ObjectiveBased on the clinical characteristics of chronic gouty arthritis （CGA） in both traditional Chinese and western medicine， this study aims to systematically evaluate the clinical concordance of existing CGA animal models， providing recommendations for establishing animal models that align with the pathological characteristics of CGA and the manifestations of traditional Chinese medicine syndromes. MethodsBy comprehensively retrieving Chinese and international databases such as China National Knowledge Infrastructure， Wanfang， VIP Chinese Science and Technology Periodical Database （VIP）， and PubMed， all relevant literature on CGA animal models was collected. Based on the guidelines， the diagnostic criteria of both traditional Chinese and western medicine were summarized and organized. The evaluation indicators for the CGA model were constructed with reference to existing evaluation modes， and the CGA animal models were analyzed to systematically evaluate the clinical concordance of existing models. ResultsThe current methods used to construct CGA animal models mainly include monosodium urate crystal induction， high-protein diet induction （poultry lack urate oxidase）， and high-fat diet combined with urate oxidase inhibitors and joint injection. Based on 11 pieces of included literature， the traditional Chinese and western medicine scoring data of each model were extracted， and the average scoring values of all models were ultimately calculated. The results show that the average clinical concordances of existing CGA animal models in both traditional Chinese and western medicine are 43.33% and 64.44%， respectively. Among them， the model with the highest clinical concordance rate is the one with a high-fat diet combined with potassium oxonate to induce hyperuricemia plus joint injection， achieving 83.33% clinical concordance in western medicine and 60% in traditional Chinese medicine. This model aligns well with the pathogenic characteristics and pathological changes of clinical CGA. ConclusionAlthough current CGA animal models can simulate some pathological characteristics of CGA， they struggle to comprehensively reflect the complex pathological processes of CGA and the characteristics of traditional Chinese medicine syndromes. Therefore， in the future， it is necessary to establish the CGA animal models that incorporate the clinical disease and syndrome characteristics of traditional Chinese and western medicine and formulate the uniform model evaluation criteria， providing more precise tools for CGA mechanism research and the development of traditional Chinese medicine.

ObjectiveTo evaluate the therapeutic effect of Huazhuo SanJie Chubi presciption （HSCD） on chronic gouty arthritis （CGA） rats with low-grade inflammation and to explore the underlying mechanism with a focus on macrophage polarization. MethodsThe 41 male 6-week-old SD rats were randomly allocated， using the random number table， to a normal group （n=8） and a model group （n =33）. CGA with low-grade inflammation was induced in the model group by daily gavage of potassium oxonate （250 mg·kg^-1·d^-1） and hypoxanthine （300 mg·kg^-1·d^-1）， combined with intra-articular injection of a monosodium urate （MSU） crystal suspension （50 μL， 25 g·L^-¹） into the left ankle twice weekly. After 4 weeks of modeling， 3 rats were randomly selected from each group for model validation. The remaining successfully modeled rats were randomly divided into a model group， an HSCD group （10.35 g·kg^-1·d^-1， gavage once daily）， an M1 polarization agonist group （L-methionine sulfoximine， 300 mg·kg^-1， subcutaneous injection every other day）， an M1 polarization agonist + HSCD group， an M2 polarization inhibitor group （PD0325901， 10 mg·kg^-1·d^-1， gavage once daily）， and M2 polarization inhibitor + HSCD group. The corresponding drug or drug combination was administered according to group assignment， whereas rats in the normal and model groups received 0.5% carboxymethyl cellulose sodium （CMC-Na） vehicle （10.35 g·kg^-1·d^-1， gavage once daily）. All interventions were continued for four weeks. During the intervention period， except for the normal group， potassium oxonate （250 mg·kg⁻¹） and hypoxanthine （300 mg·kg^-1） were co-administered by gavage every other day to maintain the model. At the end of treatment， serum uric acid （SUA）， ankle joint diameter and joint swelling index were measured. The levels of high-sensitivity C-reactive protein （hs-CRP）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， chemokine C-C motif ligand 2 （CCL2）， S100 calcium-binding protein A8/A9 （S100A8/A9）， interleukin-10 （IL-10） and arginase-1 （Arg-1） in serum and joint fluid were determined by enzyme-linked immunosorbent assay （ELISA）. High-frequency ultrasound was used to assess MSU deposition in the ankle joint. Hematoxylin-eosin （HE） staining was performed to evaluate synovial histopathological changes. Quantitative Real-time PCR and immunofluorescence were used to detect the mRNA and protein expression of the M1 macrophage polarization markers inducible nitric oxide synthase （iNOS） and the M2 macrophage polarization marker scavenger receptor cysteine-rich type 1 protein M130 （CD163） in synovial tissue. ResultsCompared with the normal group， the model group showed significantly elevated SUA level and joint swelling index， and increased levels of pro-inflammatory cytokines， CCL2， and S100A8/A9 in both serum and joint fluid （P<0.05）， accompanied by MSU deposition and synovial inflammation in the ankle joint. The mRNA and protein expression levels of macrophage polarization M1/M2 markers iNOS and CD163 in synovial tissues were also significantly up-regulated （P<0.05）. Compared with model group， rats in HSCD group had significantly lower SUA levels， attenuated joint swelling， reduced serum levels of pro-inflammatory cytokines， and decreased levels of CCL2 and S100A8/A9 in both serum and joint fluid， accompanied with alleviated MSU deposition and synovial inflammation （P<0.05）. HSCD markedly downregulated the mRNA and protein expression of M1 marker iNOS （P<0.05）， whereas it had no significant effect on the expression of M2 marker CD163. Compared with the M1 polarization agonist group， the M1 polarization agonist + HSCD group showed significantly reduced joint swelling， lower serum levels of pro-inflammatory cytokines， and decreased levels of CCL2 and S100A8/A9 in joint fluid （P<0.05）. In addition， synovial inflammatory cell infiltration and angiogenesis were attenuated， and iNOS mRNA and protein expression levels were significantly reduced （P<0.05）. Compared with the M2 polarization inhibitor group， the M2 polarization inhibitor + HSCD group exhibited reduced joint swelling， decreased levels of CCL2 and S100A8/A9 in joint fluid and ameliorated synovial inflammation （P<0.05）， whereas the levels of anti-inflammatory mediators （IL-10， Arg-1） and CD163 mRNA and protein expression were not significantly increased. ConclusionHSCD alleviates low-grade inflammation in CGA rats， at least in part， by inhibiting macrophage polarization toward the M1 phenotype.

ObjectiveThis paper aims to observe the effect of Huazhuo Sanjie Chubi prescription （HSCD） on the gouty bone erosion model rats and investigate its action mechanism. MethodsThirty-six two-month-old male SD rats were randomly divided into the blank group with nine rats and the modeling group with 27 rats. The rats in the modeling group were administered hypoxanthine solution at 300 mg·kg^-1·d^-1 and potassium oxonate solution at 250 mg·kg^-1·d^-1， combined with intra-articular injection of 200 μL monosodium urate （MSU） crystal suspension at 25 g·L^-1 into the right ankle joint （joint injection once every three days）， so as to induce the gouty bone erosion model. After four weeks of modeling， three rats were selected from these two groups to validate the model. The modeled 24 rats were randomly divided into the model group， HSCD group （10.35 g·kg^-1·d^-1）， allopurinol group （20 mg·kg^-1·d^-1）， and inhibitor group （LY294002， 10 mg·kg^-1·d^-1）， with six rats per group. Except for the blank group， rats in all other groups continued to receive hypoxanthine solution at 300 mg·kg^-1 and potassium oxonate solution at 250 mg·kg^-1 via gavage concurrently with administration to maintain modeling intervention. The rats in the HSCD group and allopurinol group received administration by gavage at the above doses. The rats in the inhibitor group received an intraperitoneal injection at the above dose. The rats in the blank group and model group received saline （10.35 g·kg^-1·d^-1） by gavage for four consecutive weeks. After administration， ankle joint swelling of the rats in all groups was observed， and the diameters were measured. Bone volume fraction （BV/TV） and bone surface area to bone volume （BS/BV） were observed and quantitatively analyzed by Micro-CT. Histopathological changes in the ankle joint were observed by hematoxylin-eosin （HE） staining and safranin O-fast green staining. The uric acid in the rats' serum was determined by enzyme colorimetry. The levels of inflammatory factors， including tumor necrosis factor-α （TNF-α）， interleukin （IL）-1β， and IL-6 were measured by enzyme-linked immunosorbent assay （ELISA）. The protein expressions of receptor activator of nuclear factor-κB ligand （RANKL） and phosphorylated （p）-phosphatidylinositol-3-kinase （PI3K） in ankle joint tissues of rats were detected by immunofluorescence staining. The mRNA levels of the proteins related to the bone erosion， including RANKL， tartrate-resistant acid phosphatase （TRAP）， cathepsin K （CTSK）， and matrix metalloproteinase-9 （MMP-9） in the ankle joint tissues of rats were determined by real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. The expressions of the proteins related to the bone erosion， including RANKL， CTSK， TRAP， MMP-9， and the proteins related to the PI3K/protein kinase B （Akt） signaling pathway， including PI3K， Akt， mammalian target of rapamycin （mTOR）， p-PI3K， phosphorylated protein kinase B （p-Akt）， and phosphorylated mammalian target of rapamycin （p-mTOR）， were detected by Western blot. ResultsCompared with the blank group， the modeling group showed marked ankle swelling and increased diameter. Micro-CT revealed an uneven articular surface and honeycomb-like bone erosion in the ankle joint. Quantitative analysis showed decreased BV/TV and increased BS/BV （P<0.05）. HE staining revealed a narrowed joint space， rough and discontinuous cartilage surfaces， reduced and unevenly distributed chondrocytes， partial hypertrophy， and blurred tidemarks， confirming successful model establishment. After four weeks of intervention， compared with those in the blank group， the rats in the model group exhibited severe ankle swelling and increased diameters （P<0.05）. Micro‑CT showed that the ankle joint surface was irregular， and bone erosion exhibited a honeycomb‑like morphology. The microstructural parameters of the bone revealed a decreased BV/TV and an increased BS/BV （P<0.05）. Histopathological examination revealed a narrowed joint space and severe articular cartilage destruction. The levels of uric acid in the serum and inflammatory factors （IL-1β， IL-6， and TNF-α） were increased （P<0.05）. The mRNA and protein levels of the proteins related to bone erosion in joint tissue， including RANKL， CTSK， TRAP， and MMP-9， were upregulated （P<0.05）. The ratios of p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR in the proteins related to the PI3K/Akt signaling pathway were increased （P<0.05）. RANKL and p-PI3K protein fluorescence intensities were elevated （P<0.05）. Compared with those in the model group， the above indicators in all other administration groups showed varying degrees of improvement. The HSCD group and inhibitor groups exhibited more significant effects in reducing ankle swelling， improving bone erosion， bone microstructure （significant decrease in BV/TV and increase in BS/BV）， and the pathology of cartilage erosion， lowering inflammatory factor levels， downregulating the proteins related to the bone erosion， and suppressing activation of the PI3K/Akt/mTOR pathway （P<0.05）. The uric acid levels in rats' serum were reduced in both HSCD and allopurinol groups （P<0.05）. Compared with those in the HSCD group， the rats in the allopurinol group had larger ankle diameters （P<0.05）， more severe bone erosion and bone microstructure damage （P<0.05）， worse improvement of the pathology of cartilage erosion， higher levels of IL-6 and TNF-α （P<0.05）， elevated expressions of the proteins related to the bone erosion， higher expression ratio of proteins related to the PI3K/Akt signaling pathway （P<0.05）， and higher fluorescence intensities of RANKL and p-PI3K proteins （P<0.05）. The inhibitor group achieved comparable results to the HSCD group in improvements of bone microstructure and the reduction of IL-1β and IL-6， stronger suppression of TNF-α and PI3K/Akt/mTOR signaling pathway activation （P<0.05）， but weaker effects on cartilage repair and serum uric acid reduction （P<0.05）. ConclusionHSCD effectively reduces uric acid levels in serum， suppresses inflammatory factor secretion， and downregulates the expressions of proteins related to bone erosion， including RANKL， CTSK， TRAP， and MMP-9 in the joint tissues. Its action mechanism of improving gouty bone erosion may be associated with inhibition of the PI3K/Akt signaling pathway.

