BACKGROUND:The inflammatory response of microglia is closely related to neuronal survival,regeneration,and functional recovery after spinal cord injury.Peroxiredoxin 1 is not only involved in the regulation of oxidative stress,but also has an important effect on cell proliferation,apoptosis,and inflammatory response.OBJECTIVE:To investigate the role and mechanism of peroxiredoxin 1 in the inflammatory response of microglia following spinal cord injury.METHODS:(1)Twelve female C57BL/6 mice were randomly divided into sham-operated(n=6)and spinal cord injury(n=6)groups.The sham-operated group was not modeled and acute spinal cord injury models were constructed in the spinal cord injury group using the modified Allen's method.Spinal cord tissue at the injured site was taken at 7 days after modeling and transcriptome sequencing was performed to identify differentially expressed genes.The expression of peroxiredoxin 1 in spinal cord tissues was verified using western blot and RT-qPCR.(2)Mouse microglia BV2 were divided into two groups:the control group was stimulated with lipopolysaccharide for 6 hours,and in the knockout group,lipopolysaccharide stimulation was applied for 6 hours at 24 hours after peroxiredoxin 1 was knocked down in the cells.RT-qPCR was performed to detect mRNA expression of peroxiredoxin 1,inflammatory factors(interleukin 1β,interleukin 6,inducible nitric oxide synthase,tumor necrosis factor α,C-C motif chemokine ligand 2,and C-X-C motif chemokine ligand 2),and western blot was performed to detect the expression of peroxiredoxin 1,inducible nitric oxide synthase,and reactive oxygen/mitogen-activated protein kinase signaling pathway proteins.Mouse microglia BV2 were treated in two groups:the control group was stimulated by hydrogen peroxide for 4 hours,and the knockout group was stimulated by hydrogen peroxide for 4 hours at 24 hours after knockdown of peroxiredoxin 1.The level of reactive oxygen species was detected by 2,7-dichlorodihydrofluorescein diacetate probe.RESULTS AND CONCLUSION:(1)Results from transcriptome sequencing,western blot and RT-qPCR confirmed that peroxiredoxin 1 expression levels in mouse spinal cord tissues were significantly higher in the spinal cord injury group than the sham-operated group(P＜0.05).(2)Peroxiredoxin 1 knockdown in microglial cells led to decreased expression of peroxiredoxin 1 mRNA and protein(P＜0.05),increased mRNA expression of interleukin 1β,interleukin 6,inducible nitric oxide synthase,tumor necrosis factor α,C-C motif chemokine ligand 2,and C-X-C motif chemokine ligand 2(P＜0.05),increased protein expression of inducible nitric oxide synthase,P-P38,P-JNK and P-ERK proteins(P＜0.05),and increased level of reactive oxygen species(P＜0.05).To conclude,peroxiredoxin 1 regulates microglial inflammation by targeting the reactive oxygen species/mitogen-activated protein kinase signaling pathway.

BACKGROUND:Mineralized collagen is the fundamental unit of bone structure and function and a major component of the extracellular matrix.Biomimetic methods have been developed to fabricate mineralized collagen with a natural bone nanostructure.Currently,mineralized collagen has been approved by regulatory authorities and applied clinically,playing a positive role in bone defect repair.OBJECTIVE:To present the integration strategies of bioactive factors with mineralized collagen,summarize schemes to enhance the osteogenic potential of mineralized collagen,emphasize the multifunctional coordination applications of mineralized collagen,and finally discuss current research focuses and future trends.METHODS:The authors searched for relevant literature in databases such as PubMed,Web of Science,Medline,WanFang,and CNKI,from 2009 to 2023,using keywords"mineralized collagen,biomimetic,functionalization,bioactive factors,osteogenesis,multi-functional coordination,bone tissue repair"in English and"mineralized collagen,biomimetic,functionalization"in Chinese.Out of 375 initially identified articles,57 were included for review after screening.RESULTS AND CONCLUSION:(1)Mineralized collagen,with its porous structure and large surface area,containing nano-hydroxyapatite,makes it an effective carrier for cells,various growth factors,and drugs.(2)Single or multiple bioactive factors can be efficiently and orderly released through different loading methods or combinations,achieving the multifunctionalization of mineralized collagen.The impact of physicochemical conditions on the bioactivity of factors and their effects on the degradability,hydroxylapatite crystal morphology,nanostructure,and content of mineralized collagen should be considered.Moreover,calcium ions in mineralized collagen can be substituted with various inorganic non-metal ions,enhancing its osteogenic,angiogenic,immunomodulatory,and anti-infective properties.(3)Ultimately,during in situ bone regeneration,functionalized mineralized collagen serves as a scaffold material,providing structural support for bone defects,and as a drug delivery system,continuously delivering various bioactive factors locally,playing roles in anti-infection,immunomodulation,promoting angiogenesis and osteogenesis,and repairing various complex bone defects.

