{"title":"Hemoglobin-to-Inflammation Marker Ratios Reflect Endoscopic Activity in Inflammatory Bowel Disease.","authors":"Zhaoyi Wu, Qian Zhang, Hui Li, Keyu Ren, Yanchun Jin, Shanwei Rong, Kuijin Xue, Bin Cao, Hongyun Wei","doi":"10.2147/JIR.S586128","DOIUrl":"https://doi.org/10.2147/JIR.S586128","url":null,"abstract":"<p><strong>Aim: </strong>To investigate the diagnostic value of hemoglobin-to-inflammation marker ratios (Hb/WBC, Hb/Neu, Hb/PLT, Hb/CRP) in assessing endoscopic activity in inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD).</p><p><strong>Methods: </strong>A single-center retrospective cross-sectional study was conducted. We screened patients diagnosed with UC or CD between January 2017 and July 2025. Patients were excluded if they had coexisting severe gastrointestinal/infectious diseases potentially affecting endoscopic or laboratory results, iron supplements intake, incomplete data, or a significant time discrepancy (>3 days) between endoscopy and laboratory testing. Ultimately, 270 IBD patients (175 UC, 95 CD) were included for the primary cross-sectional analysis. Clinical data, laboratory indicators, and endoscopic scores (Mayo Endoscopic Score, Ulcerative Colitis Endoscopic Index of Severity [UCEIS], Simplified Endoscopic Score for Crohn's Disease [SES-CD]) were collected. Receiver operating characteristic (ROC) curve analysis, correlation analysis, multivariate logistic regression, and sensitivity analyses were employed.</p><p><strong>Results: </strong>The Hb/CRP ratio demonstrated the best performance in distinguishing endoscopic active phase from remission phase in IBD. In UC patients based on the Mayo Endoscopic Score, the area under the curve (AUC) of Hb/CRP was 0.924 (95% CI: 0.884-0.964); based on the UCEIS score, the AUC was 0.890 (95% CI: 0.842-0.938); in CD patients based on the SES-CD score, the AUC was 0.839 (95% CI: 0.749-0.929). Hb/CRP significantly outperformed hemoglobin alone across all subgroups (all P<0.01), while showing comparable diagnostic accuracy to CRP alone. It also served as an independent protective factor for disease remission phase in multivariate analysis (odds ratio [OR] range = 1.007 to 1.014, all P<0.01). Sensitivity analyses stratified by anemia status confirmed the robustness of Hb/CRP, particularly in UC patients. However, the absence of fecal calprotectin (FC) data is a key limitation of the study.</p><p><strong>Conclusion: </strong>Hemoglobin-to-inflammation ratios, particularly Hb/CRP, show promising diagnostic performance for assessing endoscopic activity in IBD in this retrospective study. They may serve as non-invasive adjunctive tools for clinical disease activity monitoring, though their comparative value against established biomarkers like FC warrants further prospective validation.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"586128"},"PeriodicalIF":4.1,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13127453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147816330","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}
{"title":"Complement Components C1r and C8 Serve as Potential Inflammatory Biomarkers for Coronary Heart Disease Severity: The Mediating Role of C-Reactive Protein.","authors":"Xia Feng, Xiaoting Jiang, Shaolin Gong, Wen Liu, Qiong Yan, Hongmei Qi, Ling Yu, Xiang Wang, Xiaoping Peng","doi":"10.2147/JIR.S584396","DOIUrl":"https://doi.org/10.2147/JIR.S584396","url":null,"abstract":"<p><strong>Purpose: </strong>Inflammation plays an important role in the occurrence and development of coronary heart disease (CHD). We investigated serum complement C1r, C1s, C7, C8, C9 as potential biomarkers and the mediating role of C-reactive protein (CRP) in CHD severity. The severity of coronary artery stenosis was quantified using the validated Gensini score.</p><p><strong>Patients and methods: </strong>In this prospective cross-sectional study (n=314), patients were categorized into a control group (n=102) and a CHD group (n=212) via coronary angiography. CHD severity was quantified by the Gensini score (mild ≤31; moderate-to-severe >31). The study incorporated multiple known pathogenic factors such as demographic characteristics, underlying diseases, and metabolic indicators for comprehensive analysis. Serum complement levels were measured by ELISA. Spearman correlation, multivariate logistic regression, ROC analysis, and mediation modeling assessed associations and CRP's role.