OBJECTIVE To observe the distribution and drug resistance of pathogens isolated from the neonates with purulent meningitis and analyze the risk factors for prognosis.METHODS A total of 80 neonates with puru-lent meningitis who were treated in Maternity and Child Care Center of Xinyu and Xinyu People's Hospital from Jan.2020 to Dec.2022 were recruited as the research subjects.The distribution and drug resistance of the patho-gens isolated from the patients were observed.The neonates were divided into the poor prognosis group with 31 cases and the favorable prognosis group with 49 cases according to the treatment outcomes at the discharge from the hospital.The clinical data were compared between the two groups.The risk factors for the prognosis were ana-lyzed.RESULTS Totally 84 strains of pathogens were isolated from 80 children,the gram-positive bacteria accoun-ted for 36.90％,mainly including Staphylococcus epidermidis,Staphylococcus haemolyticus,Staphylococcus saprophyticus and Staphylococcus hominis;The gram-negative bacteria accounted for 63.10％,mainly including Escherichia coli and Klebsiella pneumoniae.The drug resistance rates of the major species of gram-positive bacte-ria to oxacillin,penicillin,cefoxitin and clindamycin were high.The drug resistance rates of the major species of gram-negative bacteria to levofloxacin,gentamycin and ceftriaxone were high.The drug resistance rates of the K.pneumoniae strains to gentamycin,levofloxacin and tobramycin were high.The proportion of neonates with coma and the total protein level of cerebrospinal fluid were higher in the poor prognosis group than in the favorable prog-nosis group(P＜0.05);the cerebrospinal fluid glucose level of the poor prognosis group was lower than that of the favorable prognosis group(P＜0.05).Coma,high level of total protein in cerebrospinal fluid and low level of cere-brospinal fluid glucose were the risk factors for the poor prognosis(P＜0.05).CONCLUSIONS The gram-negative bacteria are dominant among the pathogens isolated from the neonates with purulent meningitis.The coma,total protein of cerebrospinal fluid and cerebrospinal fluid glucose are the risk factors for the poor prognosis.It is neces-sary for the hospital to rational use of antibiotics based on the results of culture of pathogens and drug susceptibili-ty testing and take intervention measures to the risk factors for the prognosis.

Objective To summarize the outcomes of a pricing reform pilot program in a tertiary hospital in Ningxia and offer relevant suggestions.Methods The key measures used in the hospital for adjusting and optimizing the medical revenue structure were summarized.Trend and ratio analysis was employed to compare the economic performance indicators before and af-ter the pilot reform.Results During the pilot period,key performance indicators for national tertiary public hospitals demonstra-ted steady improvements.Meanwhile,the annual growth rate of medical revenue was 4.7 percentage points lower than in 2019,with medical service revenue increased by 5.6 percentage points.Moreover,outpatient and inpatient costs per visit were lower than in same-level,same-type hospitals in the region and in provincial-level general hospitals nationwide.Unreasonable growth in total medical costs was effectively curbed,and the pricing ratio of medical services became more rational.Annual management re-duced drug,consumable,examination and testing revenue by 200 million yuan,while employee average wage income rose by 10.95％from 2019 and employee satisfaction reached 85.2％,ensuring the hospital's healthy and sustainable development.Conclusion The pricing reform pilot project implemented in Ninxia provides a reference for public hospitals to adjust and opti-mize their medical revenue structure.

