Autoimmune hepatitis （AIH） is a chronic inflammatory liver disease mediated by T lymphocytes， and it can progress to liver cirrhosis or even liver failure without timely intervention. As a natural flavonoid compound， naringenin （NAR） shows a potential value in the prevention and treatment of AIH through multiple mechanisms such as remodeling immune homeostasis， targeted inhibition of inflammatory pathways， antioxidation， regulating hepatocyte metabolism and apoptosis， improving mitochondrial function， and regulating intestinal flora. However， the clinical translation and application of NAR is limited by issues such as low bioavailability and insufficient efficiency of liver-targeted delivery. This article systematically reviews the mechanism of action of NAR in the prevention and treatment of AIH， explores the potential signaling pathways involved in this process， and analyzes existing challenges in its translation and application and future research directions， so as to provide a reference for further research on NAR and its application in the prevention and treatment of AIH.

Objective:To investigate the potential of praeruptorin A (PA) in alleviating inflammatory damage in sepsis through the inhibition of ferritin expression.Methods:C57BL/6 mice were intraperitoneally injected with lipopolysaccharide (LPS) to establish the model of sepsis. After 6 and 12 h of PA intervention, serum levels of inflammatory cytokines IL-6 and TNF-α were measured by ELISA. Kidney tissues were collected at 72 h for HE staining to assess inflammatory cell infiltration and tissue damage. Human neutrophils were divided into four groups: control, LPS, ferritin, and LPS+ ferritin groups. After 12 h of intervention, qRT-PCR was used to detect the expression of IL-6 and TNF-α mRNA. In order to observe the effect of PA on the expression of inflammatory cytokines and ferritin, human neutrophils were grouped into control, LPS, and LPS+ PA (2/3/4 μmol/L) groups. After 12 h of intervention, qRT-PCR was performed to measure the expression of IL-1β, IL-6, TNF-α, and ferritin mRNA; ELISA was used to quantify the levels of IL-1β, IL-6, and TNF-α in culture supernatants; Western blot was used to analyze the expression of ferritin. Molecular docking was conducted to verify interactions between PA and ferritin.Results:Significant inflammatory cell recruitment, tissue damage, and elevated serum levels of IL-6 and TNF-α ( P<0.01) were observed in mice with LPS-induced sepsis. PA significantly inhibited cytokine secretion ( P<0.01) and alleviated tissue injury in sepsis mice. In human neutrophil models, ferritin upregulated the expression of IL-6 and TNF-α mRNA ( P<0.01); LPS stimulation alone increased the expression of IL-1β, IL-6, TNF-α, and ferritin at both mRNA and protein levels ( P<0.01), while co-stimulation with PA (3/4 μmol/L) significantly reversed the aforementioned results ( P<0.01). Molecular docking confirmed there were interaction sites between PA and ferritin. Conclusion:PA inhibits the release of inflammatory cytokines and alleviates tissue damage in sepsis, and the potential mechanism may involve modulating ferritin expression to suppress inflammatory responses.

Objective To investigate whether curcumin(CUR)can reduce chondrocyte inflammation and cartilage degradation in osteo-arthritis(OA)and the underlying mechanisms.Methods A rat model of OA was established.Rats were randomly divided into a Sham,OA,CUR+OA,and deferoxamine(DFO)+OA groups with 10 mice in each group.Chondrocytes from 5-day-old SD rats were divided into the control,interleukin-1β(IL-1β),CUR+IL-1β,and DFO+IL-1β groups.A CCK-8 assay was performed to assess the effects of CUR on cell viability alone or combined with IL-1β.Toluidine blue staining and alcian blue staining were used to observe the morphological changes of IL-1β-induced chondrocytes.The expression of inflammatory response-related proteins(COX-2 and iNOS),extracellular matrix degradation-related proteins(COL2A and MMP13),and p53,SLC7A11,and GPX4 proteins during ferroptosis were detected by Western blotting.The mitochondrial membrane potential was detected by JC-1 staining.Mitochondrial morphology was observed using transmission electron microscopy.Safranine O-fast green/HE staining was performed on cartilage tissues.Immunohistochemical staining was performed to detect COL2A and SLC7A11 expression levels.Results CUR and DFO were found to reduce IL-1β-induced inflammation,cartilage degradation,and ferroptosis,and restore mitochondrial function in chondrocytes.CUR also reversed IL-1β-induced changes in collagen Ⅱ,p53,SLC7A11,GPX4,MMP13,iNOS,and COX-2 levels.In vivo,intra-articular injection of CUR significantly improved cartilage injury in the OA rat model,and the percentages of COL2A-and SLC7A11-positive cells significantly increased in the CUR+OA and DFO+OA groups.Conclusion CUR inhibits ferroptosis and ameliorates cartilage degeneration in OA through p53 signaling pathway.

