ObjectiveTo investigate the therapeutic effect of sitravatinib on carbon tetrachloride （CCl₄）-induced liver fibrosis in mice. MethodsA total of 30 male C57BL/6J mice， aged 8 weeks， were randomly divided into control group， CCl₄ model group， and low- （5 mg/kg）， middle- （10 mg/kg）， and high-dose （20 mg/kg） sitravatinib groups. All mice except those in the control group were given intraperitoneal injection of CCl₄ for 4 consecutive weeks to induce liver fibrosis， and since the first day of modeling， the mice in the low-， middle-， and high-dose sitravatinib groups were given sitravatinib at the corresponding dose by gavage every day. The serum levels of total cholesterol （TC）， triglyceride （TG）， and alanine aminotransferase （ALT） were measured for the mice in each group； hepatic hydroxyproline content was measured； HE staining， Masson staining， and Sirius Red staining were used to observe liver histopathological changes； quantitative real-time PCR and Western blot were used to measure the mRNA and protein expression levels of α-smooth muscle actin （α-SMA） and collagen type I alpha 1 （Col1a1） in liver tissue. The therapeutic effect of sitravatinib was assessed based on the above results. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the control group， the model group had significant increases in the levels of TC， TG， and ALT （all P<0.05）， and there were no significant differences in the levels of TC， TG， and ALT between the model group and the low-， middle-， and high-dose sitravatinib groups （all P>0.05）. Hepatic hydroxyproline content decreased after sitravatinib intervention， with a significant difference between the middle-/high-dose sitravatinib groups and the CCl₄ model group （both P<0.05）. Histopathological staining showed that the sitravatinib treatment groups had a reduction in collagen deposition， along with thinning and fragmentation of fibrous septa， and in the high-dose sitravatinib group， 4 mice had a fibrosis stage of S0—S1 and 2 mice had a fibrosis stage of S2—S3， suggesting a certain degree of alleviation of liver fibrosis degree compared with the CCl₄ model group （mainly S3—S4）. The measurement of related molecules showed that sitravatinib downregulated the mRNA and protein expression levels of α-SMA and Col1a1 （all P<0.05）. ConclusionSitravatinib can effectively alleviate CCl₄-induced liver fibrosis in mice， possibly by inhibiting hepatic stellate cell activation and collagen synthesis.

ObjectiveType I interferon (IFN-I) signaling is essential for antiviral innate immunity, yet its sustained or excessive activation contributes to the pathogenesis of several autoimmune diseases and interferonopathies, such as systemic lupus erythematosus and Aicardi-Goutières syndrome. Current strategies targeting this pathway, exemplified by JAK inhibitors, act mainly on downstream signal transduction and provide limited direct control over upstream IFN-I production, while also carrying the risk of broad immunosuppression. Phyllanthus emblica L. has long been used in traditional medicine for inflammatory disorders, but the bioactive constituent responsible for its regulation of IFN-I signaling and the underlying molecular mechanism have not been clearly defined. This study aimed to identify the active anti-inflammatory component of P. emblica and to characterize its mechanism of action on the IFN-I pathway in macrophages. MethodsActive components ofP. emblica and their candidate targets were screened by network pharmacology using the TCMSP and DrugBank databases (oral bioavailability≥30%, drug-likeness≥0.18) and intersected with inflammation-related genes retrieved from public databases. The predicted interaction between EGCG and IFN-I pathway proteins (TBK1, IRF3, STAT1) was evaluated by molecular docking, with BX795 and GSK8612 used as reference TBK1 inhibitors. Mechanistic experiments were performed in THP-1-derived macrophages and primary bone marrow-derived macrophages (BMDM). Upstream signaling was activated by transfection of the nucleic acid analogs poly(I∶C) and poly(dA∶dT) or by lipopolysaccharide (LPS) stimulation, whereas downstream signaling was activated by exogenous IFN-β. An