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

ObjectiveTo investigate the effects of Huayu Jiedu prescription on brain microvascular endothelial cells （BMECs） after oxygen-glucose deprivation （OGD） injury and to explore its intervention mechanisms. MethodsThe cell counting kit-8 （CCK-8） assay was used to determine the optimal OGD duration and the effective concentration of Huayu Jiedu prescription-containing serum. Cells were randomly divided into the blank serum medium group （KBXQ）， model group （OGD）， HYXQ group （OGD + Huayu Jiedu prescription-containing serum）， and 3-methyladenine （3-MA） group （OGD + 3-MA）. Cell morphology was observed under an inverted microscope. The numbers of autophagosomes and autolysosomes in cells were observed by transmission electron microscopy. Cell viability was determined using the CCK-8 assay. Cell apoptosis rate was detected using the TdT-mediated dUTP nick-end labeling （TUNEL） assay. The expression levels of microtubule-associated protein 1 light chain 3 （LC3） and Occludin were detected by immunofluorescence. The permeability of the cell monolayer was also measured. Cells were further randomly divided into the KBXQ group， model group （OGD）， HYXQ group， phosphatidylinositol-3 kinase （PI3K） inhibitor （LY294002） group （OGD + LY294002）， and HYXQ + LY294002 group （OGD + Huayu Jiedu prescription-containing serum + LY294002）. Western blot analysis was used to detect the expression levels of the autophagy-related key molecule yeast Atg6 homolog 1 （Beclin1）， LC3Ⅱ/LC3Ⅰ， selective autophagy adaptor protein （p62）， Occludin， phosphorylated （p）-PI3K， PI3K， phosphorylated protein kinase B （p-Akt）， Akt， phosphorylated mammalian target of rapamycin （p-mTOR）， and mTOR. ResultsOGD for 6 h was selected as the optimal modeling condition， and 5% was determined as the optimal volume fraction of Huayu Jiedu prescription-containing serum. Compared with the KBXQ group， the model group showed obvious cell damage under the inverted microscope， and transmission electron microscopy revealed markedly increased numbers of autophagosomes and autolysosomes. Cell viability was significantly decreased （P<0.01）， apoptosis rate was significantly increased （P<0.01）， LC3 fluorescence intensity was significantly increased （P<0.01）， Occludin fluorescence intensity was significantly decreased （P<0.01）， and monolayer permeability was significantly increased （P<0.01）. Compared with the model group， cell damage in the HYXQ group and the 3-MA group was significantly improved， the numbers of autophagosomes and autolysosomes were markedly reduced， cell viability was significantly increased （P<0.01）， apoptosis rate was significantly decreased （P<0.01）， LC3 fluorescence intensity was significantly decreased （P<0.01）， Occludin fluorescence intensity was significantly increased （P<0.01）， and monolayer permeability was reduced （P<0.05）. Western blot results showed that， compared with the KBXQ group， the model group exhibited significantly increased expression of Beclin1 and LC3Ⅱ/LC3Ⅰ （P<0.01）， while the expression levels of p62， Occludin， p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR were significantly decreased （P<0.01）. Compared with the model group， the HYXQ group showed significantly decreased expression of Beclin1 and LC3Ⅱ/LC3Ⅰ （P<0.01） and significantly increased expression of p62， Occludin， p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR （P<0.01）. In the LY294002 group， Beclin1 and LC3Ⅱ/LC3Ⅰ expression were significantly increased （P<0.05， P<0.01）， whereas the expression levels of p62， Occludin， p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR were significantly decreased （P<0.01）. Compared with the LY294002 group， the HYXQ + LY294002 group showed significantly decreased expression of Beclin1 and LC3Ⅱ/LC3Ⅰ （P<0.01） and significantly increased expression of p62， Occludin， p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR （P<0.01）. ConclusionHuayu Jiedu prescription has a protective effect on BMECs after OGD injury， which may be achieved by activating the PI3K/Akt/mTOR autophagy-related signaling pathway and inhibiting excessive autophagy， thereby protecting Occludin protein expression and endothelial barrier function.

BACKGROUND:Although previous studies have reported associations between lipids and the risk of osteoporotic pathological fractures,the specific causal relationships between lipid level and osteoporotic pathological fractures remain unclear.OBJECTIVE:To elucidate the causal relationship between lipids and osteoporotic pathological fractures using a two-sample bidirectional Mendelian randomization analysis.METHODS:The data for 178 lipid metabolites were obtained from the IEU-GWAS database(developed by the MRC Integrative Epidemiology Unit at the University of Bristol,UK,which provides extensive summary data from genome-wide association studies),while osteoporotic pathological fracture data(from 173 619 European participants)were acquired from the FinnGen database(constructed by the Finnish national gene research program,focusing on investigating relationships between genomics and health/disease in the Finnish population).Osteoporotic pathological fracture data were used as the outcome variable,with lipids serving as exposures,for the bidirectional Mendelian randomization study to evaluate the causal effects of different lipids on osteoporotic pathological fractures.The UK Biobank database was employed as a validation set by switching the outcome variable to verify the findings horizontally.RESULTS AND CONCLUSION:(1)The inverse variance weighted analysis indicated that each unit increase in sterol ester(27∶1/20∶2)levels was associated with a 25.55％increase in the risk of osteoporotic pathological fractures(odds ratio=1.256,95％confidence interval:1.001-1.575,P=0.049),suggesting a significant positive correlation between elevated sterol ester levels and increased fracture risk.Reverse Mendelian randomization analysis revealed a significant negative association between osteoporotic pathological fractures and three types of phosphatidylcholine.Horizontal validation yielded consistent results,confirming sterol ester as a risk factor for osteoporotic pathological fractures.(2)The results indicate that sterol ester is a risk factor for osteoporotic pathological fractures,while phosphatidylcholine serves as a protective factor.These findings strengthen the evidence supporting the effect of lipids on the risk of osteoporotic pathological fractures.Although the GWAS data used in this study were derived from European populations,given the broad commonality of human genetics,the results provide valuable reference significance for improving osteoporosis in Chinese populations through lipid regulation.

