Objective To implement the disease prevention and control strategy of being ^"proactive and grassroots-focused,^" and to enhance the overall effectiveness of general hospitals in the tertiary prevention of cervical cancer, this consensus aims to provide an actionable guiding framework for the standardized construction of ^"Integrated Outpatient Clinics for Cervical Cancer Prevention and Control^" in general hospitals at all levels. Methods This consensus systematically elaborates on the specific elements for establishing such integrated clinics and formulates the corresponding standards. Results It is anticipated that the consensus will promote the establishment of standardized, homogeneous, and high-efficiency frontline positions for cervical cancer prevention and control within general hospitals, thereby contributing to the strategic vision of accelerating the elimination of cervical cancer. Conclusion The formulation and promotion of the consensus aim to provide robust clinical practice support for accelerating the realization of China's strategic vision of eliminating cervical cancer.

Olfactory receptors (ORs) form the largest superfamily of G protein-coupled receptors (GPCRs). Traditionally recognized for their role in the nasal olfactory epithelium, where they mediate the sense of smell, accumulating evidence has firmly established their ectopic expression in non-olfactory tissues, including the intestine, lungs, and kidneys. The intestine, as the primary site for nutrient digestion and absorption, harbors a highly complex chemical environment. To adapt to this environment, the gut employs a sophisticated network of “chemosensors” to monitor luminal contents and maintain homeostasis. Among these sensors, intestinal ORs have emerged as crucial functional components, serving as a molecular bridge that connects environmental chemical signals—such as food-derived odorants—to specific physiological responses. This discovery has significantly deepened our understanding of how dietary flavors and compounds influence intestinal physiology at the molecular level. This review systematically summarizes the expression profiles, ligand classification, and biological functions of ORs within the gastrointestinal tract. Studies indicate that intestinal ORs exhibit distinct spatial distribution patterns across different gut segments and display cell-type specificity, particularly within enterocytes and enteroendocrine cells. These receptors function as versatile sensors capable of recognizing a wide variety of ligands, including exogenous dietary components, gut microbiota metabolites such as short-chain fatty acids, and endogenous small molecules like azelaic acid. Upon activation by specific ligands, intestinal ORs trigger intracellular signaling cascades, primarily involving the AC-cAMP-PKA pathway or calcium influx channels. A major focus of this review is to elucidate the molecular mechanisms by which these receptors regulate the secretion of gut hormones. Activation of specific ORs in enteroendocrine cells has been shown to stimulate the release of hormones such as glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and serotonin (5-HT), thereby modulating systemic energy metabolism, glucose homeostasis, and gastrointestinal motility. Furthermore, the review addresses the critical roles of ORs in immune regulation and pathology. Evidence suggests that specific ORs contribute to the maintenance of intestinal immune homeostasis and may offer protection against inflammation. Beyond their involvement in inflammatory responses, ORs such as Olfr78 have been shown to regulate the differentiation and function of intestinal endocrine cells. Similarly, Olfr544 has been demonstrated to alleviate intestinal inflammation by remodeling the gut microbiome and metabolome. These findings collectively suggest that specific ORs hold promise as therapeutic targets for mitigating intestinal inflammation and maintaining gut homeostasis. Additionally, the review explores the emerging role of ORs in cancer. Although OR expression is often downregulated in tumor tissues compared to normal mucosa, activation of specific ORs by certain ligands can inhibit tumor cell proliferation and migration and induce apoptosis via pathways such as MEK/ERK and p38 MAPK. Conversely, other receptors, such as OR7C1, may serve as biomarkers for cancer-initiating cells. In conclusion, intestinal ORs represent a vital component of the gut’s sensory network. The review also discusses the translational potential of these findings. By elucidating the precise pairing relationships between dietary components and specific ORs, novel therapeutic strategies could be developed. Intestinal ORs may thus emerge as promising targets for nutritional and pharmacological interventions in metabolic diseases, inflammatory bowel diseases, and malignancies.