Virus-related lymphoma exhibits a dual nature as both a hematologic malignancy and a viral infectious disease， making it more resistant to treatment and associated with poorer prognosis. This paper analyzes the understanding and therapeutic advantages of traditional Chinese medicine （TCM） in virus-related lymphoma. It proposes a TCM-based approach centered around syndrome differentiation， using standardized measurements of the overall TCM condition， multi-omics research of hematologic tumors， and artificial intelligence technologies to identify the "pre-condition" of virus-related lymphoma. A risk warning model will be established to early identify high-risk populations with viral infections that may develop into malignant lymphoma， thereby establishing a risk warning system for virus-related lymphoma. At the same time， a TCM health management approach will be applied to manage and regulate virus-related lymphoma， interrupting its progression and forming a human-centered， comprehensive， continuous health service model. Based on this， a standardized， integrated clinical prevention and treatment decision-making model for virus-related lymphoma， recognized by both Chinese and western medicine， will be established to provide TCM solutions for primary prevention of major malignant tumors.

Objective: To investigate the distribution of traditional Chinese medicine (TCM) syndromes and syndrome elements in lymphoma, as well as the correlation between TCM syndromes and Western clinical indicators, in order to analyze associations between TCM syndromes and these indicators. Methods: From January 2023 to May 2024, 216 patients with lymphoma who met the inclusion criteria in the Department of Hematology, Third People′s Hospital Affiliated to Fujian University of Traditional Chinese Medicine were enrolled. Four diagnostic methods were applied to perform TCM syndrome differentiation and extract syndrome elements. The correlations between various syndromes and blood test indicators of lactate dehydrogenase (LDH), β2-microglobulin (β2-MG), immunoglobulin G (IgG), immunoglobulin M (IgM), immunoglobulin A (IgA), white blood cell (WBC), hemoglobin (Hb), platelet count (PLT), neutrophil (NEUT), immunohistochemical markers of B-cell lymphoma-6 (BCL6), B-cell lymphoma-2 (BCL2), proto-oncogene MYC, and Ki67 protein expression, Ann Arbor staging, international prognostic index (IPI) score, bone marrow infiltration, concurrent infections during chemotherapy, and post-chemotherapy bone marrow suppression rate were analyzed. Results: Five TCM syndromes, ranked by frequency, were syndromes of yin deficiency with phlegm accumulation(41.67%), qi depression with phlegm obstruction(30.56%), cold-phlegm congelation and stagnation(12.96%), phlegm-blood stasis toxin(12.04%), and lingering pathogen due to deficient vital qi(2.77%). Yin deficiency(50.93%) and phlegm(45.37%) were the more prevalent syndrome elements. The TCM syndromes were correlated with β2-MG, PLT, MYC, BCL2/MYC, Ki67 protein expression, and bone marrow infiltration (P<0.05). No statistically significant differences were observed in Ann Arbor staging or IPI score across the syndromes. Compared to the syndrome of cold-phlegm congelation and stagnation, the syndrome of qi depression with phlegm obstruction exhibited higher levels of NEUT, MYC, BCL2/MYC, and Ki67 protein expression, as well as a higher rate of post-chemotherapy bone marrow suppression (P<0.05); the syndrome of phlegm-blood stasis toxin showed higher MYC and BCL2/MYC protein expression and a higher rate of post-chemotherapy bone marrow suppression rate (P<0.05); the syndrome of yin deficiency with phlegm accumulation demonstrated higher MYC and BCL2/MYC protein expression and bone marrow infiltration rates, whereas PLT level was lower (P<0.05); the syndrome of lingering pathogen due to deficient vital qi had higher MYC, BCL2/MYC, and Ki67 protein expression levels, as well as a higher rate of post-chemotherapy bone marrow suppression rate (P<0.05). Compared to the syndrome of qi depression with phlegm obstruction, the syndrome of phlegm-blood stasis toxin exhibited lower Ki67 protein expression (P<0.05); the syndrome of yin deficiency with phlegm accumulation had higher β2-MG level, bone marrow infiltration rate, and rate of concurrent infections during chemotherapy, whereas PLT and NEUT levels and the rate of post-chemotherapy bone marrow suppression rate were lower (P<0.05). Compared to the syndrome of phlegm-blood stasis toxin, the syndrome of yin deficiency with phlegm accumulation had higher β2-MG level, whereas NEUT and the rate of post-chemotherapy bone marrow suppression were lower(P<0.05); the syndrome of lingering pathogen due to deficient vital qi exhibited a higher Ki67 protein expression (P<0.05). Compared to the syndrome of yin deficiency with phlegm accumulation, the syndrome of lingering pathogen due to deficient vital qi also showed a higher Ki67 protein expression(P<0.05). Conclusion The syndrome of yin deficiency with phlegm accumulation is relatively common in lymphoma. There is a correlation between TCM syndromes and Western medicine clinical indicators. The presence of heat signs in the syndromes may indicate active disease and poor prognosis, while the presence of strong pathogenic factors and weak vital qi in the syndromes may indicate a severer chemotherapy-related bone marrow suppression.