siRNA-mediated TREX1 knockdown model was used to mimic endogenous nucleic acid-driven interferonopathy. Expression of IFN-β1 and interferon-stimulated genes (ISGs) was measured by RT-qPCR, protein phosphorylation by Western blot, and IFN-β secretion by ELISA. Cellular thermal shift assay (CETSA) and drug affinity responsive target stability (DARTS) were used to probe the interactionbetween EGCG and IRF3. ResultsNetwork pharmacology identified (-)-epigallocatechin-3-gallate (EGCG) as a candidate IFN-I-suppressive constituent of P. emblica, with predicted binding to TBK1, IRF3, and STAT1. Molecular docking yielded binding energies of -9.2, -7.2, and -8.2 kcal/mol for TBK1, IRF3, and STAT1, respectively, indicating an affinity for TBK1 comparable to that of the reference inhibitors BX795 (-5.7 kcal/mol) and GSK8612 (-6.4 kcal/mol). EGCG suppressed IFN-β1 and ISG mRNA expression under poly (I∶C), poly (dA∶dT), and LPS stimulation in both THP-1 macrophages and BMDM. At the protein level, EGCG reduced the phosphorylation of TBK1 and IRF3 without affecting the levels of the upstream sensors cGAS and RIG-I, and lowered IFN-β secretion in a concentration-dependent manner. CETSA and DARTS showed that EGCG did not enhance the thermal stability or protease resistance of IRF3, indicating that its effect on IRF3 is indirect. Following IFN-β stimulation, prolonged EGCG treatment reduced STAT1 phosphorylation in a time-dependent manner without an apparent change in IRF9, and partially attenuated ISG transcription; this effect was not monotonicly concentration-dependent, and CXCL10 showed the most consistent suppression. In TREX1-knockdown cells, the elevated mRNA levels of ISG15, ISG56, and CXCL10 were reduced by EGCG. ConclusionEGCG suppresses IFN-I responses by concurrently inhibiting TBK1-IRF3-dependent IFN‑β production and JAK-STAT1-mediated downstream transcription. These in vitro findings provide a mechanistic basis for the anti-inflammatory use of P. emblica in traditional medicine and identify EGCG as a candidate for further evaluation in interferon-driven autoimmune disease models.

ObjectiveTo investigate the effect and mechanism of Shengxian Yixin Granule （升陷益心颗粒， SYG） in treating heart failure with preserved ejection fraction （HFpEF）. MethodsExperiment 1： Forty male C57BL/6 mice were randomly divided into control group， model group， low-dose ［25 mg/（kg·d）］， medium-dose ［50 mg/（kg·d）］， and high-dose ［（75 mg/（kg·d）］ SYG groups， with 8 mice per group. Except for the control group， HFpEF was induced by a high-fat diet combined with Nω-nitro-L-arginine methyl ester in drinking water for 16 weeks. After 10 weeks of modeling， treatment groups received corresponding doses of SYG by gavage， while the control group and model group received equal volume of normal saline， for 6 weeks. After 6 weeks of administration， the body weight， blood pressure including systolic blood pressure （SBP） and diastolic blood pressure （DBP）， and heart weight-to-tibia length ratio （HW/TL） were recorded. Echocardiography was used to evaluate left ventricular ejection fraction （LVEF） and the ratio of early to late diastolic transmitral flow velocity （E/A）. Plasma N-terminal pro-brain natriuretic peptide （NT-proBNP） and C-reactive protein （CRP） levels were measured by ELISA. The expression level of brain natriuretic peptide （BNP） in heart tissue was detected by qRT-PCR. Blood lipid levels， including low-density lipoprotein cholesterol （LDL-C）， triglycerides （TG）， and total cholesterol （TC）， were determined by a biochemical analyzer. Splenic proportions of M1 macrophages， M2 macrophages， T helper 17 （Th17） cells， and regulatory T （Treg） cells were analyzed by flow cytometry. Experiment 2： RAW 264.7 cells were stimulated with lipopolysaccharide （LPS） to establish an M1 macrophage polarization model， and then treated with SYG-containing serum for 24 h. The cells were divided into four groups， including blank serum group， high-dose SYG-containing serum group， LPS group， and LPS plus high-dose SYG-containing serum group. Combined with asignal transducer and activator of transcription 3 （Stat3） inhibitor for 24 h， the cells were divided into