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Assessment of pan-immune-inflammation value as a novel marker of proliferative diabetic retinopathy stage 认领 引用
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作者 Ozlem Candan Gözde Orman +1 位作者 NurtenÜnlü Güner Uney 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2026年第3期517-525,共9页
AIM:To evaluate the predictive value of pan-immuneinflammation value(PIV)in the diagnosis of proliferative diabetic retinopathy(PDR)and its association with the stage of PDR.METHODS:This observational case-control stu... AIM:To evaluate the predictive value of pan-immuneinflammation value(PIV)in the diagnosis of proliferative diabetic retinopathy(PDR)and its association with the stage of PDR.METHODS:This observational case-control study included participants who underwent routine complete blood count testing.Inflammation-related indices,including neutrophil-to-lymphocyte ratio,systemic immune-inflammation index(SII),and PIV,were derived and analyzed.Receiver operating characteristic curve(ROC)analysis was applied to assess the diagnostic performance of these indices in distinguishing patients with PDR,with sensitivity,specificity,area under ROC,and optimal threshold values calculated.In addition,binary logistic regression analysis was performed to evaluate the association between inflammatory indices and PDR stage.RESULTS:This study included 205 patients:60 with diabetes without retinopathy(mean age:61.81±10.76y),80 with PDR(mean age:61.63±10.03y)and 65 healthy controls(mean age:59.52±5.88y).The PDR group had significantly higher white blood cell(WBC,P527.12 and>299.08 for SII and PIV,respectively.The logistic regression analysis demonstrated that a decrease in lymphocyte(LYM)count and an increase in platelet count(PLT),glycated haemoglobin(HbA1c),SII,and PIV were all significantly associated with the development of high-risk PDR(all P345.87 area under ROC=0.871,with sensitivity of 0.827 and specificity of 0.812.CONCLUSION:PIV is a reliable,valuable,and inexpensive blood index that can be used for early detection and staging of PDR.PIV may therefore be essential to be used for the follow-up of diabetic patients. 展开更多
关键词 pan-immune-inflammation value proliferative diabetic retinopathy systemic immuneinflammation index monocyte-related inflammation systemic inflammation
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Neutrophil-initiated nociceptive ingrowth orchestrates inflammation resolution to potentiate bone regeneration 认领 引用
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作者 Xuanyu Qi Guangzheng Yang +5 位作者 Zeqian Xu Mingliang Zhou Tejing Liu Jiahui Du Sihan Lin Xinquan Jiang 《Bone Research》 SCIE CAS CSCD 2026年第1期195-209,共15页
Nociceptive pain is a cardinal feature of traumatic and inflammatory bone diseases.However,whether and how nociceptors actively regulate the immune response during bone regeneration remains unclear.Here,we found that ... Nociceptive pain is a cardinal feature of traumatic and inflammatory bone diseases.However,whether and how nociceptors actively regulate the immune response during bone regeneration remains unclear.Here,we found that neutrophil-triggered nociceptive ingrowth functioned as negative feedback regulation to inflammation during bone healing.A unique Il4ra+Ccl2high neutrophil subset drove intense postinjury TRPV1+nociceptive ingrowth,which in return dissipated inflammation by activating the production of pro-resolving mediator lipoxin A4(LXA4)in osteoblasts.Mechanistically,osteoblastic autophagy activated by nociceptor-derived calcitonin gene-related peptide(CGRP)suppressed the nuclear translocation of arachidonate 5-lipoxygenase(5-LOX)to favor the LXA4 biosynthesis.Moreover,in alveolar bone from patients with Type Ⅱ diabetes,we found diminished nociceptive innervation correlated with reduced autophagy,increased inflammation,and impaired bone formation.Activating nociceptive nerves by spicy diet or topical administration of a clinical-approved TRPV1 agonist showed therapeutic benefits on alveolar bone healing in diabetic mice.These results reveal a critical neuroimmune interaction underlying the inflammation-regeneration balance during bone repairing and may lead to novel therapeutic strategies for inflammatory bone diseases. 展开更多
关键词 inflammation resolution negative feedback regulation nociceptive pain nociceptive ingrowth lipoxin dissipated inflammation neutrophil bone regeneration
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Tocilizumab as an effective treatment option for idiopathic orbital inflammation:a case report and literature review 认领 引用
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作者 Hai-Yang Zhang Hui-Jie Zhang Hui-Fang Zhou 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2026年第1期199-201,共3页
Dear Editor,Idiopathic orbital inflammation(IOI),also known as orbital inflammatory pseudotumor,is a relatively common orbital disorder[1].Its pathogenesis remains unclear,often regarded as a nonspecific immune-mediat... Dear Editor,Idiopathic orbital inflammation(IOI),also known as orbital inflammatory pseudotumor,is a relatively common orbital disorder[1].Its pathogenesis remains unclear,often regarded as a nonspecific immune-mediated response[2].IOI presents with symptoms such as pain,photophobia,proptosis,eyelid swelling,edema,conjunctival congestion,and diplopia,with possible vision loss occurring in some cases.Based on the soft tissue structures involved,IOI can be classified into subtypes such as myositis,optic neuritis,dacryoadenitis,diffuse orbital inflammation,and orbital inflammatory masses[2]. 展开更多