Objective To investigate whether curcumin(CUR)can reduce chondrocyte inflammation and cartilage degradation in osteo-arthritis(OA)and the underlying mechanisms.Methods A rat model of OA was established.Rats were randomly divided into a Sham,OA,CUR+OA,and deferoxamine(DFO)+OA groups with 10 mice in each group.Chondrocytes from 5-day-old SD rats were divided into the control,interleukin-1β(IL-1β),CUR+IL-1β,and DFO+IL-1β groups.A CCK-8 assay was performed to assess the effects of CUR on cell viability alone or combined with IL-1β.Toluidine blue staining and alcian blue staining were used to observe the morphological changes of IL-1β-induced chondrocytes.The expression of inflammatory response-related proteins(COX-2 and iNOS),extracellular matrix degradation-related proteins(COL2A and MMP13),and p53,SLC7A11,and GPX4 proteins during ferroptosis were detected by Western blotting.The mitochondrial membrane potential was detected by JC-1 staining.Mitochondrial morphology was observed using transmission electron microscopy.Safranine O-fast green/HE staining was performed on cartilage tissues.Immunohistochemical staining was performed to detect COL2A and SLC7A11 expression levels.Results CUR and DFO were found to reduce IL-1β-induced inflammation,cartilage degradation,and ferroptosis,and restore mitochondrial function in chondrocytes.CUR also reversed IL-1β-induced changes in collagen Ⅱ,p53,SLC7A11,GPX4,MMP13,iNOS,and COX-2 levels.In vivo,intra-articular injection of CUR significantly improved cartilage injury in the OA rat model,and the percentages of COL2A-and SLC7A11-positive cells significantly increased in the CUR+OA and DFO+OA groups.Conclusion CUR inhibits ferroptosis and ameliorates cartilage degeneration in OA through p53 signaling pathway.

Objective:To investigate the potential of praeruptorin A (PA) in alleviating inflammatory damage in sepsis through the inhibition of ferritin expression.Methods:C57BL/6 mice were intraperitoneally injected with lipopolysaccharide (LPS) to establish the model of sepsis. After 6 and 12 h of PA intervention, serum levels of inflammatory cytokines IL-6 and TNF-α were measured by ELISA. Kidney tissues were collected at 72 h for HE staining to assess inflammatory cell infiltration and tissue damage. Human neutrophils were divided into four groups: control, LPS, ferritin, and LPS+ ferritin groups. After 12 h of intervention, qRT-PCR was used to detect the expression of IL-6 and TNF-α mRNA. In order to observe the effect of PA on the expression of inflammatory cytokines and ferritin, human neutrophils were grouped into control, LPS, and LPS+ PA (2/3/4 μmol/L) groups. After 12 h of intervention, qRT-PCR was performed to measure the expression of IL-1β, IL-6, TNF-α, and ferritin mRNA; ELISA was used to quantify the levels of IL-1β, IL-6, and TNF-α in culture supernatants; Western blot was used to analyze the expression of ferritin. Molecular docking was conducted to verify interactions between PA and ferritin.Results:Significant inflammatory cell recruitment, tissue damage, and elevated serum levels of IL-6 and TNF-α ( P<0.01) were observed in mice with LPS-induced sepsis. PA significantly inhibited cytokine secretion ( P<0.01) and alleviated tissue injury in sepsis mice. In human neutrophil models, ferritin upregulated the expression of IL-6 and TNF-α mRNA ( P<0.01); LPS stimulation alone increased the expression of IL-1β, IL-6, TNF-α, and ferritin at both mRNA and protein levels ( P<0.01), while co-stimulation with PA (3/4 μmol/L) significantly reversed the aforementioned results ( P<0.01). Molecular docking confirmed there were interaction sites between PA and ferritin. Conclusion:PA inhibits the release of inflammatory cytokines and alleviates tissue damage in sepsis, and the potential mechanism may involve modulating ferritin expression to suppress inflammatory responses.