ObjectiveTo investigate the effects and underlying mechanisms of polydatin in delaying the progression of colitis-associated colorectal cancer （CAC） by constructing an azoxymethane （AOM）/dextran sulfate sodium （DSS）-induced CAC mouse model and conducting in vitro experiments. MethodsFifty-four male C57BL/6J mice were randomly divided into normal， model， and polydatin groups （0.045 g·kg^-1）. The CAC mouse model was established using AOM/DSS， and samples were collected at 4， 7， and 10 weeks. Body weight change rate， disease activity index （DAI）， and tumor formation were assessed. Hematoxylin-eosin （HE） staining was used to observe pathological injury in intestinal tissues. Immunohistochemistry （IHC） was performed to detect zonula occludens-1 （ZO-1） expression in colonic tissues， and Western blot was used to detect the expression of E-cadherin， N-cadherin， and Vimentin in colonic epithelial cells. Real-time PCR was used to measure mRNA expression of interleukin-17A （IL-17A）， Wnt3a， β-catenin， T cell factor 1 （Tcf1）， E-cadherin， N-cadherin， and Vimentin in colonic tissues. Flow cytometry was used to analyze the proportion of CD8⁺T cells and the expression of exhaustion-related molecules in tumors. Human colon cancer DLD-1 cells were cultured in a polydatin-containing medium， and wound healing assays were performed to observe migration changes. Real-time PCR was used to detect mRNA expression of interleukin-17 receptor A （IL-17RA）， Wnt3a， β-catenin， Tcf1， E-cadherin， N-cadherin， and Vimentin in DLD-1 cells. ResultsCompared with the normal group， the model group at all three time points showed significantly decreased body weight change rate （P<0.01）， significantly shortened colon length （P<0.01）， and markedly increased DAI scores （P<0.01）. HE staining revealed significant inflammatory cell infiltration in the submucosa of the colon in the model group， accompanied by epithelial dysplasia. ZO-1 expression in colonic tissues was significantly reduced （P<0.01）. The mRNA expression of the pro-inflammatory factor IL-17A and key molecules of the Wnt/β-catenin pathway （Wnt3a， β-catenin， Tcf1） was significantly elevated （P<0.05）. The mRNA and protein expression of epithelial-mesenchymal transition （EMT） markers N-cadherin and Vimentin was significantly upregulated （P<0.05）， while E-cadherin expression was significantly downregulated （P<0.05）. The proportion of tumor-infiltrating CD8⁺T cells expressing immunosuppressive molecules （TIM-3， LAG-3， PD-1） was significantly increased （P<0.05）. Compared with the model group， the polydatin group showed significant improvement in body weight and DAI score （P<0.01）， as well as recovery of colon length and tissue injury. ZO-1 expression in colonic tissue was significantly increased （P<0.01）， while IL-17A， Wnt3a， β-catenin， Tcf1， N-cadherin， and Vimentin expression levels were significantly decreased （P<0.05）， and E-cadherin expression was significantly increased （P<0.01）. Tumor-infiltrating CD8⁺ T cells expressing immunosuppressive molecules were significantly reduced （P<0.05）. In vitro experiments showed that polydatin significantly inhibited migration of DLD-1 cells （P<0.01） and reversed the upregulation of IL-17RA， Wnt3a， β-catenin， N-cadherin， and Vimentin mRNA， as well as the downregulation of E-cadherin mRNA （P<0.05）. ConclusionPolydatin inhibits IL-17A secretion and IL-17RA expression， improves the immune microenvironment， blocks activation of the Wnt/β-catenin signaling pathway， suppresses EMT markers （N-cadherin and Vimentin）， and restores tight junction protein expression in intestinal epithelial cells， thereby delaying the progression from colitis to colorectal cancer in mice.

Allergic conjunctivitis is a common ocular inflammatory disease, with intense itching being the most typical and distressing symptom for patients. In recent years, with the in-depth study of the interaction between the nervous and immune systems, significant progress has been made in understanding the mechanism of itching in allergic conjunctivitis. This review elaborates on the neurobiological basis of itching in allergic conjunctivitis, with a focus on the complex dialogue between immune cells and sensory neurons, particularly the core role of the IL-33-ST2-CGRP signaling axis in mediating itching. Additionally, this article introduces new findings in genetic susceptibility research, including the identification of susceptibility genes for allergic conjunctivitis through transcriptome-wide association studies. The sensory nervous system not only transmits itch signals but also actively participates in the formation of antigen channels related to conjunctival goblet cells, thereby regulating the local uptake of allergens and the initiation of the immune response. Moreover, targeted novel therapeutic strategies offer hope for patients with refractory allergic conjunctivitis. Exploring the molecular and cellular mechanisms of itching in allergic conjunctivitis will provide a theoretical basis for the development of more effective treatment methods.