BACKGROUND:With the development of oral implantology,implant restoration has gradually become the first choice of restoration after missing teeth,and bone augmentation procedures have led to the expansion of implant indications and the improvement of the success rate of implant restoration.However,the long-term stability of bone height,width and volume after bone augmentation surgery has been one of the clinical difficulties for oral implantologists.OBJECTIVE:To measure and analyze the bone width,height,and volume of different sites in the bone augmentation area at different time points using cone-beam CT and an automatic image alignment program.METHODS:Seventeen patients with severe bone defects in the upper anterior region who underwent Onlay bone block grafting in the external oblique region were recruited from the Department of Stomatology,Zhejiang Tongde Hospital.There were 10 males and 7 females,with a mean age of(45.88±12.47)years.The cone-beam CT scans of the patients' Onlay bone grafts were taken at five time points:preoperatively,immediately postoperatively,6 months postoperatively,immediately post implantation,and 6 months post implantation,and then were statistically analyzed for alveolar bone volume,width,and height in the bone augmentation area,as well as for the difference in the alveolar bone volume of the bone incremental area between patients of different sexes and age.RESULTS AND CONCLUSION:(1)The alveolar bone volume in the bone augmentation area was higher immediately and 6 months after bone grafting than before bone grafting(P＜0.05)as well as was higher immediately after bone grafting than 6 months after bone grafting(P＜0.05).The alveolar bone height in the bone augmentation area was higher immediately and 6 months after bone grafting than before bone grafting(P＜0.05).The horizontal width of the alveolar bone at various sites in the bone augmentation area immediately and 6 months after bone grafting was higher than that before bone grafting(P＜0.05).(2)There was no significant difference in the volume of bone graft resorption at various sites in the bone augmentation area between males and females immediately and 6 months after bone grafting(P＞0.05).Pearson correlation analysis showed a positive correlation between age and the change in bone augmentation area volume immediately and 6 months after bone grafting,but the difference was not statistically significant(P＞0.05).(3)Twenty-five dental implants with completed implant restorations functioned normally,and the survival rate of the implants was 100％.To conclude,Onlay bone graft implant restoration in the upper anterior region can significantly improve insufficient bone with favorable outcomes.However,there is some amount of bone resorption in the bone augmentation area at 6 months after Onlay bone grafting and it is necessary to open up the second surgical area.Clinicians should consider different bone augmentation procedures in accordance with the specific circumstances.

BACKGROUND:The inflammatory response of microglia is closely related to neuronal survival,regeneration,and functional recovery after spinal cord injury.Peroxiredoxin 1 is not only involved in the regulation of oxidative stress,but also has an important effect on cell proliferation,apoptosis,and inflammatory response.OBJECTIVE:To investigate the role and mechanism of peroxiredoxin 1 in the inflammatory response of microglia following spinal cord injury.METHODS:(1)Twelve female C57BL/6 mice were randomly divided into sham-operated(n=6)and spinal cord injury(n=6)groups.The sham-operated group was not modeled and acute spinal cord injury models were constructed in the spinal cord injury group using the modified Allen's method.Spinal cord tissue at the injured site was taken at 7 days after modeling and transcriptome sequencing was performed to identify differentially expressed genes.The expression of peroxiredoxin 1 in spinal cord tissues was verified using western blot and RT-qPCR.(2)Mouse microglia BV2 were divided into two groups:the control group was stimulated with lipopolysaccharide for 6 hours,and in the knockout group,lipopolysaccharide stimulation was applied for 6 hours at 24 hours after peroxiredoxin 1 was knocked down in the cells.RT-qPCR was performed to detect mRNA expression of peroxiredoxin 1,inflammatory factors(interleukin 1β,interleukin 6,inducible nitric oxide synthase,tumor necrosis factor α,C-C motif chemokine ligand 2,and C-X-C motif chemokine ligand 2),and western blot was performed to detect the expression of peroxiredoxin 1,inducible nitric oxide synthase,and reactive oxygen/mitogen-activated protein kinase signaling pathway proteins.Mouse microglia BV2 were treated in two groups:the control group was stimulated by hydrogen peroxide for 4 hours,and the knockout group was stimulated by hydrogen peroxide for 4 hours at 24 hours after knockdown of peroxiredoxin 1.The level of reactive oxygen species was detected by 2,7-dichlorodihydrofluorescein diacetate probe.RESULTS AND CONCLUSION:(1)Results from transcriptome sequencing,western blot and RT-qPCR confirmed that peroxiredoxin 1 expression levels in mouse spinal cord tissues were significantly higher in the spinal cord injury group than the sham-operated group(P＜0.05).