关键词 soft tissue structures idiopathic orbital inflammation orbital disorder its vision loss myositisoptic neuriti orbital inflammatory pseudotumoris orbital inflammation ioi also orbital inflammatory pseudotumor
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Adenosine:A key player in neuroinflammation 认领 引用
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作者 Qilin Guo Rhea Seth Wenhui Huang 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第4期1556-1557,共2页
Neuroinflammation,the inflammatory response of the central nervous system(CNS),is a common feature of many neurological disorders such as sepsis-associated encephalopathy(SAE),multiple sclerosis(MS),and Parkinson'... Neuroinflammation,the inflammatory response of the central nervous system(CNS),is a common feature of many neurological disorders such as sepsis-associated encephalopathy(SAE),multiple sclerosis(MS),and Parkinson's disease(PD).Prior studies identified cytokines(e.g.,tumor necrosis factor[TNF],interleukin[IL]-1,and IL-6)delivered by resident glial cells and brain-invading peripheral immune cells as the major contributor to neuroinflammation(Becher et al.,2017).In addition to pro-inflammatory cytokines,elevated levels of extracellular purine molecules such as adenosine triphosphate(ATP)and adenosine can be detected upon any pathological insults(e.g.,injury,ischemia,and hypoxia),contributing to the progression of neurological disorders(Borea et al.,2017). 展开更多
关键词 adenosine sepsis associated encephalopathy central nervous system cns neuroinflammation cerebral inflammation neurological disorders inflammatory response parkinsons disease pd prior
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Inflammation,immunity,and gastric ulcer—clinical insights from routine haematology 认领 引用
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作者 Hui Wang Shi-San Bao 《World Journal of Gastroenterology》 SCIE CAS 2026年第3期189-191,共3页
Gastric ulcer remains a common cause of morbidity,yet marked clinical variability suggests contributors beyond established risk factors such as Helicobacter pylori,non-steroidal anti-inflammatory drug exposure,and exc... Gastric ulcer remains a common cause of morbidity,yet marked clinical variability suggests contributors beyond established risk factors such as Helicobacter pylori,non-steroidal anti-inflammatory drug exposure,and excess gastric acid.To clarify the role of systemic inflammation,Shen et al evaluated six complete blood count(CBC)-derived inflammatory indices in patients with gastric ulcer.All indices showed significant associations,with the systemic inflammatory response index demonstrating the strongest discriminatory value.Given that CBC testing is routine,inexpensive,and widely accessible,these indices may offer practical adjunctive markers for identifying individuals at increased risk.However,the cross-sectional design and lack of adjustment for major confounders limit causal interpretation.Prospective validation is required to determine whether these indices predict ulcer development,recurrence,or clinical outcomes,and to assess their potential integration with established risk factors. 展开更多
关键词 Inflammation Immunity Gastric ulcer Systemic immune-inflammation index Routine haematology
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Neuroinflammation strokes the brain:A double-edged sword in ischemic stroke 认领 引用 被引量：5
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作者 Giorgia Lombardozzi Vanessa Castelli +2 位作者 Chiara Giorgi Annamaria Cimini Michele d’Angelo 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第5期1715-1722,共8页
Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response pla... Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response plays a crucial role in worsening brain injury.Neuroinflammation,a key player in the pathophysiology of stroke,has a dual role.In the acute phase of stroke,neuroinflammation exacerbates brain injury,contributing to neuronal damage and blood–brain barrier disruption.This aspect of neuroinflammation is associated with poor neurological outcomes.Conversely,in the recovery phase following stroke,neuroinflammation facilitates brain repair processes,including neurogenesis,angiogenesis,and synaptic plasticity.The transition of neuroinflammation from a harmful to a reparative role is not well understood.Therefore,this review seeks to explore the mechanisms underlying this transition,with the goal of informing the development of therapeutic interventions that are both time-and context-specific.This review aims to elucidate the complex and dual role of neuroinflammation in stroke,highlighting the main actors,biomarkers of the disease,and potential therapeutic approaches. 展开更多
关键词 brain repair euinflammation inflammation ischemia mechanisms microglia oxidative stress stroke therapeutic approaches
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Effects and mechanisms of adipose tissue-derived extracellular vesicles in vascular inflammation and dysfunction 认领 引用 被引量：1
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作者 Daphne Lintsen Bieke Broux 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第5期2005-2006,共2页