ObjectiveTo explore the effect of gypenosides （GPs） on liver lipid deposition in metabolism-associated fatty liver disease （MAFLD） mice and its mechanism based on classical/non-classical ferroptosis. MethodsEight male C57BL/6 mice in a blank group and 32 male apolipoprotein E gene knockout （ApoE^-/-） mice were randomly divided into a model group， a low-dose GPs （GPs-L） group， a high-dose GPs （GPs-H） group， and a simvastatin （SV） group. Starting from the second week， mice in the blank group were given a maintenance diet， and the other four groups were fed a high-fat diet daily. After eight weeks of feeding， mice in the GPs-L and GPs-H groups were given GPs of 1.487 mg·kg^-1·d^-1 and 2.973 mg·kg^-1·d^-1， respectively， and mice in the SV group were given simvastatin of 2.275 mg·kg^-1·d^-1. Mice in the blank group and the model group were given saline of equal volume by gavage for four weeks. The content of total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， high-density lipoprotein cholesterol （HDL-C）， alanine aminotransferase （ALT）， and aspartate aminotransferase （AST） in the serum of mice in each group was detected by an automatic biochemical analyzer. The level of non-esterified fatty acid （NEFA） and TG in the mouse liver was measured by the kit. The change in liver tissue structure and lipid deposition was observed by hematoxylin-eosin （HE） and oil red O staining. The levels of coenzyme Q₁₀ （CoQ₁₀）， glutathione （GSH）， malondialdehyde （MDA）， and Fe²⁺ in serum， as well as nicotinamide adenine dinucleotide phosphate ［NAD（P）H］ in the liver were detected by enzyme-linked immunosorbent assay （ELISA）. The expression of ferroptosis suppressor protein 1 （FSP1） in the liver of mice was observed by the immunohistochemical （IHC） method， and the expression of genes and proteins related to classical and non-classical ferroptosis pathways was analyzed by real-time polymerase chain reaction （Real-time PCR） and Wes automated protein expression analysis system. ResultsCompared with those in the blank group， the levels of TC， TG， LDL-C， ALT， and AST in serum and TG and NEFA in the liver in the model group were significantly increased， and the level of HDL-C in serum was significantly decreased （P<0.01）. The liver tissue structure changed， and there were fat vacuoles of different sizes and a large number of red lipid droplets， with obvious lipid deposition. The level of CoQ10 and GSH in serum and NADH in the liver were significantly decreased， while the level of MDA and Fe²⁺ in serum was significantly increased （P<0.01）. The mRNA and protein expressions of cystine/glutamate transporter （xCT/SLC7A11）， glutathione peroxidase （GPX4）， p62， nuclear factor E₂-related factor 2 （Nrf2）， and FSP1 were significantly decreased， and the mRNA and protein expressions of tumor antigen （p53）， spermidine/spermine N1-acetyltransferase 1 （SAT1）， arachidonate 15-lipoxygenase （ALOX15）， and Kelch-like epichlorohydrin-associated protein-1 （Keap1） were significantly increased （P<0.01）. Compared with those in the model group， the level of TC， TG， LDL-C， ALT， and AST in serum and TG and NEFA in the liver of mice in the GPs-L， GPs-H， and SV groups were decreased， while the level of HDL-C in serum was significantly increased （P<0.05， P<0.01）. The liver tissue structure and lipid deposition were improved. The levels of CoQ10 and GSH in serum and NADH in the liver were significantly increased， while the levels of MDA and Fe²⁺ in serum were significantly decreased （P<0.05， P<0.01）. The mRNA and protein expressions of xCT， GPX4， p62， Nrf2， and FSP1 were significantly increased， while the mRNA and protein expressions of p53， SAT1， ALOX15， and Keap1 were significantly decreased （P<0.05， P<0.01）. ConclusionGPs can interfere with liver lipid deposition in MAFLD mice through classical/non-classical ferroptosis pathways.