a lipopolysaccharide group， a high-dose SYG-containing serum group， an inhibitor group， and high-dose SYG-containing serum plus inhibitor group. The expression levels of inducible nitric oxide synthase （iNOS） and interleukin-1β （IL-1β） in each group were detected by qRT-PCR. The protein levels of iNOS， IL-1β， Stat3， and phosphorylated Stat3 （p-Stat3） were detected by Western Blotting. ResultsExperiment 1： Compared to the control group， the model group showed significantly decreased E/A ratio， and increased cardiac BNP expression， plasma NT-proBNP，HW/TL ratio， body weight， TC， LDL-C， SBP， and DBP， as well as shortened exhaustion distance and exhaustion time （P＜0.05 or P＜0.01）. Compared to the model group， the E/A ratio increased in the low-， medium-， and high-dose SYG groups； cardiac BNP expression decreased in the low- and high-dose groups， and plasma NT-proBNP levels decreased in the high-dose group； the HW/TL ratio and body weight decreased， while exhaustion distance and exhaustion time increased in the medium- and high-dose groups； TG levels decreased in the low- and medium-dose groups， and LDL-C levels decreased in the medium- and high-dose groups； SBP and DBP decreased in the low-， medium-， and high-dose groups （P＜0.05 or P＜0.01）. Compared to the low-dose SYG group， body weight decreased， and both exhaustion distance and exhaustion time increased in the medium- and high-dose groups （P＜0.05 or P＜0.01）. Compared to the medium-dose SYG group， the exhaustion time increased in the high-dose SYG group （P＜0.01）. Experiment 2： In the LPS‑induced M1 macrophage polarization model， compared to the blank serum group， the LPS group showed significantly increased mRNA and protein expression of iNOS and IL‑1β， as well as the p‑Stat3/Stat3 ratio （P＜0.01）. Compared to the LPS group， the high‑dose SYG-containing serum plus LPS group showed significantly decreased mRNA and protein expression of iNOS and IL‑1β， as well as the p‑Stat3/Stat3 ratio （P＜0.05 or P＜0.01）. Compared to the LPS group， the inhibitor group also showed significantly reduced these parameters （P＜0.05 or P＜0.01）. ConclusionSYG can improve cardiac function， ventricular remodeling， exercise capacity， and lipid metabolism in HFpEF mice， while inhibiting inflammatory responses. Its mechanism may be related to the regulation of the Stat3 signaling pathway and inhibition of M1 macrophage polarization.

ObjectiveTo investigate the effect and mechanism of Shengxian Yixin Granule （升陷益心颗粒， SYG） in treating heart failure with preserved ejection fraction （HFpEF）. MethodsExperiment 1： Forty male C57BL/6 mice were randomly divided into control group， model group， low-dose ［25 mg/（kg·d）］， medium-dose ［50 mg/（kg·d）］， and high-dose ［（75 mg/（kg·d）］ SYG groups， with 8 mice per group. Except for the control group， HFpEF was induced by a high-fat diet combined with Nω-nitro-L-arginine methyl ester in drinking water for 16 weeks. After 10 weeks of modeling， treatment groups received corresponding doses of SYG by gavage， while the control group and model group received equal volume of normal saline， for 6 weeks. After 6 weeks of administration， the body weight， blood pressure including systolic blood pressure （SBP） and diastolic blood pressure （DBP）， and heart weight-to-tibia length ratio （HW/TL） were recorded. Echocardiography was used to evaluate left ventricular ejection fraction （LVEF） and the ratio of early to late diastolic transmitral flow velocity （E/A）. Plasma N-terminal pro-brain natriuretic peptide （NT-proBNP） and C-reactive protein （CRP） levels were measured by ELISA. The expression level of brain natriuretic peptide （BNP） in heart tissue was detected by qRT-PCR. Blood lipid levels， including low-density lipoprotein cholesterol （LDL-C）， triglycerides （TG）， and total cholesterol （TC）， were determined by a biochemical analyzer. Splenic proportions of M1 macrophages， M2 macrophages， T helper 17 （Th17） cells， and regulatory T （Treg） cells were analyzed by flow cytometry. Experiment 2： RAW 264.7 cells were stimulated with lipopolysaccharide （LPS） to establish an M1 macrophage polarization model， and then treated with SYG-containing serum for 24 h. The cells