Neuroinflammation is a key process in the pathogenesis of various neurodegenerative diseases,such as multiple sclerosis(MS),Alzheimer's disease,and traumatic brain injury.Even for disorders historically unrelated ... Neuroinflammation is a key process in the pathogenesis of various neurodegenerative diseases,such as multiple sclerosis(MS),Alzheimer's disease,and traumatic brain injury.Even for disorders historically unrelated to neuroinflammation,such as Alzheimer's disease,it is now shown to precede pathological protein aggregations. 展开更多
关键词 pathological protein aggregations vascular inflammation neuroinflammation neurodegenerative diseasessuch multiple sclerosis Alzheimers disease adipose tissue derived extracellular vesicles alzheimers diseaseit
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Melatonin alleviates neuroinflammation in ischemic stroke by regulating cyclic GMP-AMP synthase-mediated microglial pyroptosis signaling 认领 引用 被引量：3
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作者 Qian Li Lin Feng +7 位作者 Yu Tian Erliang Guo Yiran Li Jingyan Niu Haodong Pan Chun Dang Yaoheng Lu Lihua Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第6期2380-2388,共9页
Inflammation plays a key role in driving the secondary brain injury that follows ischemic stroke.Melatonin is an endogenous neuroendocrine hormone that regulates mitochondrial homeostasis.However,the role and mechanis... Inflammation plays a key role in driving the secondary brain injury that follows ischemic stroke.Melatonin is an endogenous neuroendocrine hormone that regulates mitochondrial homeostasis.However,the role and mechanisms by which melatonin regulates microglial pyroptosis and the inflammatory cascade through double-stranded DNA(dsDNA)-sensing cyclic GMP-AMP synthase(cGAS)signaling warrant further study.Using middle cerebral artery occlusion mice,we investigated the effects of melatonin on cGAS-mediated pyroptosis and neuroinflammation.Middle cerebral artery occlusion model mice exhibited significantly increased DNA damage and cytoplasmic dsDNA release,as reflected byγH2AX staining,as well as heightened activation of the cytosolic dsDNA-sensing cGAS-STING pathway,both of which were notably suppressed by melatonin treatment.Melatonin also mitigated NOD-like receptor family pyrin domain-containing protein 3(NLRP3)inflammasome activation and nuclear factor(NF)-κB/gasdermin D-mediated pyroptosis in microglia following ischemic stroke,while exhibiting the capacity to attenuate the immune response to ischemia in mice.This led to reduced infiltration of peripheral neutrophils and monocytes/macrophages in the ischemic brain.Specifically,melatonin administration resulted in reductions in the numbers of ionized calcium-binding adapter molecule 1-positive cells and production of interleukin-6 and tumor necrosis factor-αby microglia.Regarding neurological outcomes,melatonin significantly reduced cerebral infarct volume and ameliorated neurological deficits in mice.Notably,the neuroprotective effect of melatonin was correlated with the inhibition of cGAS activity.We also developed and tested melatonin co-loaded macrophage membrane-biomimetic reactive oxygen species-responsive nanoparticles(Mф-MLT@FNGs),which exhibited therapeutic properties in middle cerebral artery occlusion mice.Our findings suggest that melatonin acts on microglial pyroptosis to inhibit neuroinflammation and reshape the immune microenvironment through regulation of the cGAS-STING-NF-κB signaling pathway.By doing so,melatonin rescues damaged brain tissue and protects neurological function,highlighting its potential as a neuroprotective treatment for ischemic stroke. 展开更多
关键词 cGAS immune injury inflammation ischemic stroke melatonin pyroptosis STING microglia
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Effects and mechanism of Bifidobacterium on intestinal inflammation resulting from deoxycholic acid-induced M1 polarization of macrophages 认领 引用 被引量：2
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作者 Peng-Chun Yang Chun-Yan Xiao +6 位作者 Jing Wang Cai-Hua Yan Qi-Yi Li Shi-Yu Li Jian Li Li-Jing Zhang Chi-Bing Dai 《World Journal of Gastroenterology》 SCIE CAS 2026年第6期77-96,共20页
BACKGROUND A high-fat diet(HFD)can cause systemic low-grade inflammation,metabolic and inflammatory diseases,and alter the composition of intestinal microbiota.Although probiotics mitigate intestinal inflammation,it i... BACKGROUND A high-fat diet(HFD)can cause systemic low-grade inflammation,metabolic and inflammatory diseases,and alter the composition of intestinal microbiota.Although probiotics mitigate intestinal inflammation,it is still unclear whether they can directly inhibit the production of deoxycholic acid(DCA)to prevent or alleviate intestinal inflammation.AIM To investigate changes in intestinal flora,fecal DCA levels,and cytokine profiles.METHODS Vancomycin was administered to significantly reduce the population of intestinal gram-positive bacteria,which helped in reducing the fecal DCA levels.Recruitment of pro-inflammatory macrophages,polarization of macrophages,and the inflammation associated with the intestinal flora of the HFD animal model were assessed.Their expression levels were analyzed through real-time polymerase chain reaction,immunofluorescence staining,liquid chromatography-mass spectrometry,and 16S rRNA high-throughput sequencing.RESULTS HFD or DCA promotes the infiltration of colon macrophages,causing their polarization toward the M1 phenotype.This polarization can be inhibited by both vancomycin and Bifidoba-cterium.Bifidobacterium enhances the species richness and uniformity of the intestinal microbiota in HFD mice;however,it does not improve these parameters in the presence of vancomycin.Bifidobacterium also does not increase the abundance of microbiota in HFD-fed or HFD-and-vancomycin-treated mice.HFD alters the relative abundance of intestinal microbiota at the phylum and genus levels.Bifidobacterium or vancomycin can partially mitigate these changes.CONCLUSION Bifidobacterium can inhibit HFD-induced intestinal inflammation or that resulting from DCA-induced M1 polarization of macrophages.It may also regulate bile acid levels and target cholesterol metabolism pathways,which may serve as potential therapeutic strategies for HFD-associated colitis. 展开更多