</p><p><strong>Results: </strong>Serum C1r and C8 were significantly elevated in CHD and severe stenosis groups. While C1s showed a slight increase in the severe stenosis group, it, along with C7 and C9, showed limited overall diagnostic utility for CHD. Spearman analysis revealed that C1r and C8 were positively correlated with both Gensini score and cTnT levels. In the fully adjusted model (Model 4), C1r remained a robust independent predictor of moderate-to-severe stenosis (continuous OR=2.10, 95% CI: 1.41-3.12; Q4 vs Q1 OR=5.61, 95% CI: 2.12-14.89). C8 also maintained statistical significance as a continuous variable (OR=1.98, P=0.004). Furthermore, mediation analysis indicated that CRP mediated 31.6% and 46.2% of the effects of C1r and C8 on disease severity, respectively. The combined AUC of C1r and C8 for predicting CHD was 0.769.</p><p><strong>Conclusion: </strong>C1r is an independent predictor of CHD severity, while C8 exhibits a dose-dependent association modulated by systemic status. Integrating anatomical and physiological markers confirms the complement-CRP axis's pivotal role in CHD risk stratification, providing evidence for inflammatory biomarkers in lesion assessment.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"584396"},"PeriodicalIF":4.1,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13127450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147816374","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}
{"title":"Methodological and Clinical Gaps in Biomarker-Guided Weaning for Sepsis-Induced ARDS [Letter].","authors":"Cheng-Wei Lu, Kuo-Chen Chang","doi":"10.2147/JIR.S612924","DOIUrl":"https://doi.org/10.2147/JIR.S612924","url":null,"abstract":"","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"612924"},"PeriodicalIF":4.1,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13127430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147816340","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}
Maiara Piva, Marília F Manchope, Fernanda Barbosa-Costa, Beatriz H S Bianchini, Ketlem C Andrade, Letícia Coelho Silva, Cássia Calixto-Campos, Fernanda S Rasquel-Oliveira, Victor Fattori, Ana Carla Zarpelon-Schutz, Doumit Camilios-Neto, Sergio M Borghi, Rubia Casagrande, Waldiceu A Verri
{"title":"<i>Trans</i>-Chalcone Reduces Inflammation and Pain Triggered by Superoxide Anion: Neuronal and Non-Neuronal Mechanisms.","authors":"Maiara Piva, Marília F Manchope, Fernanda Barbosa-Costa, Beatriz H S Bianchini, Ketlem C Andrade, Letícia Coelho Silva, Cássia Calixto-Campos, Fernanda S Rasquel-Oliveira, Victor Fattori, Ana Carla Zarpelon-Schutz, Doumit Camilios-Neto, Sergio M Borghi, Rubia Casagrande, Waldiceu A Verri","doi":"10.2147/JIR.S590675","DOIUrl":"https://doi.org/10.2147/JIR.S590675","url":null,"abstract":"<p><strong>Background: </strong>Potassium superoxide (KO<sub>2</sub>), a superoxide anion donor, can be applied to induce reactive oxygen species (ROS) triggered pain and inflammation. <i>trans</i>-Chalcone (TC) is an atypical flavonoid because its molecular structure does not possess intrinsic antioxidant properties. This characteristic allows investigating the mechanisms of action of flavonoids excluding inherent chemical antioxidant effect. In the present study, we investigated the activity and mechanisms of TC in a model of inflammation and pain triggered by a superoxide anion donor, which to our knowledge have not been assessed yet.</p><p><strong>Methods: </strong>Overt pain-like behavior, mechanical hyperalgesia, edema, leukocyte recruitment, oxidative stress markers, cytokine dosage by enzyme-linked immunosorbent assay (ELISA), nuclear factor kappa B (NF-κB) phosphorylation by Western blotting, mRNA expression by reverse transcription quantitative polymerase chain reaction (RT-qPCR), and neuronal activity by calcium levels were assessed. TC was administered orally 30 min before stimulation with KO<sub>2</sub>, and a dose of 30 mg/kg was selected based on previous study.