(2)Peroxiredoxin 1 knockdown in microglial cells led to decreased expression of peroxiredoxin 1 mRNA and protein(P＜0.05),increased mRNA expression of interleukin 1β,interleukin 6,inducible nitric oxide synthase,tumor necrosis factor α,C-C motif chemokine ligand 2,and C-X-C motif chemokine ligand 2(P＜0.05),increased protein expression of inducible nitric oxide synthase,P-P38,P-JNK and P-ERK proteins(P＜0.05),and increased level of reactive oxygen species(P＜0.05).To conclude,peroxiredoxin 1 regulates microglial inflammation by targeting the reactive oxygen species/mitogen-activated protein kinase signaling pathway.

ObjectiveTo investigate the material basis of the pathogenesis of cerebral ischemic injury with blood stasis and toxin syndrome and to explore the protective effects of Huayu Jiedu prescription （HYJDP） on neutrophil extracellular trap-related cell death （NETosis） in cerebral ischemic injury following acute cerebral infarction. MethodsSeventy-two Sprague-Dawley （SD） rats were randomly divided into six groups （n=12 per group）： sham operation （Sham） group， blood stasis and toxin model （Model） group， low-， medium-， and high-dose HYJDP groups （HYJDP-L， HYJDP-M， and HYJDP-H； 9， 18， and 36 g·kg^-1， respectively）， and butylphthalide （NBP） group （0.06 g·kg^-1）. Except for the Sham group， rats in all other groups were subjected to carrageenan/dry yeast combined with a modified intraluminal filament method to establish a focal cerebral ischemia model of the middle cerebral artery with blood stasis and toxin syndrome. Neurological function was evaluated at 24 h after modeling using the Zea-Longa neurological deficit score. Cerebral infarction rate was assessed by 2，3，5-triphenyltetrazolium chloride （TTC） staining. Pathological morphology of brain tissue was observed using hematoxylin-eosin （HE） staining. Enzyme-linked immunosorbent assay （ELISA） was used to determine serum levels of interleukin-8 （IL-8）， myeloperoxidase-DNA complexes （MPO-DNA）， and citrullinated histone H3 （CitH3）. Protein expression of phosphorylated phosphatidylinositol 3-kinase （p-PI3K）， protein kinase B （p-Akt）， mammalian target of rapamycin （p-mTOR）， sequestosome 1 （p62）， and CitH3 in brain tissue was detected by Western blot. Immunofluorescence （IF） was used to detect the expression of neutrophil-specific marker Ly6G， CitH3， and neuron-specific nuclear protein （NeuN） in brain tissue. ResultsCompared with the Sham group， neurological deficit scores and cerebral infarction rates in the model group were significantly increased （P<0.01 for both）. HE staining showed varying degrees of neuronal degeneration and necrosis， characterized by blurred neuronal structures， nuclear pyknosis and fragmentation， cytoplasmic dissolution into a vacuolated reticular pattern， and mild glial cell proliferation. ELISA results showed that serum levels of IL-8， MPO-DNA， and CitH3 were significantly increased （P<0.01）. Western blot analysis demonstrated decreased expression of p-PI3K， p-Akt， p-mTOR， and p62， while CitH3 expression was significantly increased （P<0.01）. IF results showed an increased number of NETs⁺ cells and a significant decrease in NeuN⁺ cells （P<0.01）. Compared with the Model group， neurological deficit scores in the HYJDP-H group were significantly decreased （P<0.05）， and cerebral infarction rates in the HYJDP-H and NBP groups were significantly reduced （P<0.01）. HE staining showed that brain tissue damage was markedly alleviated in the HYJDP-H group. ELISA results showed that levels of IL-8， MPO-DNA， and CitH3 were significantly decreased in the HYJDP-M， HYJDP-H， and NBP groups （P<0.01）. Western blot analysis showed that expression of p-PI3K， p-Akt， p-mTOR， and p62 was significantly increased in the HYJDP-H and NBP groups， while CitH3 expression was significantly reduced in all drug intervention groups （P<0.01）. IF results showed that the number of NETs⁺ cells was significantly decreased and the number of NeuN⁺ cells was significantly increased in all drug intervention groups （P<0.01）. ConclusionNETs may be the material basis of the pathogenesis of cerebral ischemic injury characterized by blood stasis and toxin. HYJDP can regulate the PI3K/Akt/mTOR signaling pathway， reduce the release of pro-inflammatory mediators and NETosis-related products， alleviate cerebral ischemic injury caused by autophagy-dependent NETosis， and thereby exert a neuroprotective effect.