关键词 High-fat diet Bifidobacterium Deoxycholic acid Macrophage polarization Microbiota Intestinal inflammation
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Depression induces ocular surface inflammation and dry eye-like changes in mice 认领 引用 被引量：1
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作者 Xiang Lin Yu-Wen Liu +7 位作者 Jia-Ni Li Wei-Jie Ouyang Li-Ying Tang Jie-Li Wu Zhao-Lin Liu Shi-Nan Wu Jiao-Yue Hu Zu-Guo Liu 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2026年第3期434-442,共9页
AIM:To investigate the impact of depression-like behavior on ocular surface homeostasis in a mouse model,with a focus on dry eye-like alterations.METHODS:Male C57BL/6J mice(10-12 weeks old)were randomly assigned to co... AIM:To investigate the impact of depression-like behavior on ocular surface homeostasis in a mouse model,with a focus on dry eye-like alterations.METHODS:Male C57BL/6J mice(10-12 weeks old)were randomly assigned to control or restraint stress(RS)groups.The RS group underwent three intermittent 24-hour restraint sessions to induce depressive-like behavior.Behavioral testing,tear secretion measurement,and corneal Oregon Green Dextran(OGD)staining were performed.Postmortem analyses included histological evaluation of lacrimal glands,goblet cell quantification using periodic acid-Schiff staining,and assessment of key inflammatory and apoptotic markers:interleukin(IL)-17,matrix metalloproteinases(MMP)-3,MMP-9,IL-13,interferon(IFN)-γ,and cleaved caspase-3 and-8.RESULTS:Repeated RS induced depression-like behavior and significant ocular surface changes.RStreated mice showed increased corneal OGD uptake and upregulation of gene/protein expression of IL-17,MMP-3,and MMP-9(P<0.05).Goblet cell density and IL-13 protein expression were reduced,while IFN-γprotein expression was elevated(P<0.05).Cleaved caspase-3 and-8 levels were significantly increased in both cornea and conjunctiva.Tear volume and lacrimal gland size were unchanged;however,mild inflammatory infiltration was observed in lacrimal glands.CONCLUSION:Repeated RS leads to ocular surface inflammation and dry eye-like pathology,including corneal barrier disruption,goblet cell loss,and epithelial apoptosis.These findings suggest that depression contributes to the pathogenesis of dry eye disease via immune-mediated mechanisms. 展开更多
关键词 depression restraint stress dry eye ocular surface damage inflammation mice
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Co-exposure of PFASs,PAHs and metals,immune inflammation and triglyceride-glucose index:Exploring associations and mediation effects in children 认领 引用 被引量：1
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作者 Miao Liu Biao Zhang +11 位作者 Yuanyuan Zhang Jie Wang Lei Zhao Wenting Guo Meng Li Huihua Yang Xuefeng Lai Liangle Yang Xiao Meng Cuijuan Wang Zhihu Zhang Xiaomin Zhang 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第2期384-393,共10页
The associations of co-exposure to per-and polyfluoroalkyl substances(PFAS),polycyclic aromatic hydrocarbons(PAHs),and metals with children’s glycometabolism and the underlying mechanism of immune inflammation are la... The associations of co-exposure to per-and polyfluoroalkyl substances(PFAS),polycyclic aromatic hydrocarbons(PAHs),and metals with children’s glycometabolism and the underlying mechanism of immune inflammation are largely unclear.We conducted a longitudinal panel study to explore the effects of individual and mixture of 27 contaminants on an emerging surrogate indicator of insulin resistance,triglyceride-glucose index(TyG),and the mediation of immunoglobulins and cytokines in children aged 4–6 years and 11–13 years.The results showed robust associations of perfluorooctanoic acid(PFOA),perfluorononanoic acid(PFNA),perfluoroundecanoic acid(PFUnDA),and arsenic(As)with elevated TyG.The interaction of PFNA with PFOA was significant,showing a synergistic effect on TyG.And combined association of each pair of PFOA,PFNA,and As with TyG were enhanced.Meanwhile,the effect of contaminants mixture on TyG was significant for polyfluoroalkyl substances(PFAS)mixture,of which 6:2 Chlorinated polyfluorinated ether sulfonates(Cl-PFESA),PFNA,and PFUnDA weighted more than others.Notably,contaminants were related to immune globulins and cytokines,of which chemokine ligand(CCL)4,interleukin(IL)-1β,IL-9,and tumor necrosis factor(TNF)-α significantly mediated associations of PFOA,PFNA,and PFUnDA with TyG.Accordingly,PFAS and metals were individually and jointly associated with TyG elevation,with 6:2 Cl-PFESA,PFNA,and PFUnDA contributing the most,and CCL4,IL-1β,IL-9,and TNF-α might be the underlying mediators in children. 展开更多
关键词 Priority-controlled contaminants mixture Triglyceride-glucose index Mediation of immune inflammation Panel study