ObjectiveTo explore the effect of gypenosides （GPs） on liver lipid deposition in metabolism-associated fatty liver disease （MAFLD） mice and its mechanism based on classical/non-classical ferroptosis. MethodsEight male C57BL/6 mice in a blank group and 32 male apolipoprotein E gene knockout （ApoE^-/-） mice were randomly divided into a model group， a low-dose GPs （GPs-L） group， a high-dose GPs （GPs-H） group， and a simvastatin （SV） group. Starting from the second week， mice in the blank group were given a maintenance diet， and the other four groups were fed a high-fat diet daily. After eight weeks of feeding， mice in the GPs-L and GPs-H groups were given GPs of 1.487 mg·kg^-1·d^-1 and 2.973 mg·kg^-1·d^-1， respectively， and mice in the SV group were given simvastatin of 2.275 mg·kg^-1·d^-1. Mice in the blank group and the model group were given saline of equal volume by gavage for four weeks. The content of total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， high-density lipoprotein cholesterol （HDL-C）， alanine aminotransferase （ALT）， and aspartate aminotransferase （AST） in the serum of mice in each group was detected by an automatic biochemical analyzer. The level of non-esterified fatty acid （NEFA） and TG in the mouse liver was measured by the kit. The change in liver tissue structure and lipid deposition was observed by hematoxylin-eosin （HE） and oil red O staining. The levels of coenzyme Q₁₀ （CoQ₁₀）， glutathione （GSH）， malondialdehyde （MDA）， and Fe²⁺ in serum， as well as nicotinamide adenine dinucleotide phosphate ［NAD（P）H］ in the liver were detected by enzyme-linked immunosorbent assay （ELISA）. The expression of ferroptosis suppressor protein 1 （FSP1） in the liver of mice was observed by the immunohistochemical （IHC） method， and the expression of genes and proteins related to classical and non-classical ferroptosis pathways was analyzed by real-time polymerase chain reaction （Real-time PCR） and Wes automated protein expression analysis system. ResultsCompared with those in the blank group， the levels of TC， TG， LDL-C， ALT， and AST in serum and TG and NEFA in the liver in the model group were significantly increased， and the level of HDL-C in serum was significantly decreased （P<0.01）. The liver tissue structure changed， and there were fat vacuoles of different sizes and a large number of red lipid droplets， with obvious lipid deposition. The level of CoQ10 and GSH in serum and NADH in the liver were significantly decreased， while the level of MDA and Fe²⁺ in serum was significantly increased （P<0.01）. The mRNA and protein expressions of cystine/glutamate transporter （xCT/SLC7A11）， glutathione peroxidase （GPX4）， p62， nuclear factor E₂-related factor 2 （Nrf2）， and FSP1 were significantly decreased， and the mRNA and protein expressions of tumor antigen （p53）， spermidine/spermine N1-acetyltransferase 1 （SAT1）， arachidonate 15-lipoxygenase （ALOX15）， and Kelch-like epichlorohydrin-associated protein-1 （Keap1） were significantly increased （P<0.01）. Compared with those in the model group， the level of TC， TG， LDL-C， ALT， and AST in serum and TG and NEFA in the liver of mice in the GPs-L， GPs-H， and SV groups were decreased， while the level of HDL-C in serum was significantly increased （P<0.05， P<0.01）. The liver tissue structure and lipid deposition were improved. The levels of CoQ10 and GSH in serum and NADH in the liver were significantly increased， while the levels of MDA and Fe²⁺ in serum were significantly decreased （P<0.05， P<0.01）. The mRNA and protein expressions of xCT， GPX4， p62， Nrf2， and FSP1 were significantly increased， while the mRNA and protein expressions of p53， SAT1， ALOX15， and Keap1 were significantly decreased （P<0.05， P<0.01）. ConclusionGPs can interfere with liver lipid deposition in MAFLD mice through classical/non-classical ferroptosis pathways.

Objective: To investigate the association of serum alanine aminotransferase (ALT) with left ventricular hypertrophy (LVH) in adolescents, and to provide scientific evidence for the early screening and intervention strategy of cardiac structure damage. Methods: Data were obtained from the third follow up survey (October 2023) of the "Huantai Childhood Cardiovascular Health Cohort Study", including 1 156 healthy adolescents aged 12-17 with complete information. The sample population was stratified into low ( Q 1 group), medium ( Q 2 group), and high ( Q 3 group) ALT levels based on tertiles within the same gender and age groups. Inter group comparisons were conducted using analysis of variance and trend test. A multivariate Logistic regression model was used to analyze the association between ALT levels and LVH, and stratified analyses were performed by gender and age groups. Results: With the increase of ALT quantile level, the detection rate of LVH showed an increasing trend ( Q 1: 3.7%; Q 2: 10.6%; Q 3: 16.7%, Z= 5.89 , P <0.01). After adjusting for potential covariates, compared with the ALT group ( Q 1), the group ( Q 3) increased the risk of developing LVH in adolescents ( OR=2.09, 95%CI =1.21-4.12). Stratified analyses by age and sex showed a significant association only in boys and younger individuals aged 12 to 14 years [ OR (95% CI ) were 2.64(1.04-7.67) and 3.24( 1.35 -9.06), both P <0.05)]. Conclusion Elevated serum ALT levels are associated with an increased risk of LVH in adolescents, and early detection and control of abnormal liver enzyme levels can help reduce early vascular structural damage and prevent adverse cardiovascular events.