were divided into four groups， including blank serum group， high-dose SYG-containing serum group， LPS group， and LPS plus high-dose SYG-containing serum group. Combined with asignal transducer and activator of transcription 3 （Stat3） inhibitor for 24 h， the cells were divided into a lipopolysaccharide group， a high-dose SYG-containing serum group， an inhibitor group， and high-dose SYG-containing serum plus inhibitor group. The expression levels of inducible nitric oxide synthase （iNOS） and interleukin-1β （IL-1β） in each group were detected by qRT-PCR. The protein levels of iNOS， IL-1β， Stat3， and phosphorylated Stat3 （p-Stat3） were detected by Western Blotting. ResultsExperiment 1： Compared to the control group， the model group showed significantly decreased E/A ratio， and increased cardiac BNP expression， plasma NT-proBNP，HW/TL ratio， body weight， TC， LDL-C， SBP， and DBP， as well as shortened exhaustion distance and exhaustion time （P＜0.05 or P＜0.01）. Compared to the model group， the E/A ratio increased in the low-， medium-， and high-dose SYG groups； cardiac BNP expression decreased in the low- and high-dose groups， and plasma NT-proBNP levels decreased in the high-dose group； the HW/TL ratio and body weight decreased， while exhaustion distance and exhaustion time increased in the medium- and high-dose groups； TG levels decreased in the low- and medium-dose groups， and LDL-C levels decreased in the medium- and high-dose groups； SBP and DBP decreased in the low-， medium-， and high-dose groups （P＜0.05 or P＜0.01）. Compared to the low-dose SYG group， body weight decreased， and both exhaustion distance and exhaustion time increased in the medium- and high-dose groups （P＜0.05 or P＜0.01）. Compared to the medium-dose SYG group， the exhaustion time increased in the high-dose SYG group （P＜0.01）. Experiment 2： In the LPS‑induced M1 macrophage polarization model， compared to the blank serum group， the LPS group showed significantly increased mRNA and protein expression of iNOS and IL‑1β， as well as the p‑Stat3/Stat3 ratio （P＜0.01）. Compared to the LPS group， the high‑dose SYG-containing serum plus LPS group showed significantly decreased mRNA and protein expression of iNOS and IL‑1β， as well as the p‑Stat3/Stat3 ratio （P＜0.05 or P＜0.01）. Compared to the LPS group， the inhibitor group also showed significantly reduced these parameters （P＜0.05 or P＜0.01）. ConclusionSYG can improve cardiac function， ventricular remodeling， exercise capacity， and lipid metabolism in HFpEF mice， while inhibiting inflammatory responses. Its mechanism may be related to the regulation of the Stat3 signaling pathway and inhibition of M1 macrophage polarization.

Aim To explore the therapeutic effects of resveratrol(Res)on hepatic inflammation and oxida-tive stress in rheumatoid arthritis(RA),and to eluci-date the relationship of the regulatory mechanism of the Nrf2/Keap1 signaling pathway in it.Methods A mouse model of arthritis was induced using chicken type Ⅱ collagen in combination with complete Freund's adjuvant,and Res was administered by tube feeding for treatment.Serum liver function indices and levels of hepatic inflammation and oxidative stress were detected in mice.An in vitro cellular model of hepatic inflam-mation and oxidative stress was established by treating mouse primary hepatocytes(MPHs)with TNF-α(5μg·L-1),cell proliferation inhibition was detected by CCK-8,and inflammation and oxidative stress-relat-ed indices were detected by protein blotting.The in-trinsic mechanisms by which Res attenuated hepatic in-flammation and oxidative stress in rheumatoid arthritis were explored by treating MPHs with Nrf2 inhibitor and Keap1 overexpression plasmid.Results Res signifi-cantly reduced the levels of inflammation and oxidative stress in hepatic tissues of collagen-induced arthritis mice as well as TNF-α-treated MPHs,and activated the Nrf2/Keap1 signaling pathway.Inflammation and oxidative stress levels in MPHs were exacerbated by the use of Nrf2 inhibitors and Keap1 overexpression,which promoted apoptosis.Conclusion Res attenuates he-patic inflammation and oxidative stress in rheumatoid arthritis via the Nrf2/Keap1 pathway.