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Chitosan alleviates symptoms of Parkinson's disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier 认领 引用 被引量：1
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作者 Yinying Wang Rongsha Chen +7 位作者 Guolin Shi Xinwei Huang Ke Li Ruohua Wang Xia Cao Zhongshan Yang Ninghui Zhao Jinyuan Yan 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第1期377-391,共15页
Studies have shown that chitosan protects against neurodegenerative diseases. However, the precise mechanism remains poorly understood. In this study, we administered chitosan intragastrically to an MPTP-induced mouse... Studies have shown that chitosan protects against neurodegenerative diseases. However, the precise mechanism remains poorly understood. In this study, we administered chitosan intragastrically to an MPTP-induced mouse model of Parkinson's disease and found that it effectively reduced dopamine neuron injury, neurotransmitter dopamine release, and motor symptoms. These neuroprotective effects of chitosan were related to bacterial metabolites, specifically shortchain fatty acids, and chitosan administration altered intestinal microbial diversity and decreased short-chain fatty acid production in the gut. Furthermore, chitosan effectively reduced damage to the intestinal barrier and the blood–brain barrier. Finally, we demonstrated that chitosan improved intestinal barrier function and alleviated inflammation in both the peripheral nervous system and the central nervous system by reducing acetate levels. Based on these findings, we suggest a molecular mechanism by which chitosan decreases inflammation through reducing acetate levels and repairing the intestinal and blood–brain barriers, thereby alleviating symptoms of Parkinson's disease. 展开更多
关键词 acetate adenosine 5′-monophosphate-activated protein kinase blood–brain barrier chitosan dopamine neurons inflammation intestinal barrier Parkinson's disease peroxisome proliferator-activated receptor delta short-chain fatty acids
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Dysregulated insulin signaling and inflammation contribute to the pathogenesis of Alzheimer’s disease:From animal models to human cells 认领 引用
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作者 Marcus Elo Rytter Cecilie Amalie Brøgger Svane +1 位作者 Joachim Størling Wenqiang Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第3期1126-1127,共2页
The shared links between Alzheimer’s disease and type 2 diabetes mellitus:Alzheimer’s disease(AD)and type 2 diabetes mellitus(T2DM)are two prevalent conditions that come with substantial daily struggles.Emerging evi... The shared links between Alzheimer’s disease and type 2 diabetes mellitus:Alzheimer’s disease(AD)and type 2 diabetes mellitus(T2DM)are two prevalent conditions that come with substantial daily struggles.Emerging evidence highlights that these diseases share similar pathophysiological features,including insulin resistance and chronic inflammation,which contribute to their rapid progression(Chen et al.,2022).Insulin resistance,a hallmark of T2DM,has been suggested to exacerbate neurodegeneration in AD.Similarly,chronic low-grade inflammation in T2DM parallels with neuroinflammation,which is observed in AD,suggesting overlapping pathophysiological mechanisms in T2DM and AD. 展开更多
关键词 alzheimer s disease chronic inflammationwhich type diabetes mellitus alzheimer s disease ad inflammation exacerbate neurodegeneration Alzheimers disease insulin resistance type diabetes mellitus t dm
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Prognostic value of pan-immune-inflammation index in hepatocellular carcinoma compared with albumin-bilirubin and model for end-stage liver disease sodium 认领 引用
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作者 Salih Karatlı Doğan Yazılıtaş +3 位作者 Seher Kaya GökşenI Imamoğlu Selahattin Celik Galip C Uyar 《World Journal of Gastrointestinal Oncology》 SCIE 2026年第7期103-113,共11页
BACKGROUND Hepatocellular carcinoma(HCC)prognosis is influenced by tumor burden,liver function,performance status,and systemic inflammation.Conventional prognostic systems such as the albumin-bilirubin(ALBI)and model ... BACKGROUND Hepatocellular carcinoma(HCC)prognosis is influenced by tumor burden,liver function,performance status,and systemic inflammation.Conventional prognostic systems such as the albumin-bilirubin(ALBI)and model for end-stage liver disease-sodium(MELD-Na)scores mainly reflect hepatic functional reserve but may not adequately capture the host inflammatory response.AIM To evaluate the prognostic significance of the pan-immune-inflammation value(PIV)compared with ALBI and MELD-Na scores in patients with HCC.METHODS This retrospective cohort study included 97 patients diagnosed with HCC and treated at the Medical Oncology Department of Ankara Etlik City Hospital between September 2022 and September 2025.Overall survival(OS)was analyzed using Kaplan-Meier survival analysis,Cox regression models,and receiver operating characteristic(ROC)curve analysis.Univariate and multivariable Cox regression analyses were performed to identify independent prognostic factors,and optimal cut-off values were determined using the Youden index.RESULTS Median follow-up was 10 months,and 58 deaths occurred.In univariate analysis,Eastern Cooperative Oncology Group(ECOG)performance status,Barcelona clinic liver cancer stage,cirrhosis,treatment modality,ALBI,MELD-Na score,and PIV were significantly associated with OS(all P<0.05).In multivariable Cox regression analysis,ECOG performance status(P<0.001)and PIV(P=0.016)remained independent prognostic factors.ROC analysis demonstrated that PIV had the highest discriminatory ability for predicting OS(AUC=0.794,P<0.001),followed by ALBI(AUC=0.781,P<0.001),alpha-fetoprotein(AUC=0.712,P<0.001),and MELD-Na(AUC=0.699,P=0.001).Patients with high PIV had significantly poorer survival,with a median OS of 5 months compared with 30 months in the low-PIV group.CONCLUSION These findings demonstrate that PIV provides superior prognostic performance compared with conventional liver function-based scores and may serve as a robust biomarker for risk stratification in patients with HCC. 展开更多