Objective:To compare the consistency of lymphoma multigene detection panels based on next-generation sequencing (NGS) with FISH detection of B-cell lymphoma gene rearrangement.Methods:From January 2019 to May 2023, fusion genes detected by lymphoma-related 413 genes that targeted capture sequencing of 489 B-cell lymphoma tissues embedded in paraffin were collected from Henan Cancer Hospital, and the results were compared with simultaneous FISH detection of four break/fusion genes: BCL2, BCL6, MYC, and CCND1. Consistency was defined as both methods yielding positive or negative results for the same sample. The relationship between fusion mutation abundance in NGS and the positivity rate of cells in FISH was also analyzed.Results:Kappa consistency analysis revealed high consistency between NGS and FISH in detecting the four B-cell lymphoma-related gene rearrangement ( P<0.001 for all) ; however, the detection rates of positive individuals differed for the four genes. Compared with FISH, NGS demonstrated a higher detection rate for BCL2 rearrangement, a lower detection rate for BCL6 and MYC rearrangement, and a similar detection rate for CCND1 rearrangement. No correlation was found between fusion mutation abundance in NGS and the positivity rate of cells in FISH. Conclusions:NGS and FISH detection of B-cell lymphoma gene rearrangement demonstrate overall good consistency. NGS is superior to FISH in detecting BCL2 rearrangement, inferior in detecting MYC rearrangement, and comparable in detecting CCND1 rearrangement.

Objective: To investigate the prevalence, awareness, treatment and control rates of diabetes among residents in Fangshan District, Bejing Municipality, so as to provide reference for strengthening the prevention and control of diabetes. Methods: The residents aged 18 to 79 years were selected in Fangshan District using multistage stratified cluster sampling method from March to June 2023. Demographic information, lifestyle, body mass index, fasting blood glucose, and blood lipid were collected through questionnaire surveys, physical examinations and laboratory tests. The prevalence, awareness, treatment and control rates of diabetes among residents were analyzed and their influencing factors were identified using a multivariable logistic regression model. Results: A total of 4 438 residents were enrolled, including 2 367 males (53.33%) and 2 071 females (46.67%), and had a mean age of (44.99±14.90) years. The prevalence, awareness, treatment and control rates of diabetes were 15.75%, 57.37%, 56.22% and 22.90%, respectively. Multivariable logistic regression analysis showed that age (aged 30 to 39 years, OR=1.624, 95%CI: 1.011-2.609; aged 40 to 49 years, OR=3.469, 95%CI: 2.163-5.561; aged 50 to 59 years, OR=4.202, 95%CI: 2.595-6.803; aged 60 to 69 years, OR=7.229, 95%CI: 4.406-11.862; aged 70 to 79 years, OR=7.929, 95%CI: 4.665-13.479), obesity (OR=1.368, 95%CI: 1.071-1.748), hypertension (OR=1.943, 95%CI: 1.601-2.359) and dyslipidemia (OR=2.754, 95%CI: 2.287-3.317) were the factors affecting the prevalence of diabetes. Sex (women, OR=1.529, 95%CI: 1.019-2.293), age (aged 40 to 49 years, OR=4.971, 95%CI: 1.681-14.698; aged 50 to 59 years, OR=6.070, 95%CI: 2.045-18.020; aged 60 to 69 years, OR=6.902, 95%CI: 2.287-20.832; aged 70 to 79 years, OR=6.954, 95%CI: 2.191-22.070) and hypertension (OR=1.906, 95%CI: 1.337-2.718) were the factors affecting the awareness of diabetes. Age (aged 40 to 49 years, OR=4.699, 95%CI: 1.594-13.855; aged 50 to 59 years, OR=5.990, 95%CI: 2.023-17.732; aged 60 to 69 years, OR=7.134, 95%CI: 2.370-21.470; aged 70 to 79 years, OR=6.639, 95%CI: 2.102-20.964) and hypertension (OR=1.857, 95%CI: 1.304-2.645) were the factors affecting the treatment of diabetes. Age (aged 40 to 49 years, OR=2.948, 95%CI: 1.349-6.438; aged 60 to 69 years, OR=2.344, 95%CI: 1.049-5.234) was the factor affecting the control of diabetes. Conclusions The prevalence rate of diabetes among residents in Fangshan District was high, and the improvements of awareness rate, treatment rate and control rate were not obvious. Health education and management of diabetes should be strengthened for elderly, hypertensive and dyslipidemic residents.

Objective To establish a safe disposal management program for home used sharps waste of insulin injection so as to provide a reference for the standardised management of sharps waste after insulin.injection.Methods Based on the model of information-motivation-behavioural skills,the safe disposal management program for insulin needles used at home was developed by literature reviews and semi-structured interviews to investigate the perceptions and requirements of patients.The program was then modified and refined by two rounds of expert consultation with Delphi method.Results The effective retrieval rates of questionnaire for two rounds of expert consultations were 88.89%and 93.75%,with an expert authority coefficient at 0.93.In the second round,the mean importance scores of the items were 4.40 to 5.00,with a coefficient of variation ranged from 0 to 0.168.The established program consisted of three primary items,six secondary items,and 20 tertiary items.Conclusion The safe disposal management program for home used sharps waste of insulin injection established from the perspectives of information,motivation and behavioural skills was scientific and practical,which offered a guidance to healthcare professionals in the clinical practices.