</p><p><strong>Results: </strong>TC inhibited abdominal contortion, mechanical hyperalgesia, paw edema, and myeloperoxidase activity (an indirect marker of macrophage/neutrophil recruitment). TC induced antioxidant activity (assessed by ferric reducing ability and free radical scavenging), while reducing superoxide anion production and lipid peroxidation, at least in part, by upregulating <i>Nrf2</i> and downregulating <i>Gp91<sup>phox</sup></i> and <i>Cox-2</i> mRNA expression. TC inhibited KO<sub>2</sub>-induced NF-κβ phosphorylation as well as interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, and IL-33 production. Finally, TC reduced the activation of transient receptor potential vanilloid 1 (TRPV1<sup>+</sup>) and transient receptor potential ankyrin 1 (TRPA1<sup>+</sup>) nociceptive neurons in the dorsal root ganglia.</p><p><strong>Conclusion: </strong>These results demonstrate that the in vivo anti-inflammatory and analgesic activities of TC involve neuronal and non-neuronal mechanisms, and that non-antioxidant flavonoids are still biologically active.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"590675"},"PeriodicalIF":4.1,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13127440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147816368","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}
Haoyue Zhu, Xiaohan Yu, Yazhuo Wang, Ning Zhao, Baoquan Qu, Huike Ma, Yujiao Meng, Jingxia Zhao, Yan Wang, Ping Li
{"title":"A Novel Chronic Psoriasis Mouse Model via Optimized Imiquimod Dosing and Machine Learning Evaluation.","authors":"Haoyue Zhu, Xiaohan Yu, Yazhuo Wang, Ning Zhao, Baoquan Qu, Huike Ma, Yujiao Meng, Jingxia Zhao, Yan Wang, Ping Li","doi":"10.2147/JIR.S590945","DOIUrl":"https://doi.org/10.2147/JIR.S590945","url":null,"abstract":"<p><strong>Scope: </strong>Imiquimod (IMQ)-induced psoriasis-like mouse models are widely used for psoriasis research, but existing methods fail to sustain disease manifestation over time. This study explores the effect of different IMQ dosing frequencies on maintaining psoriasis symptoms in mice.</p><p><strong>Methods and results: </strong>We compared a general IMQ model (General Model) with models that used spaced dosing (D-D Model) or 5-6 doses per week (3D-D Model) over a 28-day duration. Each experimental group consisted of eight mice (n=8) to ensure statistical significance. Both the D-D and 3D-D models maintained classic pathological features of psoriasis, including immune cell accumulation in skin and sustained levels of psoriasis-related inflammatory factors in the blood, compared to the control and General Model groups. Transcriptomic analysis revealed that D-D Model and 3D-D models mice exhibited more severe psoriasis-like lesions and significantly increased expression of IL-17 and IL-23 signaling genes (IL-17A, IL-17F, S100A9) compared to the General Model. Furthermore, adjusted dosing frequencies influenced the metabolic profile, with higher regulation of TRP channels and 2-oxocarboxylic acid metabolism in the skin of D-D mice. Subsequent, Identification and validation of a conserved psoriasis biomarker signature via machine learning and cross-species analysis.</p><p><strong>Conclusion: </strong>Adjusting the dosing frequency of conventional imiquimod-induced psoriasis-like mouse models to alternate-day administration (D-D) or three days on followed by one day off (3D-D) maintained long-term psoriasis symptoms. enhancing IL-17/IL-23 signaling pathways. This modification resulted in a model exhibiting biological characteristics more closely resembling those in humans, thereby providing a more clinically relevant model for chronic psoriasis. Despite these advantages, the current model has not yet fully recapitulated the complex seasonal and cyclical nature of clinical psoriasis.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"590945"},"PeriodicalIF":4.1,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13118704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773696","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}