关键词 Hepatocellular carcinoma Pan-immune-inflammation value Systemic inflammation Prognostic biomarkers Albumin-bilirubin score Model for end-stage liver disease-sodium score Survival Prognosis
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Single-Cell RNA Sequencing Reveals 7-Ketositosterol Exacerbates Aortic Inflammation Through TLR4 Signaling-Regulated IRF5 Mediated M1 Macrophage Polarization 认领 引用
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作者 Qinjun Zhang Weisu Huang +3 位作者 Cheng Chen Jianfu Shen Baiyi Lu Peiwu Li 《Engineering》 SCIE EI CSCD 2026年第5期280-293,共14页
Atherosclerosis(AS)is a chronic inflammatory disease in which macrophages play an indispensable role.Exploration of the effects of aortic cell subpopulations in AS remains challenging due to cellular heterogeneity.Phy... Atherosclerosis(AS)is a chronic inflammatory disease in which macrophages play an indispensable role.Exploration of the effects of aortic cell subpopulations in AS remains challenging due to cellular heterogeneity.Phytosterol oxidation products(POPs)are key dietary factors influencing AS due to their potential pro-inflammatory effects in atherosclerotic mice.However,the contribution of alterations in cellular heterogeneity to this outcome and the exact mechanisms remain elusive.Here,we constructed a novel single-cell transcriptomic landscape of arteries in ApoE-/-mice fed an atherosclerotic diet without or with POPs,Combining single-cell RNA sequencing(scRNA-seq)with in vitro functional validation,we demonstrated that 7-ketositosterol(7-KS),a major component of POPs,induced macrophages to skew the pro-inflammatory(M1)phenotype through the toll-like receptor 4(TLR4)-interferon regulatory factor 5(IRF5)axis,thereby amplifying the inflammatory response.Notably,we verified the presence of this pro-inflammatory immune niche with the same molecular features using publicly available human arterial scRNA-seq data.This demonstrates that this is a reproducible characteristic in human AS.Our study shifts the current paradigm of exploring the biological effects of food components,and provides unprecedented perspectives for the application of single-cell technology to food nutrition research. 展开更多
关键词 Single-cell analysis 7-ketositosterol Macrophage Inflammation Polarization
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Polystyrene microplastics impaired decidualization in mice via oxidative stress and inflammation and disrupted the reproductive function of their female offspring 认领 引用
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作者 Weike Li Boyin Tan +12 位作者 Jun Xiong Jiani Diao Jing Wang Jing Long Zhenyin Chen Yuguang He Xuemei Chen Fei Han Fangfang Li Junlin He Yingxiong Wang Yan Su Rufei Gao 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第4期51-63,共13页
The extensive utilization of plastics has heightened concerns regarding microplastics exposure.However,the effects of polystyrene microplastics(PS-MPs)on early pregnancy remain inadequately investigated.This study aim... The extensive utilization of plastics has heightened concerns regarding microplastics exposure.However,the effects of polystyrene microplastics(PS-MPs)on early pregnancy remain inadequately investigated.This study aimed to examine the impact of PS-MPs on decidualization and embryo implantation in female mice,as well as the reproductive function of their offspring following maternal exposure to PS-MPs.We investigated the harmful effects of different PS-MPs sizes on mouse endometrial stromal cells(mESCs)during in vitro decidualization.Pregnant mice were orally given various concentrations of PS-MPs to examine their impact on decidualization.We evaluated oxidative stress and inflammation markers to understand their roles in abnormal decidualization.Additionally,we assessed potential reproductive health impacts on female offspring.Our findings indicated that 5μm PS-MPs effectively penetrated mESCs and significantly disrupted decidualization compared to smaller or larger particles.Pregnant mice that were exposed to 5μm PS-MPs at a dose of 1000 mg/(kg・day)exhibited substantial reductions in the decidual area and downregulation of decidualization markers such as BMP2.Inflammatory cytokines increased significantly in mESCs following 5μm PS-MPs exposure,and the elevated malondialdehyde levels in uterine tissue were mitigated by antioxidant treatment.Moreover,offspring exhibited decreased uterine wet weight,uterine organ coefficients,decidual areas,and expression of BMP2 due to maternal exposure to PS-MPs.These results highlighted the detrimental effects of PS-MPs on maternal decidualization and embryo implantation,suggesting a link to oxidative stress and inflammation,and maternal exposure to PS-MPs during pregnancy impaired reproductive function in offspring females. 展开更多