Objective:To report two cases of anti-glomerular basement membrane (GBM) disease with IgA nephropathy (IgAN), and summarize the clinical characteristics of these patients through systematic literature review, for providing clinical data for the diagnosis and treatment of this disease.Methods:It was a case-series analysis. Clinical data of two cases with anti-GBM disease and IgAN diagnosed in the First Affiliated Hospital of Guangxi Medical University were collected. The course of their diagnosis and treatment was described. Besides, the relevant literature of anti-GBM disease with IgAN cases reported in PubMed and CNKI databases from the establishment of the database to June 30, 2024 were retrived, and the relevant clinical data were extracted for analysis and summary. Patients were divided into end-stage renal disease (ESRD) group and non-ESRD group according to renal outcome, and the differences in age, gender, hemoglobin, creatinine at diagnosis, proportion of hypuria/anuria, qualitative grade of urinary protein, and proportion of renal crescent were compared between the two groups.Results:Two patients were both young women. The pathology of renal tissue suggested crescentic glomerulonephritis. The pathological manifestations were linear deposition of IgG along GBM and deposition of immune complex dominated by IgA in mesangial region. At the initial diagnosis, the renal function damage of the case one was not severe. After plasma exchange, glucocorticoid and cyclophosphamide treatment, the renal function recovered. The kidney function of the case two was obviously impaired at the initial diagnosis, and was improved after the above treatment, but aggravated due to infection, and continued to progress into ESRD. Twenty-six literates involving 40 cases of anti-GBM disease with IgAN were retrieved. A total of 42 cases of anti-GBM disease with IgAN, including 2 cases in this report, were analyzed and summarized. The age was (41.3±17.5) years old, 45.2% were male, 39 cases (92.9%) were from Asia. The hemoglobin was (94.4±15.1) g/L, the serum creatinine was 450.8 (284.4, 755.8) μmol/L, 83.3% (35/42) patients had crescent ratio greater than 50% and 37 patients (88.1%) patients were treated with intravenous methylprednisolone and cytotoxic immunosuppressive drugs. Plasma exchange was performed in 34 patients (81.0%) patients, 23 patients (54.8%) had renal function recovered and 17 patients (40.5%) entered ESRD. Compared with the non-ESRD group, the serum creatinine in the ESRD group was higher at initial diagnosis ( P<0.01), and the proportion of hypuria/anuria was higher ( P=0.03). There were no statistically significant differences in age, sex, hemoglobin, urinary protein and crescent proportion between the two groups (all P>0.05). Conclusions:Compared with anti-GBM disease, anti-GBM with IgAN has a smoother course and a better prognosis. Infection should be actively prevented during treatment.