ObjectiveTo explore the mechanisms of Yangjing Tongluo prescription （YJTL） in the treatment of intrauterine adhesion （IUA） from the perspective of oxidative stress mediated by the Kelch-like ECH-associated protein 1/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 （Keap1/Nrf2/HO-1） signaling pathway. MethodsA total of 48 rats with normal estrous cycles were selected and randomly divided into a normal group （n=8） and a modeling group （n=40）. An IUA rat model was established using a dual-injury method combining surgical curettage and infection. Eight rats were randomly selected from the modeling group for a pilot experiment to confirm successful model establishment. After successful modeling， the remaining 32 rats were randomly divided into a model group， a low-dose YJTL group （YJTL-L）， a high-dose YJTL group （YJTL-H）， and a Progynova group. Rats in the normal and model groups were administered purified water （15 mL·kg^-1） by gavage daily， while rats in the YJTL-L， YJTL-H， and Progynova groups received YJTL at doses of 6.43 and 12.86 g·kg^-1 and Progynova at 2.06 × 10^-4 g·kg^-1， respectively， for 14 consecutive days. The general condition， uterine morphology， and uterine index of the rats were monitored. Histopathological changes in uterine tissue were observed using hematoxylin-eosin （HE） staining. Serum levels of reactive oxygen species （ROS） and glutathione peroxidase （GSH-Px） were measured by enzyme-linked immunosorbent assay （ELISA）. Protein expression levels of Keap1， Nrf2， and HO-1 in endometrial tissue were detected by Western blot. Immunofluorescence （IF） was used to assess the distribution of Nrf2 and HO-1， as well as the expression of Nrf2 in the cytoplasm and nucleus. ResultsCompared with the normal group， rats in the model group exhibited poor mental status and reduced mobility， markedly edematous and tortuous uterine morphology， decreased gland number， and inflammatory reactions in the endometrium， along with an increased uterine organ index （P<0.05）. Serum ROS levels were significantly increased （P<0.05）， while serum GSH-Px levels were significantly decreased （P<0.05）. In endometrial tissue， Keap1 protein expression was increased （P<0.05）， whereas Nrf2 and HO-1 protein expression was decreased. Mild nuclear translocation of Nrf2 was observed， accompanied by increased relative fluorescence intensity of nuclear Nrf2 and decreased relative fluorescence intensity of cytoplasmic HO-1. Compared with the model group， all treatment groups showed varying degrees of improvement in the above symptoms and pathological changes. Serum ROS levels were reduced （P<0.05）， serum GSH-Px levels were increased （P<0.05）， Keap1 protein expression in endometrial tissue was decreased， and Nrf2 and HO-1 protein expression was increased in a dose-dependent manner （P<0.05）. Notably， significant nuclear translocation of Nrf2 was observed， with correspondingly increased relative fluorescence intensity of nuclear Nrf2 and enhanced relative fluorescence intensity of cytoplasmic HO-1. ConclusionYJTL may enhance antioxidant capacity and repair oxidative damage to the endometrial basal layer by regulating the Keap1/Nrf2/HO-1 signaling pathway.