{"title":"Construction and Validation of a Nomogram Based on Preoperative Inflammatory Indicators for Predicting Acute Kidney Injury After Pancreaticoduodenectomy.","authors":"Wenwen Zhang, Zengyuan Qin, JunTao Wang, Chunling Huang, Xiaoru Zhao, Ziyang Liu, Limeng Wang, Lei Yan, Yue Gu, Fengmin Shao","doi":"10.2147/JIR.S588367","DOIUrl":"https://doi.org/10.2147/JIR.S588367","url":null,"abstract":"<p><strong>Background: </strong>Acute kidney injury (AKI) after pancreaticoduodenectomy is common and early identification of such patients is critical. Inflammation contributes significantly to the onset of postoperative acute kidney injury. We aimed to construct and evaluate a predictive nomogram based on preoperative inflammatory indicators for postoperative AKI in patients undergoing pancreaticoduodenectomy.</p><p><strong>Methods: </strong>In the current retrospective cohort study, we included 844 adult patients who underwent pancreaticoduodenectomy between December 2016 and June 2020. All enrolled patients were randomly assigned to the training and validation cohorts in a 7:3 ratio. We utilized least absolute shrinkage and selection operator (LASSO) regression for feature selection and multivariable logistic regression analyses to identify key risk factors in the training cohort. These selected factors were subsequently used to construct a nomogram. The nomogram's performance was assessed using various metrics such as the receiver operating characteristic (ROC) curve, calibration curves, Hosmer-Lemeshow goodness of fit, and decision curve analysis (DCA).</p><p><strong>Results: </strong>In this cohort, AKI was observed in 98 out of 844 patients, representing an incidence rate of 11.6%. LASSO regression and multivariable logistic analysis showed that monocyte-to-lymphocyte ratio (MLR), red blood cell distribution width (RDW), and alkaline phosphatase (ALP) were independent influencing factors of postoperative AKI. The nomogram, which integrated the three identified factors, demonstrated an area under the curve (AUC) of 0.799 in both the training and validation cohorts, indicating moderate discriminative ability. The Hosmer-Lemeshow goodness of fit test and the calibration curve demonstrate good agreement between predicted and observed values. The DCA indicated a positive net clinical benefit.</p><p><strong>Conclusion: </strong>We developed and validated a nomogram based on preoperative MLR that could help identify individuals at risk of AKI following pancreaticoduodenectomy. This model may help clinicians optimize perioperative management for these patients.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"588367"},"PeriodicalIF":4.1,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13116534/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773739","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}
{"title":"Traditional Chinese Medicine Treatment for Coronary Heart Disease: Pathological Mechanisms of Modulating Cell Death Pathways.","authors":"Wanying Jia, Jinwei Liu, Zhibo Zhu","doi":"10.2147/JIR.S590293","DOIUrl":"https://doi.org/10.2147/JIR.S590293","url":null,"abstract":"<p><p>Coronary heart disease (CHD) is one of the most prevalent cardiovascular pathologies, with complications significantly increasing mortality rates. The pathogenesis of CHD is complex and multidimensional, and its cellular and molecular basis remains incompletely understood. Recent studies indicate that multiple forms of cell death participate in the initiation and progression of CHD, including inflammation-driven factors (Pyroptosis- Necroptosis- Ferroptosis), context-dependent modulators (Apoptosis- Autophagy), and emerging/hypothetical mechanisms (PANoptosis- Cuproptosis- Disulfidptosis). Meanwhile, traditional Chinese medicine (TCM) is gaining increasing attention in the management of cardiovascular diseases, particularly CHD. This research summarizes the roles of multiple cell death pathways in the pathogenesis of CHD and provides a detailed review and comprehensive analysis of the mechanisms underlying existing experimental studies on TCM formulas and active components used to treat CHD. We highlight representative TCM metabolites and TCM formulas, such as resveratrol, TongMai YangXin Wan, Gualoupi Injection, etc. It concludes that TCM counteracts CHD by inhibiting various cell death pathways. Current basic research primarily focuses on signaling pathways such as PI3K/Akt, TNF, and MAPK. This work provides new insights and approaches for the treatment of CHD and further research. Finally, it identifies current challenges, including unclear compositions of TCM and insufficient validation of mechanisms, and proposes new directions for future research.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"590293"},"PeriodicalIF":4.1,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13118658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773710","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}