Objective:To report two cases of anti-glomerular basement membrane (GBM) disease with IgA nephropathy (IgAN), and summarize the clinical characteristics of these patients through systematic literature review, for providing clinical data for the diagnosis and treatment of this disease.Methods:It was a case-series analysis. Clinical data of two cases with anti-GBM disease and IgAN diagnosed in the First Affiliated Hospital of Guangxi Medical University were collected. The course of their diagnosis and treatment was described. Besides, the relevant literature of anti-GBM disease with IgAN cases reported in PubMed and CNKI databases from the establishment of the database to June 30, 2024 were retrived, and the relevant clinical data were extracted for analysis and summary. Patients were divided into end-stage renal disease (ESRD) group and non-ESRD group according to renal outcome, and the differences in age, gender, hemoglobin, creatinine at diagnosis, proportion of hypuria/anuria, qualitative grade of urinary protein, and proportion of renal crescent were compared between the two groups.Results:Two patients were both young women. The pathology of renal tissue suggested crescentic glomerulonephritis. The pathological manifestations were linear deposition of IgG along GBM and deposition of immune complex dominated by IgA in mesangial region. At the initial diagnosis, the renal function damage of the case one was not severe. After plasma exchange, glucocorticoid and cyclophosphamide treatment, the renal function recovered. The kidney function of the case two was obviously impaired at the initial diagnosis, and was improved after the above treatment, but aggravated due to infection, and continued to progress into ESRD. Twenty-six literates involving 40 cases of anti-GBM disease with IgAN were retrieved. A total of 42 cases of anti-GBM disease with IgAN, including 2 cases in this report, were analyzed and summarized. The age was (41.3±17.5) years old, 45.2% were male, 39 cases (92.9%) were from Asia. The hemoglobin was (94.4±15.1) g/L, the serum creatinine was 450.8 (284.4, 755.8) μmol/L, 83.3% (35/42) patients had crescent ratio greater than 50% and 37 patients (88.1%) patients were treated with intravenous methylprednisolone and cytotoxic immunosuppressive drugs. Plasma exchange was performed in 34 patients (81.0%) patients, 23 patients (54.8%) had renal function recovered and 17 patients (40.5%) entered ESRD. Compared with the non-ESRD group, the serum creatinine in the ESRD group was higher at initial diagnosis ( P<0.01), and the proportion of hypuria/anuria was higher ( P=0.03). There were no statistically significant differences in age, sex, hemoglobin, urinary protein and crescent proportion between the two groups (all P>0.05). Conclusions:Compared with anti-GBM disease, anti-GBM with IgAN has a smoother course and a better prognosis. Infection should be actively prevented during treatment.

Objective:To compare the dose-response effects of single-fraction ultra-high dose rate (FLASH) and conventional dose rate (CONV) whole abdominal irradiation (WAI) with X-rays on acute radiation-induced intestinal injury in mice, in order to identify optimal dose parameters and potential mechanisms.Methods:A total of 186 male C57BL/6J mice were randomly assigned to a non-irradiation group ( n=6), FLASH irradiation groups ( n=90), and CONV irradiation groups ( n=90). Acute radiation-induced intestinal injury models were established using single-fraction WAI with 11, 12, 13, 14, and 15 Gy X-rays (200 Gy/s for FLASH and 4 Gy/min for CONV). Changes in body weight, stool characteristics, and disease activity index (DAI) scores were assessed at 9 d post-irradiation. At 7 d post-irradiation at 11, 12, and 13 Gy, the intestines were collected for macroscopic examination and length measurement. The small intestine was selected for HE staining and quantitative analysis of intestinal crypt number and mucosal epithelial thickness. The survival of mice was assessed at 15 d post-WAI across all dose groups. Results:After single-fraction WAI at 11, 12, and 13 Gy, the body weight was higher in the FLASH group than that in the CONV group ( t=10.17, 12.65, 10.16, P<0.05). The DAI scores for the FLASH group were 1.00±1.10, 3.17±0.75, and 2.83±1.17, respectively, which were lower than those of the CONV group (4.33±0.52, 7.00±0.00, 8.60±0.55; t=8.70, 11.71, 14.99, P<0.05). However, after WAI at 14 Gy and 15 Gy, there were no significant differences in body weight and DAI between the FLASH group and the CONV group ( P>0.05). At 7 d after single-fraction WAI at 11, 12, and 13 Gy, mice in the FLASH group exhibited less intestinal congestion, edema, and shortening compared with the CONV group. The difference between the FLASH and CONV groups were statistically significant in small intestine length at 11 and 13 Gy ( t=4.42, 3.78, P<0.05), and in colorectal length at 11 and 12 Gy ( t=3.97, 3.12, P<0.05). Small intestine HE staining revealed superior preservation of intestinal architecture in the FLASH group compared with the CONV group, characterized by longer villi, increased crypt numbers, thicker mucosal epithelium, and enhanced structural integrity. The differences in crypt number and mucosal epithelial thickness were statistically significant ( tcrypt=13.10, 23.80, 11.90; tmucosal=5.75, 2.64, 7.74; P<0.05). At 15 d post-irradiation, the survival rate in the 15 Gy FLASH group was higher than that in the CONV group (50% vs. 10%, χ2=5.39, P<0.05), with a median survival extension of 6 d ( HR=0.340, 95% CI: 0.115 4-0.999 9). No significant survival differences were observed between the FLASH group and the CONV group at 11, 12, 13, and 14 Gy ( P>0.05). Conclusions:FLASH irradiation significantly alleviated acute radiation-induced intestinal injury from medium single-fraction WAI with 11, 12, and 13 Gy X-rays compared with CONV irradiation, and showed potential to improve mouse survival after single-fraction WAI at 15 Gy. This effect is likely associated with the preservation of intestinal crypts and exhibits a dose-dependent relationship.