OBJECTIVE: Asthma imposes a significant global health burden. This study examines changes in the asthma-related disease burden from 1990 to 2021 and projects future burdens for 2050 under different scenarios. METHODS: Using data from the Global Burden of Disease 2021 study, we analyzed asthma incidence, prevalence, mortality, and disability-adjusted life years (DALYs) from 1990 to 2021. We projected the disease burden for 2050 based on current trends and hypothetical scenarios in which all risk factors are controlled. Temporal trends in age-standardized incidence, prevalence, mortality, and DALY rates were explored using Annual Percent Change. RESULTS: In 2021, the age-standardized rates for asthma incidence, prevalence, mortality, and DALYs in China were 364.17 per 100,000 (95% uncertainty interval [ UI]: 283.22-494.10), 1,956.49 per 100,000 (95% UI: 1,566.68-2,491.87), 1.47 per 100,000 (95% UI: 1.15-1.79), and 103.76 per 100,000 (95% UI: 72.50-145.46), respectively. A higher disease burden was observed among Chinese men and individuals aged 70 years or older. Compared to the current trend, a combined scenario involving improvements in environmental factors, behavioral and metabolic health, child nutrition, and vaccination resulted in a greater reduction in the disease burden caused by asthma. CONCLUSION Addressing modifiable risk factors is essential for further reducing the asthma-related disease burden.
Humans ; Asthma/mortality* ; China/epidemiology* ; Male ; Female ; Adult ; Middle Aged ; Aged ; Child ; Adolescent ; Global Burden of Disease/trends* ; Child, Preschool ; Young Adult ; Infant ; Cost of Illness ; Disability-Adjusted Life Years ; Prevalence ; Incidence ; Infant, Newborn ; Aged, 80 and over ; Risk Factors

Aim To explore the therapeutic effects of resveratrol(Res)on hepatic inflammation and oxida-tive stress in rheumatoid arthritis(RA),and to eluci-date the relationship of the regulatory mechanism of the Nrf2/Keap1 signaling pathway in it.Methods A mouse model of arthritis was induced using chicken type Ⅱ collagen in combination with complete Freund's adjuvant,and Res was administered by tube feeding for treatment.Serum liver function indices and levels of hepatic inflammation and oxidative stress were detected in mice.An in vitro cellular model of hepatic inflam-mation and oxidative stress was established by treating mouse primary hepatocytes(MPHs)with TNF-α(5μg·L-1),cell proliferation inhibition was detected by CCK-8,and inflammation and oxidative stress-relat-ed indices were detected by protein blotting.The in-trinsic mechanisms by which Res attenuated hepatic in-flammation and oxidative stress in rheumatoid arthritis were explored by treating MPHs with Nrf2 inhibitor and Keap1 overexpression plasmid.Results Res signifi-cantly reduced the levels of inflammation and oxidative stress in hepatic tissues of collagen-induced arthritis mice as well as TNF-α-treated MPHs,and activated the Nrf2/Keap1 signaling pathway.Inflammation and oxidative stress levels in MPHs were exacerbated by the use of Nrf2 inhibitors and Keap1 overexpression,which promoted apoptosis.Conclusion Res attenuates he-patic inflammation and oxidative stress in rheumatoid arthritis via the Nrf2/Keap1 pathway.

Objective:To investigate whether brown adipose tissue-derived exosomes(BAT-exos) could ameliorate endothelial cell injury by activating Pink1-Parkin pathway-mediated mitophagy.Methods:Endothelial cell injury was induced with angiotensin Ⅱ(Ang Ⅱ) to establish a cellular injury model. Exosomes were isolated from both brown adipose tissue and white adipose tissue and characterized by transmission electron microscopy(TEM), nanoparticle tracking analysis(NTA), fluorescence labeling, and Western blot. Cell viability was assessed using the CCK-8 assay, and apoptosis rates were determined by flow cytometry. Levels of tumor necrosis factor-α(TNF-α), interleukin(IL)-6, and IL-8 were measured by ELISA. Mitochondrial autophagy was assessed by immunofluorescence colocalization, and protein expression levels of Pink1, Parkin, and LC3 Ⅱ/I were determined by Western blot.Results:Ang Ⅱ induced endothelial cell apoptosis, activated inflammatory responses, and suppressed mitophagy, as evidenced by decreased expression of mitophagy-related proteins. Following the successful characterization of BAT-exos, we found that BAT-exos activated mitophagy and alleviated endothelial cell injury, whereas white adipose tissue-derived exosomes(WAT-exos) inhibited mitophagy and exacerbated injury. Mechanistically, BAT-exos targeted the Pink1-Parkin signaling pathway to activate mitophagy.Conclusion:BAT-exos markedly improve endothelial cell injury by activating mitophagy through the Pink1-Parkin pathway, providing new insights and potential therapeutic targets for cardiovascular diseases.