{"title":"Exploring the Protective Mechanism of Xuebijing Injection Against Sepsis.","authors":"Zhouguang Jiao, Haikuan Yu, Xuekong Li, Xiaoqing Chen, Fangfang Jiao, Taojin Feng, Dewen Kong, Rongxian Jiang, Jingguang Jin, Yulong Song, Xinhua Luo","doi":"10.2147/JIR.S586204","DOIUrl":"https://doi.org/10.2147/JIR.S586204","url":null,"abstract":"<p><strong>Purpose: </strong>Xuebijing (XBJ) injection is a traditional Chinese medicine (TCM) injection prepared using modern pharmaceutical techniques. Approved as a State Category II New Drug for sepsis, XBJ has demonstrated significant clinical efficacy in China. However, the bioactive components of XBJ and the mechanisms underlying its anti-sepsis effects remain to be fully elucidated. This study aimed to elucidate the regulatory network among herbs, compounds, genes, and signaling pathways.</p><p><strong>Methods: </strong>We conducted a network pharmacology analysis by integrating published RNA-sequencing data from the BioProject database and experimental evidence from 27 relevant studies identified in PubMed. And the anti-sepsis effects of XBJ and its main component, Hydroxysafflor Yellow A, were validated in a CLP-induced murine model.</p><p><strong>Results: </strong>Our results demonstrate that XBJ modulates 21 target genes through at least 18 of its bioactive compounds (e.g. Quercetin, Kaempferol). The majority of these genes, including IL6, TNF, and HMGB1, were down-regulated after XBJ treatment. Using a cecal ligation and puncture (CLP)-induced murine sepsis model, we demonstrated that by 24 hours post-operation, the survival rate in the XBJ-treated group was twice that of the PBS-treated group (66.7% vs. 33.3%). Finally, a comprehensive herb-compound-gene-pathway regulatory network was established to illustrate the potential mechanisms of action.</p><p><strong>Conclusion: </strong>In summary, this study reveals that XBJ may alleviate sepsis by modulating target genes via its compounds, primarily through anti-inflammatory and antioxidant pathways. This study provides a systematic elucidation of XBJ's anti-sepsis mechanism, and the research strategy established here offers a valuable framework for investigating the mechanisms of other complex traditional Chinese medicine formulae.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"586204"},"PeriodicalIF":4.1,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13117868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773680","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}
Yiwen Sun, Shengze Li, Jiming Duan, Jiaxing Li, Wenxing Li
{"title":"Using the Phillygenin Ameliorates the Severe Acute Pancreatitis in Rats by Inhibiting TLR4/NF-κB Pathway.","authors":"Yiwen Sun, Shengze Li, Jiming Duan, Jiaxing Li, Wenxing Li","doi":"10.2147/JIR.S590483","DOIUrl":"https://doi.org/10.2147/JIR.S590483","url":null,"abstract":"<p><strong>Background: </strong>There is no effective agent against the inflammation in severe acute pancreatitis (SAP). Phillygenin (PHI) exhibits potent anti-inflammatory activity. However, the molecular mechanisms underlying its effects on SAP remain unclear. The aim of the study was to explore the therapeutic effects and regulatory mechanism of PHI on SAP.</p><p><strong>Methods: </strong>Thirty male SD rats were randomly divided into control, SAP and PHI (30 mg/kg) treated groups. The effectiveness of the PHI treatment was determined by looking at the histological scores of the pancreas, the levels of serum amylase and lipase, pathological changes and myeloperoxidase (MPO) activity. The affinity between PHI and the TLR4/NF-κB proteins were predicted using molecular docking. Rat pancreatic AR42J cells were divided into control, cerulein plus LPS and PHI-treated groups (12.5, 25 and 50 μg/mL). In vivo and vitro experiments, the effect of PHI on the release of TNF-α, IL-6, and IL-1β were measured by ELISA. The Western blot and immunohistochemistry were used to uncover the underlying molecular mechanisms targeting on TLR4/NF-κB.