BACKGROUND:Currently,research both domestically and internationally on patellofemoral pain syndrome has explored the kinematics and dynamics during daily activities such as stair ascent and descent,and walking. However,there is a lack of studies examining the lower limb biomechanical characteristics of young female patients with patellofemoral pain syndrome in different squatting conditions.OBJECTIVE:To investigate the lower limb biomechanical characteristics among young female patients with patellofemoral pain syndrome in different functional states of the subtalar joint,providing theoretical support for the clinical treatment of various types of patellofemoral pain syndrome.METHODS:A total of 33 participants were included in this study. There were 10 subjects in the healthy control group (group C). The other 27 subjects with patellofemoral pain syndrome were divided into two groups according to the foot posture index:14 subjects in the normal subtalar joint group (group A,foot posture index 0-6 points) and 13 subjects in the abnormal subtalar joint group (group B,foot posture index 7-12 points). The biomechanical indices of thesubjects in each group were collected and compared when they walked on stairs at normal speed. The kinematic indices included the three-dimensional joint angles of the hip and knee and the sagittal plane joint angles of the ankle at the initial contact moment and the moment of maximum knee flexion angle during the stance period. The dynamic indices included the three-dimensional joint torques of the hip and knee and the sagittal plane joint torques of the ankle at the moment of maximum knee flexion angle during the stance period. The surface electromyography indices included the root mean square amplitudes of the vastus medialis,vastus lateralis,rectus femoris,semitendinosus and semimembranosus,biceps femoris,and gluteus medius in the pre-activation stage and the buffering stage.RESULTS AND CONCLUSION:(1) At the initial ground contact moment,group A exhibited a greater knee flexion angle (P<0.05),greater hip external rotation angle (P<0.01),and smaller knee external rotation angle (P<0.01) compared to group B. Compared to group C,group A showed a greater knee flexion angle and smaller hip flexion angle (both P<0.01). Group B demonstrated a greater knee external rotation angle and smaller hip external rotation angle and hip flexion angle (all P<0.01) compared to group C. (2) At the moment of maximum knee flexion,group A had a smaller knee valgus angle (P<0.05),smaller knee external rotation angle (P<0.05),and greater knee flexion angle (P<0.01) compared to group B. Compared to group C,group A showed a smaller knee valgus angle (P<0.05),smaller hip flexion angle (P<0.01),and smaller hip external rotation angle (P<0.05). Group B had a smaller knee flexion angle,hip flexion angle,hip external rotation angle,and greater knee external rotation angle (all P<0.01) compared to group C. Additionally,group A exhibited a greater hip internal rotation moment (P<0.05) and plantarflexion moment (P<0.01) compared to group C. (3) At normal speed during the staircase buffering phase,group C showed higher activation levels than group A in the vastus lateralis (P<0.05),vastus medialis (P<0.01),gluteus medius (P<0.01),and biceps femoris (P<0.05). Group C also had higher activation levels than group B in the vastus medialis (P<0.01),gluteus medius (P<0.01),and biceps femoris (P<0.05). Additionally,group A showed higher activation in the semitendinosus and semimembranosus muscles compared to group B (P<0.05). (4) These findings indicate that young female patients with patellofemoral pain syndrome have stiffer hip and knee joint buffering while descending stairs,potentially compensated by the ankle joint. Low muscle activation levels contribute to patellofemoral pain,with those having normal subtalar joints but experiencing pain showing the lowest and most abnormal activation. ③ Abnormal biomechanics in the normal subtalar joint group are mainly due to insufficient hip and knee flexion. Abnormal biomechanics in the abnormal subtalar joint group are mainly due to excessive subtalar joint pronation.