Objective:This study aimed to integrate RNA-seq data to identify key genes associated with macrophage-ferroptosis and develop a prognostic model for hepatocellular carcinoma(HCC).Methods:We retrieved a dataset from the GEO database containing transcriptome data and clinical information for 163 samples.Macrophage-related genes were identified using WGCNA and immune infiltration analyses.Ferroptosis-related genes from the FerrDbV2 database were intersected with differentially expressed genes to obtain significant macrophage-ferroptosis-related genes.Hub genes were screened via protein interaction network construction,and key genes were identified using four machine learning algorithms.These genes exhibited significant expression differences between cancer and normal tissues and were closely linked to patient prognosis.ROC curve and KM survival analyses were performed,and expression levels were validated at the transcriptome and proteome levels.Results:Four key genes RRM2,KIF20A,PCK2,and PDK4 were identified and evaluated.RRM2 and KIF20A demonstrated high importance in classification prediction models and reliable performance in ROC and KM analyses(AUC＞0.9,P＜0.05).These genes regulate cancer cell proliferation/survival and macrophage polarization/function,influencing the tumor microenvironment and HCC progression.Conclusion:RRM2 and KIF20A regulate cancer cell proliferation and survival,modulate macrophage polarization and function,and influence the immune response in the tumor microenvironment.They can serve as prognostic biomarkers and potential immunotherapy targets for hepatocellular carcinoma.

OBJECTIVE To investigate the time-effect relationship of ginger-partitioned moxibustion in treating fecal inconti-nence in patients with mild to moderate active Crohn's disease so as to optimize moxibustion duration and provide a basis for clinical application.METHODS A total of 128 patients with Crohn's disease complicated by fecal incontinence who met the inclusion crite-ria were selected as the study subjects.They were divided into a control group and three experimental groups(experimental group Ⅰ,Ⅱ,and Ⅲ)of 32 patients each using a stratified random method(with 1 dropout in experimental group Ⅰ).Patients in the control group received routine anti-tumor necrosis factor-α monoclonal antibody(adalimumab)treatment,while patients in the experimental groups received ginger moxibustion therapy in addition to the treatment provided to the control group.Among them,experimental groupⅠ received treatment for 20 minutes,experimental group Ⅱ for 40 minutes,and experimental group Ⅲ for 60 minutes.The course of treatment for all four groups was 3 months.Changes in TCM syndrome scores were compared before and after treatment in the four groups to assess clinical efficacy.The cleveland clinic incontinence score(CCIS)was used to assess the severity of fecal incontinence,the Crohn's disease activity index(CDAI)was used to assess the degree of disease activity,and the inflammatory bowel disease ques-tionnaire(IBDQ)was used to evaluate the quality of life.Anal pressure index and peripheral blood CRP and ESR levels were mea-sured,and the relationship between moxibustion time and effect was analyzed.RESULTS After 3 months of treatment,the total TCM syndrome scores of all four groups improved to varying degrees(P<0.05,P<0.01).The total scores of groups Ⅰ,Ⅱ,and Ⅲ were supe-rior to those of the control group(P<0.05,P<0.01),while group Ⅱ had the lowest total TCM syndrome score.Group Ⅱ had the high-est overall clinical effective rate,significantly better than both the control and group Ⅰ(P<0.05,P<0.01).CCIS scores,IBDQ scores and total scores,and peripheral blood ESR levels were significantly reduced in all four groups(P<0.01),with group Ⅱ having the low-est score,lower than both the control and group Ⅰ(P<0.05,P<0.01).CRP levels were significantly reduced in groups Ⅱ and Ⅲ(P<0.05,P<0.01),both lower than the control group(P<0.05,P<0.01),with group Ⅱ lower than group Ⅰ(P<0.01).Intestinal symptom scores in the IBDQ of groups Ⅱ and Ⅲ were significantly higher than those in the control group and group Ⅰ(P<0.05,P<0.01).The maximum resting pressure of the anal canal,rectal defecation threshold,and maximum tolerance capacity all increased significantly in the four groups(P<0.05,P<0.01),but there were no significant differences among the groups(P>0.05).During the treatment,two cases of mild skin redness occurred in group Ⅲ,which resolved after treatment,with no serious adverse reactions.CONCLUSION Ginger moxibustion in the treatment of Crohn's disease complicated by fecal incontinence exhibits a time-effect relationship,with 40 minutes as the optimal duration.It can effectively improve symptoms,control inflammation,enhance quality of life,and has good safety.