ObjectiveTo investigate the characteristics and potential mechanisms of Luotong Xianrong Yin （LTXRY） in improving lung injury in rats with idiopathic pulmonary fibrosis （IPF） by regulating glycolysis. MethodsForty specific pathogen-free （SPF） Sprague-Dawley （SD） rats were randomly divided into a sham-operated group （10 mL·kg^-1）， model group （10 mL·kg^-1）， LTXRY group （15.18 g·kg^-1）， and nintedanib group （0.1 g·kg^-1）， with 10 rats in each group. The IPF rat model was established by intratracheal instillation of bleomycin. After 28 days of gavage intervention， pulmonary function was assessed. Lung pathological changes were observed by hematoxylin-eosin （HE） and Masson staining. Enzyme-linked immunosorbent assay （ELISA） was used to determine the levels of inflammatory factors， including tumor necrosis factor-α （TNF-α）， interleukin （IL）-1β， and IL-6， in lung tissue. Chemiluminescence assays were employed to detect lactate content and lactate dehydrogenase activity in lung tissue. Western blot was used to measure the protein expression of transforming growth factor-β₁ （TGF-β₁）， CollagenⅠ and CollagenⅢ to evaluate collagen deposition， as well as hexokinase 2 （HK2）， pyruvate kinase M2 （PKM2）， and 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3） to assess glycolysis levels. Network pharmacology was applied to analyze the potential targets and signaling pathways of LTXRY in IPF， and molecular docking was conducted to evaluate the binding energy between active components and potential targets. Western blot was further used to detect the expression of target- and pathway-related proteins. ResultsCompared with the sham-operated group， rats in the model group showed significantly increased main airway resistance （Rn） and respiratory system resistance （Rrs）， and significantly decreased respiratory system compliance （Crs）. Inflammatory infiltration and collagen deposition were observed in lung tissue， with significantly increased levels of TNF-α， IL-1β， and IL-6， as well as elevated protein expression of TGF-β₁， CollagenⅠ and CollagenⅢ. Lactate content， lactate dehydrogenase activity， and the protein expression of HK2， PKM2， and PFKFB3 in lung tissue were significantly increased. Network pharmacology analysis indicated that signal transducer and activator of transcription 3 （STAT3） was a key target of LTXRY in IPF， and hypoxia-inducible factor-1 （HIF-1） was a critical signaling pathway. The expression levels of phosphorylated STAT3 （p-STAT3） and HIF-1α in lung tissue were significantly higher than those in the sham-operated group. Compared with the model group， rats in the LTXRY group showed significantly decreased Rn and Rrs and significantly increased Crs. Lung inflammatory infiltration and collagen deposition were markedly alleviated， with significantly reduced levels of TNF-α， IL-1β， and IL-6， and decreased protein expression of TGF-β₁， CollagenⅠ and CollagenⅢ. Lactate content， lactate dehydrogenase activity， and the protein expression of HK2， PKM2， and PFKFB3 were significantly decreased， accompanied by markedly reduced expression of p-STAT3 and HIF-1α. ConclusionLTXRY alleviates lung tissue injury in IPF rats by regulating glycolysis mediated by the STAT3/HIF-1α signaling pathway.

Over the past two decades, genome-wide association study(GWAS) has identified numerous genetic variants and loci associated with heritable diseases. With the gradual maturation and saturation of GWAS methodologies, transcriptome-wide association study(TWAS) offers a novel perspective by linkinggenetic phenotypes to gene expression levels. By integrating TWAS with other multi-omics analyses, researchers can gain a deeper understanding of heritable diseases. This article provides an overview of recent groundbreaking and representative TWAS methods and tools, analyzes their strengths and limitations, and discusses future trends in TWAS development.