Background and Aims:According to the Chinese Guidelines for the Diagnosis and Treatment of Colorectal Cancer(2023 Edition),patients with early-stage colorectal cancer who present with high-risk factors require additional radical surgery following endoscopic resection.However,due to the relatively low rate of lymph node metastasis in early colorectal cancer,some patients may not benefit from such supplemental surgery.Therefore,accurately identifying patients who are truly likely to benefit and refining the indications for supplemental surgery are pressing clinical challenges.This study was conducted to investigate the risk factors and distribution patterns of lymph node metastasis following additional radical surgery through retrospectively analyzing a large single-center cohort,thereby providing evidence-based support for clinical decision-making.Methods:Clinicopathologic data were retrospectively reviewed for patients with early-stage colorectal cancer who underwent additional radical surgery at Fudan University Shanghai Cancer Center between 2008 and 2023.Binary Logistic regression and multivariate analyses were performed to identify risk factors associated with lymph node metastasis,and the distribution characteristics of metastatic lymph nodes were further examined.Results:A total of 417 patients were included in the study,with lymph node metastasis confirmed in 36 cases(8.63％)postoperatively.Over time,the number of patients undergoing supplemental surgery increased,while the proportion of cases with residual cancer decreased.Among 243 patients included in the risk factor analysis,univariate analysis indicated that submucosal invasion depth of SM2 or greater,poor tumor differentiation,positive vascular invasion,and tumor location were high-risk factors for lymph node metastasis.Multivariate analysis identified invasion depth(P=0.039)and tumor location(P=0.014)as independent risk factors.Among the metastatic cases,58.3％involved a single lymph node;63.9％of metastases were limited to the first station,and 36.1％extended to the second station,with no metastasis found at the third station.Only four patients had preoperative imaging suggestive of lymph node enlargement.Conclusion:Although the number of supplemental surgeries following endoscopic resection of early-stage colorectal cancer has increased significantly,the actual rate of lymph node metastasis remains low,suggesting a potential risk of overtreatment.Submucosal invasion depth ≥SM2 and tumor location are independent risk factors for metastasis.D2 lymph node dissection is deemed necessary,while the diagnostic value of imaging remains limited.Clinical decisions should prioritize precision and individualized treatment planning.

Aim To investigate the intervention effect of Rehmannia radix water extract on bleomycin(BLM)-induced pulmonary fibrosis in mice combined with metabolomics and to reveal the potential mechanism,in order to provide new ideas for clinical treatment of pul-monary fibrosis.Methods Male C57BL/6N mice were randomly divided into the control group,model group,pirfenidone group(positive control,PFD,270 mg·kg-1),and low dose(DH-L,4.55 g·kg-1)group,medium dose(DH-M,9.1 g·kg-1)group and high dose(DH-H,18.2 g·kg-1)group of Rehman-nia.Except for the control group,BLM(5 mg·kg-1)was instilled into the trachea to establish the model of pulmonary fibrosis in the other groups.The survival rate,lung index and blood oxygen saturation of mice in each group were evaluated.HE and Masson staining were used to observe the pathological changes of lung tissue.WBP was used to detect lung function.Flow cytometry was used to detect the apoptosis of primary lung cells,ROS and immune cells.ELISA was used to detect the levels of fibrosis markers and inflammatory factors(α-SMA,collagen Ⅰ,collagen Ⅲ,TGF-β1,TNF-α,IL-1 β,and IL-6).Biochemical method was employed to detect the contents of GSH-Px,T-SOD and MDA.Liquid chromatograph mass spectrometer(LC-MS)metabolomics was used to analyze the changes of serum metabolic profile.Results Water extract of Re-hmannia significantly increased the survival rate,oxy-gen saturation and lung function of mice with pulmona-ry fibrosis,reduced the lung coefficient,ameliorated pathological damage and collagen deposition in lung tissue,reduced the levels of apoptosis and oxidative stress,and down-regulated the levels of inflammatory factors in lung tissue.It regulated the levels of metabo-lites such as bile acid metabolism,sphingolipid metabo-lism,and unsaturated fatty acid metabolism.Conclu-sions Water extract of Rehmannia inhibits lung injury and collagen deposition in mice with pulmonary fibrosis by inhibiting inflammatory response,which may be a-chieved by regulating the levels of inflammatory factors through the metabolic pathways of bile acid and sphin-golipid.