</p><p><strong>Results: </strong>PHI treatment significantly improved pancreatic pathology (<i>P < 0.001</i>), decreased the levels of serum amylase and lipase (<i>P < 0.05</i>), reduced pancreatic MPO activity (<i>P < 0.01</i>). Additionally, PHI reduced the release of TNF-α (<i>P < 0.01</i>), IL-6 (<i>P < 0.05</i>), and IL-1β (<i>P < 0.01</i>) in rats. Furthermore, PHI exhibited strong binding ability to both TLR4 and NF-κB. The protein expression of TLR4, NF-κB, and phospho-NF-κB proteins in vivo and in vitro models were downregulated by PHI (<i>P < 0.05</i>). The transfer of phospho-NF-κB to the nucleus was also reduced in the rat pancreas (<i>P < 0.05</i>).</p><p><strong>Conclusion: </strong>PHI exhibits a protective effect against SAP. It can alleviate SAP in rats by inhibiting TLR4/NF-κB pathway. Therefore, PHI may be considered as a novel therapeutic agent against SAP.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"590483"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13110813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773708","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}
{"title":"The Association Between C-Reactive Protein-to-Albumin Ratio and in-Hospital Mortality in Patients with <i>Klebsiella pneumoniae</i> Bloodstream Infection: A Retrospective Cohort Study.","authors":"Yingxiu Huang, Ting Ao, Ming Hu, Peng Zhen","doi":"10.2147/JIR.S588368","DOIUrl":"https://doi.org/10.2147/JIR.S588368","url":null,"abstract":"<p><strong>Background: </strong>The C-reactive protein-to-albumin ratio (CAR), integrating inflammation (CRP) and physiological reserve (albumin), shows promise as a prognostic biomarker in critical illness, but its specific role in <i>Klebsiella pneumoniae</i> bloodstream infection (KP-BSI) mortality has not been confirmed.</p><p><strong>Methods: </strong>Between 2019 and 2024, 264 adult patients with KP-BSI at a tertiary medical center were included in this retrospective cohort study. The primary endpoint was in-hospital mortality, Patients were categorized into three groups according to tertiles of the CAR: T1 < 3.91, T2 3.91-6.91, and T3 > 6.91. To assess the relationship between serum CAR levels and mortality risk, we applied multivariable Cox proportional hazards models and constructed Kaplan-Meier survival curves, with subgroup analyses incorporating interaction testing across sex, age, diabetes, septic shock, and CRKP status, as well as sensitivity analyses excluding patients with chronic liver disease, those with missing covariates, and including those with a length of hospital stay exceeding 180 days. The discriminatory performance of CAR was further assessed using receiver operating characteristic (ROC) curve analysis.</p><p><strong>Results: </strong>Among the 264 patients included in the final analysis, 121 (45.8%) died during hospitalization. Non-survivors showed significantly higher CAR (7.1 ± 3.4) than survivors (4.8 ± 3.0) (p<0.001). After adjusting for potential confounders, each unit increase in CAR was independently associated with a higher risk of in-hospital mortality (hazard ratio (HR)=1.12, 95% confidence interval (CI): 1.07-1.19, p<0.001). When treated as a categorical variable, compared to the reference group (T1 group), patients in the highest tertile (T3) had a substantially elevated mortality risk (HR=3.12, 95% CI: 1.83-5.34, P<0.001). Subgroup analyses and sensitivity analyses consistently supported the robustness of the results. The ROC analysis demonstrated that CAR had moderate discriminatory ability.</p><p><strong>Conclusion: </strong>CAR is independently associated with in-hospital mortality in patients with KP-BSI. This readily available biomarker offers meaningful early risk stratification and may help identify patients at elevated risk who could benefit from closer monitoring and targeted clinical intervention.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"19 ","pages":"588368"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13110735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773698","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}