关键词 Polystyrene microplastics Decidualization Endometrial stromal cell Oxidative stress Inflammation Offspring
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Dual targeting of cutaneous inflammation and vasculopathy via STING-NF-κB blockade underlies the anti-psoriatic efficacy of Yinxie Granules 认领 引用
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作者 Jueyao Zou Tongyao Hu +11 位作者 Zhengyu Zhang Yong He Yuxin Wang Yixiao Zhou Ziyan Zhu Suyun Yu Wei Zou Zhonghong Wei Yang Zhao Yanhong Pan Wenxing Chen Yin Lu 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2026年第7期832-848,共17页
Psoriasis is a chronic skin disease driven by skin inflammation and abnormal subcutaneous blood vessels.Yinxie Granules(YXKL)is a clinically effective traditional Chinese medicine(TCM)formula that has shown promise in... Psoriasis is a chronic skin disease driven by skin inflammation and abnormal subcutaneous blood vessels.Yinxie Granules(YXKL)is a clinically effective traditional Chinese medicine(TCM)formula that has shown promise in psoriasis treatment,but its pharmacological mechanisms and material basis remain unclear,limiting its clinical application and co-administration with other drugs.In this study,we explored the mechanism and active components of YXKL in the treatment of psoriasis using patient samples,IMQ-induced psoriatic mice,zebrafish,and in vitro assays.We discovered that YXKL alleviated skin inflammation and restored the skin barrier by reducing M1 macrophage/Th17 infiltration,lowering pro-inflammatory cytokines(IL-6,IFN-β,IL-23,IL-17),and increasing loricrin expression.Mechanistically,we identified a dynamic transition in STING signaling during psoriasis progression.Both the STING/IRF3 and STING/NF-κB pathways were activated in moderate psoriasis,while only the STING/NF-κB pathway was hyperactivated in severe disease.YXKL specifically targeted the STING/NF-κB pathway to mitigate inflammation and vasculopathy but had no significant impact on the upstream regulators,including TRAF6,LKB1,AMPK,and ULK1.Quercetin and kaempferol were identified as the primary STING-modulating components in YXKL,binding to STING proteins and inhibiting downstream pathway activation.These flavonoid components mediate the anti-psoriatic effects of YXKL by simultaneously suppressing skin inflammation and angiogenesis while enhancing vascular integrity through STING inhibition in both keratinocytes and endothelial cells.Our results elucidated the molecular basis of YXKL for psoriasis treatment,highlighting STING/NF-κB as a pivotal therapeutic target in mitigating psoriasis development and providing natural candidate compounds as potential STING inhibitors. 展开更多
关键词 Psoriasis Yinxie Granules STING-NF-κB Skin inflammation Vascular remodeling STING inhibitor
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Effect of moxibustion at Zusanli(ST36)on beclin 1-solute carrier family 7 member 11 gene ferroptosis-related proteins in synovial inflammation of rats with rheumatoid arthritis 认领 引用
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作者 HAO Feng SANG Jiajia +4 位作者 PENG Chuanyu HU Jun WU Zijian HU Ling GU Yihuang 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2026年第3期594-604,共11页
OBJECTIVE:To investigate the effects of moxibustion at Zusanli(ST36)on ferroptosis-related proteins in synovial inflammation of rats with rheumatoid arthritis(RA)and verify the mechanism by cell experiments.METHODS:A ... OBJECTIVE:To investigate the effects of moxibustion at Zusanli(ST36)on ferroptosis-related proteins in synovial inflammation of rats with rheumatoid arthritis(RA)and verify the mechanism by cell experiments.METHODS:A RA rat model was established using a"disease-syndrome integration"modeling method.The rats were randomly divided into a blank control group(Control group)and a model replication group.Rats with successfully replicated RA models were further divided into a model control group(RA group)and a moxibustion treatment group(RA+Mox group).After intervention,the rats'ankle swelling degree and small animal ultrasound examination were conducted and synovial tissue was examined for pathology,lipid reactive oxygen species(ROS)detection,ferrous ion Fe2+double staining,and immunohistochemistry analysis.Serum from three groups of rats were extracted and used for cellular assays,cell counting kit-8 and Western blot validation.RESULTS:(a)Compared to Control group rats,RA rats showed significantly increased footpad swelling(P0.05),but the lipid ROS levels in the synovial tissue of RA+Mox rats were significantly increased(P0.05),but BECN1 expression in the synovial tissue of RA+Mox rats was significantly increased(P<0.01)compared to RA rats.Compared to Control group rats,RA rats had significantly higher Solute Carrier Family 7 Member 11 Gene(SLC7A11)levels in synovial tissue(P<0.05);compared to RA rats,the SLC7A11 levels in RA+Mox rats were significantly decreased(P<0.05).(c)In the lipopolysaccharides(10 ng/mL)model,50%concentration of RA rats serum promoted human RA fibroblast-like synovial cell line(MH7A)proliferation(48 h)(P<0.05)and 50%concentration of RA+Mox rat serum inhibited MH7A proliferation(48,72 h)(P<0.001).Both 25%and 50%concentrations of RA+Mox rat serum upregulated BECN1 and downregulated SLC7A11 expression in MH7A.CONCLUSION:Moxibustion at Zusanli(ST36)suggests a potential to relieve footpad swelling and synovial inflammation in RA rats,alleviate synovial tissue hyperplasia and thickening.It may induce lipid ROS accumulation in synovial tissue,upregulating Fe1+levels,upregulating BECN1 expression,and downregulating SLC7A11 expression in RA rats.Moreover,50%concentration of rat serum after moxibustion inhibited the proliferation of synovial fibroblasts and regulated the expression of ferroptosis-related proteins. 展开更多