The morbidity and mortality associated with diphtheria have been effectively managed through mass immunization strategies. Nevertheless, recent outbreaks of diphtheria have been reported in various regions of Africa and Asia. In addition to infections among children, there has been a notable increase in cases among middle-aged and elderly individuals, underscoring the necessity of continued vigilance in the control of diphtheria. This paper reviewed the epidemiology of diphtheria, the current application of vaccines, and immunization strategies, with the aim of providing evidence for the prevention and control of this disease.

Objective To investigate the neuroprotective effects and mechanisms of the alcoholic extract of the Yi drug(Rubia yunnanensis)on the Alzheimer's disease(AD)model of Caenorhabditis elegans(C.elegans).Methods Based on a transgenic C.elegans model of AD,the efficacy and mechanism of alcoholic extracts of Rubia yunnanensis against β-amyloid(Aβ)-induced toxic effects were explored.C.elegans were synchronized and divided into a control group and low and high dose groups of the alcoholic extract of Rubia yunnanensis to study the effects of the alcoholic extract of Rubia yunnanensis on C.elegans paralysis,lifespan,lipofuscin levels,behavior,growth and development,heat stress and oxidative stress,ROS levels,and Aβ aggregation,as well as the key transcription factors in the insulin/insulin-like growth factor 1 signaling pathway were investigated by GFP reporter gene worm assay and RNAi assay DAF-16 expression.Results Compared with the Control group,the intervention of the alcoholic extracts of Rubia yunnanensis could effectively improve the paralyzed phenotype of C.elegans(P<0.001),prolong the lifespan of C.elegans and reduce the level of lipofuscin in C.elegans significantly(P<0.001),improve the mobility of C.elegans significantly(P<0.001),and improve its resistance to oxidative stress and heat stress damage significantly(P<0.001),and reduce the level of ROS in C.elegans significantly(P<0.001),and reduce the deposition of Aβ protein in the head of C.elegans significantly(P<0.01),and had no effect on the growth and development of C.elegans(P>0.05),and also promoted the nuclear translocation of DAF-16 in the reporter gene C.elegans TJ356,and the effect of the alcoholic extracts of Rubia yunnanensis in delaying the degree of paralysis of C.elegans was lost after silencing the expression of C.elegans DAF-16 by RNAi,whereas the L4440 empty vector control group in the administration of Rubia yunnanensis alcohol extract significantly reduced the level of C.elegans paralysis(P<0.001).Conclusion The alcoholic extract of Rubia yunnanensis can significantly ameliorate the paralyzed phenotype in the C.elegans model of Alzheimer's disease with certain antioxidant,anti-aging and anti-Aβ protein activities,and the mechanism may be related to the activation of DAF-16,a downstream transcription factor of the insulin signaling pathway.