AIM:To investigate the visual development of children under 6 years old in Wuhan, and provide evidence-based support for the formulation and optimization of regional policies for children's eye health care.METHODS:Suresight refractive screener was applied to rapid refractive status examination in 4 989 preschool children under 6 years old in Wuhan City, with results determined according to the manufacturer's age-specific referral criteria. All screened pre-school children completed vision screening and comprehensive ophthalmic examination.RESULTS: A total of 4 989 children under 6 years old were screened out, including 2 641 males and 2 348 females. They were divided into 6 groups according to age: 426 aged from 6-month to 1-year-old, 903 aged >1 to 2 years old, 1 078 aged >2 to 3 years old, 442 aged >3 to 4 years old, 808 aged >4 to 5 years old, and 1 332 aged >5 to 6 years old. The abnormal rate in the 6-month to 1-year-old group was 44.60%, in the >1 to 2 years old group was 26.02%, in the >2 to 3 years old group was 15.58%, in the >3 to 4 years old group was 10.86%, in the >4 to 5 years old group was 21.91%, in the >5 to 6 years old group was 23.27%, and the total refractive abnormal rate for children aged 6 mo to 6 years old was 22.61%. The refractive abnormal rate generally showed a decreasing trend with increasing age(P<0.001); the refractive abnormal rate in boys aged 6-month to 6 years old was 12.33%, and in girls was 10.28%, with no statistically significant difference in the abnormal rate between boys and girls(P>0.05); among children aged 6-month to 6 years old, the abnormal rate of single-eye myopia was 0.98%, of single-eye hyperopia was 5.41%, of single-eye astigmatism was 9.92%, of binocular myopia was 0.98%, of binocular hyperopia was 2.79%, and of binocular astigmatism was 8.14%; the prevalence of astigmatism in children aged 6-month to 1-year-old was 40.38%, in those aged >1 to 2 years old was 19.82%, in those aged >2 to 3 years old was 12.34%, in those aged >3 to 4 years old was 9.05%, in those aged >4 to 5 years old was 18.81%, and in those aged >5 to 6 years old was 16.89%; the prevalence of astigmatism in children aged 6-month to 6 years old was 18.06%. The abnormal rate of astigmatism in the four age groups ranging from 6-month to 4 years old decreased continuously with age(P<0.001). There was no statistically significant difference in the abnormal rate of astigmatism between the >4 to 5 years old group and the >5 to 6 years old group(P>0.05).CONCLUSION:Refractive error has become a common eye disease among preschool children. Through early vision screening, establishing a systematic refractive management file, and early intervention, the best treatment period can be seized to avoid missing it and causing adverse consequences.

ObjectiveTaking Aurantii Fructus Immaturus juice（AFI）-processed Atractylodis Macrocephalae Rhizoma（AMR） as an example， this study aims to systematically compare the volatile and non-volatile components of AMR and its processed products， investigate the key differential components， evaluate their anti-inflammatory activities， and elucidate the synergistic mechanism of processing. MethodsThe chemical compositions of volatile and non-volatile components in AMR and AFI-processed AMR were systematically characterized using gas chromatography-mass spectrometry（GC-MS） and ultra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry（UPLC-Q-TOF-MS）， with relative mass fractions and response values determined separately. Volatile components were identified through searches in the National Institute of Standards and Technology（NIST）17 database， comparison with retention index（RI） and fragmentation pattern matching. Non-volatile components were identified by searching Waters Traditional Chinese Medicine （TCM） spectral library， in conjunction with PubChem and MassBank， characteristic fragmentation patterns and response values were also used to support identification. Differential components were screened using principal component analysis（PCA）， orthogonal partial least squares-discriminant analysis（OPLS-DA）， with variable importance in the projection（VIP） value >1. Components with high log₂fold change（FC） among major differential groups were selected as those exhibiting significant changes before and after processing. The anti-inflammatory activity of the differential compounds was evaluated by assessing their effects on nitric oxide（NO） production in a lipopolysaccharide（LPS）-induced RAW264.7 macrophage model. Enzyme-linked immunosorbent assay（ELISA） was used to detect the effects of the differential components on tumor necrosis factor（TNF）-α， interleukin（IL）-1β， IL-6， and monocyte chemotactic protein（MCP）-1 levels， and immunofluorescence（IF） was employed to assess their effects on nuclear transcription factor（NF）-κB p65 translocation， thereby elucidating the underlying molecular mechanisms. ResultsA total of 36 compounds were identified in the volatile components of AMR and AFI-processed AMR， among which， sesquiterpenes and monoterpenes were significantly increased after processing. In the non-volatile components， 36 compounds were identified， and the main differential components were flavonoids， sesquiterpenoids， and triterpenoids. Flavonoids were the primary differential components distinguishing AMR from its processed products， representing compounds directly introduced during processing. Five compounds， including atractylenolide Ⅲ， tangeritin， nobiletin， hesperidin and narirutin， were selected as representatives of three classes based on their most prominent differential expression among different compound types for subsequent anti-inflammatory activity studies. The results showed that 100 μmol·L^-1 tangerine and narirutin could significantly inhibit LPS-induced NO production（P<0.01） in a concentration-dependent manner. Tangeritin was able to significantly inhibit the levels of TNF-α and MCP-1 secreted by RAW264.7（P<0.05）， while narirutin significantly inhibited the levels of TNF-α， IL-1β， MCP-1 and IL-6（P<0.01）. IF revealed that both tangeritin and narirutin significantly blocked the translocation of NF-κB p65 from the cytoplasm to the nucleus. ConclusionAFI-processed AMR significantly alters the chemical composition profile of AMR， and the newly introduced flavonoid components during processing may be key to its enhanced anti-inflammatory effects.