关键词 moxibustion arthritis rheumatoid ferroptosis Zusanli(ST36) synovial inflammation
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Semaglutide ameliorates coronary microembolization-induced injury by suppressing apoptosis and inflammation via the HMGB1/RAGE/NF-κB p65 pathway 认领 引用
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作者 Hua-Feng YANG Hong-Qing LI +2 位作者 Qiang WANG Xian-Tao WANG Lang LI 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2026年第2期83-99,共17页
BACKGROUND Coronary microembolization(CME)is the major leading cause of perioperative myocardial injury during coronary revascularization.Semaglutide exerts multiple protective biological activities,but its cardioprot... BACKGROUND Coronary microembolization(CME)is the major leading cause of perioperative myocardial injury during coronary revascularization.Semaglutide exerts multiple protective biological activities,but its cardioprotective effects on CME remain unclear.Thus,this experiment studied the impact of semaglutide on CME-induced myocardial injury.METHODS A rat CME model was generated by injecting microspheres into the left ventricle while clamping the ascending aorta.A H9c2 cardiomyocyte model was constructed by stimulation of lipopolysaccharide combined with hypoxia.Semaglutide or the high mobility group box 1(HMGB1)antagonist glycyrrhizin administrations were ahead of CME and cell modeling.Cardiac function,myocardial injury markers,cell viability and morphological alternations were detected.Apoptotic and inflammatory factors,cytosolic HMGB1 and its translocation,advanced glycosylation end-product specific receptor(RAGE),and nuclear factor kappa B p65(NF-κB p65)were evaluated.RESULTS Semaglutide pretreatment ameliorated CME-induced cardiac systolic dysfunction and relieved the cardiac injury.Semaglutide attenuated myocardial apoptosis and inflammatory response following CME in vivo and in vitro.Moreover,semaglutide downregulated HMGB1 expression and suppressed its nuclear-cytoplasmic translocation.Both glycyrrhizin and semaglutide administration affected the HMGB1/RAGE/NF-κB p65 pathway after CME.CONCLUSIONS Semaglutide pretreatment attenuates CME-induced myocardial injury by suppressing apoptosis and inflammation through the HMGB1/RAGE/NF-κB p65 pathway. 展开更多
关键词 injecting microspheres semaglutide inflammation h c cardiomyocyte model myocardial injury coronary microembolization apoptosis coronary revascularizationsemaglutide
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Associations of indoor airborne microbiome with systemic inflammation in the context of indoor particulate matter pollution and the metabolic mechanisms 认领 引用
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作者 Yetong Zhao Luyi Li +8 位作者 Wenlou Zhang Shan Liu Wanzhou Wang Xuezhao Ji Di Yang Lifang Zhao Zhihong Zhang Xinbiao Guo Furong Deng 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第1期187-198,共12页
Microorganisms constitute an essential component in the indoor environment,which is closely related to hu-man health.However,there is limited evidence regarding the associations between indoor airborne microbiome and ... Microorganisms constitute an essential component in the indoor environment,which is closely related to hu-man health.However,there is limited evidence regarding the associations between indoor airborne microbiome and systemic inflammation,as well as whether this association is modified by indoor particulate matter and the underlying mechanisms.In this prospective repeated-measure study among 66 participants,indoor airborne mi-crobiome was characterized using amplicon sequencing and qPCR.Indoor fine particulate matter(PM2.5)and inhalable particulate matter(PM10)were measured.Systemic inflammatory biomarkers were assessed,including white blood cell(WBC),neutrophil(NEUT),monocyte,eosinophil counts,and their proportions.Targeted serum amino acid metabolomics were conducted to explore the underlying mechanisms.Linear mixed-effect models re-vealed that bacterial and fungal Simpson diversity were significantly associated with decreased WBC and NEUT.For example,for each interquartile range increase in the bacterial Simpson diversity,WBC and NEUT changed by-4.53%(95%CI:-8.25%,-0.66%)and-5.95%(95%CI:-11.3%,-0.27%),respectively.Notably,increased inflammatory risks of airborne microbial exposure were observed when indoor PM2.5 and PM10 levels were below the WHO air quality guidelines.Mediation analyses indicated that dopamine metabolism partially mediated the anti-inflammatory effects of fungal diversity exposure.Overall,our study indicated protection from a diverse indoor microbial environment on cardiovascular health and proposed an underlying mechanism through amino acid metabolism.Additionally,health risks associated with microbial exposure deserve more attention in con-texts of low indoor particulate matter pollution.Further research is necessary to fully disentangle the complex relationships between indoor microbiome,air pollutants,and human health. 展开更多
关键词 Indoor air Bioaerosols Microbiome Particulate matter Systemic inflammation Amino acid metabolism
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