinflammatory and profibrotic genes in heart tissue of CDDP-treated animals. In vitro lipopolysaccharide (LPS)-stimulated macrophages cultured in the presence of TNE adopted immunosuppressive phenotype characterized by decreased production of proinflammatory cytokines and prooxidative mediators. <b>Conclusion:</b> Our study provides the evidence that TNE ameliorates cisplatin-induced cardiotoxicity in rats by reducing inflammation and oxidative stress via promoting M2 macrophage polarization.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"6587305"},"PeriodicalIF":4.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11779992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066486","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":"METTL3/miR-192-5p/SCD1 Axis Regulates Lipid Metabolism to Affect T Cell Differentiation in Asthma.","authors":"Zhengrong Chen, Dingwei Yan, Suyu Guo, Yiyi Song, Xinxing Zhang, Wenjing Gu, Heting Dong, Li Huang","doi":"10.1155/mi/4955849","DOIUrl":"10.1155/mi/4955849","url":null,"abstract":"<p><p><b>Background:</b> This study aimed to explore the mechanisms underlying T-cell differentiation in asthma. <b>Methods and Results:</b> Flow cytometry was performed to detect Th cells. LC-MS/MS was performed to assess lipid metabolism. HE staining was performed to assess the pathological changes of the lung tissues. ELISA was performed to detect cytokine levels. The results of quantitative real-time polymerase chain reaction (qRT-PCR) and western blot showed that miR-192-5p expression was decreased, while SCD1 expression was increased in CD4⁺T cells isolated from the peripheral blood of children with asthma. The dual luciferase reporter assay determined the direct interaction between miR-192-5p and SCD1. MiR-192-5p inhibitor reduced ASCL3 and PPARα, increased FASN and SREBP1c mRNA expression and protein levels in mouse spleen CD4⁺T cells, and elevated Th2 and Th17 cells, but these effects were reversed by the SCD1 inhibitor. Oleic acid (OA) reduced Th1 cells and increased Th2 and Th17 cells in mouse spleen CD4⁺T cells treated with an SCD1 inhibitor. Additionally, pri-miR-192-5p expression was increased in CD4⁺T cells isolated from the peripheral blood of asthmatic children, and the deletion of METTL3 upregulated pri-miR-192-5p expression in an m6A-dependent manner. MiR-192-5p mimic and inhibitor both reversed miR-192-5p and SCD1 expression affected by overexpression or deletion of METTL3, both <i>in vivo</i> and <i>in vitro</i>. Furthermore, METTL3 overexpression attenuated lung inflammation, elevated Th1 cells, and reduced Th2 and Th17 cells in CD4⁺T cells isolated from the peripheral blood of asthmatic mice. These effects were reversed by the miR-192-5p inhibitor. <b>Conclusion:</b> These results suggest that METTL3/miR-192-5p/SCD1 axis regulates lipid metabolism and affects T cell differentiation, thus affecting asthma progression. This study may provide novel insights into the pathogenesis of asthma and a new treatment strategy.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"4955849"},"PeriodicalIF":4.4,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11769594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047232","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":"Modified Gegen Qinlian Decoction Ameliorates DSS-Induced Colitis in Mice via the Modulation of NF-<i>κ</i>B and Nrf2/HO-1 Pathways.","authors":"Jinke Huang, Jiaqi Zhang, Zhihong Liu, Jing Ma, Yifan Wang, Fengyun Wang, Xudong Tang","doi":"10.1155/mi/7468297","DOIUrl":"10.1155/mi/7468297","url":null,"abstract":"<p><p><b>Background:</b> This study aims to reveal the potential molecular mechanisms of modified Gegen Qinlian decoction (MGQD) in relieving ulcerative colitis (UC). <b>Methods:</b> C57BL/6J mice were used to establish experimental colitis via dextran sodium sulfate (DSS). Body weight, disease activity index (DAI), spleen weight, colon length, and histopathologic features were measured to evaluate the therapeutic effects of MGQD on mice with UC. The ELISA kits were employed to assess the concentrations of interleukin (IL)-6, IL-1β, tumor necrosis factor-α (TNF-α), glutathione (GSH), reactive oxygen species (ROS), and malondialdehyde (MDA). Western blot analyses were used to assess the levels of IκBα, p65, p-IκBα, p-p65, HO-1, and Nrf2. Moreover, the protein levels of Nrf2 and p-p65 were assessed by immunofluorescence. <b>Results:</b> Colitis-related symptoms in mice were significantly alleviated by MGQD. Moreover, MGQD inhibited the levels of TNF-α, IL-1β, IL-6, MDA, and ROS and increased the level of GSH in mice with UC. Mechanistically, MGQD prevented the activation of the NF-κB pathway and concomitantly promoted the activation of the Nrf2/HO-1 pathway. <b>Conclusion:</b> MGQD alleviated UC by suppressing inflammation and oxidative stress via the modulation of NF-κB and Nrf2/HO-1 pathways, suggesting that MGQD may be a candidate therapy for UC.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"7468297"},"PeriodicalIF":4.4,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029160","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":"Characteristics of Pediatric Allergic Rhinitis With Different Disease Severity.","authors":"Yinhui Zeng, Ting Lin, Wanhua Xie, Shengli Gao, Qingxiang Zeng, Xi Luo, Wenlong Liu","doi":"10.1155/mi/5553039","DOIUrl":"10.1155/mi/5553039","url":null,"abstract":"<p><p><b>Background:</b> Although numerous studies have focused on diagnostic biomarkers to help identify allergic rhinitis (AR), data on the characteristics of pediatric AR with different severity is limited. We aimed to compare the characteristics of pediatric AR with different severity. <b>Methods:</b> A total of 1054 children with AR were enrolled and classified into mild intermittent AR, mild persistent AR, moderate-to-severe intermittent AR, and moderate-to-severe persistent AR. All children were surveyed using a questionnaire that included detailed demographic information. Blood cell analysis was performed using an automatic hematology analyzer. <b>Results:</b> No significant differences were observed in feeding patterns, dietary habits, outdoor activity time, total IgE, eosinophil count, and eosinophil percentage among the different AR subgroups. However, a higher prevalence of a family history of AR was noted in the moderate-to-severe persistent group. Symptoms were more likely to exacerbate when using air conditioning in children with moderate-to-severe persistent AR. Multivariate regression analysis also showed that symptom exacerbation when using air conditioning was associated with disease severity. <b>Conclusions:</b> This study suggests that exacerbation of symptoms during air conditioning use can be considered a predictive factor for the severity of pediatric AR. Doctors and parents should pay special attention to these children to prevent more severe symptoms and improve the quality of life of these patients as early as possible.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2025 ","pages":"5553039"},"PeriodicalIF":4.4,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029159","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}