BACKGROUND:Although previous studies have reported associations between lipids and the risk of osteoporotic pathological fractures,the specific causal relationships between lipid level and osteoporotic pathological fractures remain unclear.OBJECTIVE:To elucidate the causal relationship between lipids and osteoporotic pathological fractures using a two-sample bidirectional Mendelian randomization analysis.METHODS:The data for 178 lipid metabolites were obtained from the IEU-GWAS database(developed by the MRC Integrative Epidemiology Unit at the University of Bristol,UK,which provides extensive summary data from genome-wide association studies),while osteoporotic pathological fracture data(from 173 619 European participants)were acquired from the FinnGen database(constructed by the Finnish national gene research program,focusing on investigating relationships between genomics and health/disease in the Finnish population).Osteoporotic pathological fracture data were used as the outcome variable,with lipids serving as exposures,for the bidirectional Mendelian randomization study to evaluate the causal effects of different lipids on osteoporotic pathological fractures.The UK Biobank database was employed as a validation set by switching the outcome variable to verify the findings horizontally.RESULTS AND CONCLUSION:(1)The inverse variance weighted analysis indicated that each unit increase in sterol ester(27∶1/20∶2)levels was associated with a 25.55％increase in the risk of osteoporotic pathological fractures(odds ratio=1.256,95％confidence interval:1.001-1.575,P=0.049),suggesting a significant positive correlation between elevated sterol ester levels and increased fracture risk.Reverse Mendelian randomization analysis revealed a significant negative association between osteoporotic pathological fractures and three types of phosphatidylcholine.Horizontal validation yielded consistent results,confirming sterol ester as a risk factor for osteoporotic pathological fractures.(2)The results indicate that sterol ester is a risk factor for osteoporotic pathological fractures,while phosphatidylcholine serves as a protective factor.These findings strengthen the evidence supporting the effect of lipids on the risk of osteoporotic pathological fractures.Although the GWAS data used in this study were derived from European populations,given the broad commonality of human genetics,the results provide valuable reference significance for improving osteoporosis in Chinese populations through lipid regulation.

ObjectiveTo explore the regulation of hypothalamic-pituitary-gonadal （HPG） axis by modified Erxian decoction in rats with perimenopausal syndrome （PMS） and to further analyze the expression of proteins related to the silent information regulator 1 （SIRT1）/hypothalamic kisspeptin （Kisspeptin）/gonadotropin-releasing hormone （GnRH） signaling pathway in the arcuate nucleus region （ARC） of the hypothalamus， so as to reveal the potential target of action and molecular biological mechanism of modified Erxian decoction for the treatment of perimenopausal syndrome. MethodsAn animal model was established via the incomplete castration method， with successful modeling confirmed by the exfoliated cervical cell smear method. The 48 rats were divided into six groups based on the randomization principle after successful modeling， including a sham operation group， a model group， an estradiol valerate group （0.09 mg∙kg^-1∙d^-1）， high-， medium-， and low-dose modified Erxian decoction groups （7.614， 3.807，1.903 5 g∙kg^-1∙d^-1）， with 8 rats in each group. The estradiol valerate group and the high-， medium- and low-dose modified Erxian decoction groups were continuously administered by gavage for 28 days， and the indicators were detected 24 hours after the last administration. Body weights and uterine indices were measured. The pathological changes of the uterus were observed by hematoxylin-eosin （HE） staining. Enzyme-linked immunosorbent assay （ELISA） was performed to measure the levels of estradiol （E₂）， follicle-stimulating hormone （FSH）， luteinizing hormone （LH）， and gonadotropin-releasing hormone （GnRH）. Real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot were used to determine the expression levels of SIRT1， Kisspeptin， kisspeptin receptor （GPR54）， and GnRH in the ARC region of the hypothalamus and gonadotropin-releasing hormone receptor （GnRH-R） in pituitary. ResultsCompared with the sham operation group， rats in the model group had a significantly increased body weight （P0.01）， reduced wet weight and index of uterus （P0.01）， endometrial thinning or atrophy， glandular atrophy， and a decreasing number of glands. Additionally， serum levels of E₂ and the expression of SIRT1 in the ARC region of the hypothalamus significantly decreased （P0.01）. Serum levels of FSH， LH， and GnRH， the expression of Kisspeptin， GPR54， and GnRH in the ARC region of the hypothalamus， and GnRH-R in pituitary significantly increased （P0.01）. Compared with the model group， the estradiol valerate group and the high-， medium-dose modified Erxian decoction groups had significantly reduced body weight， serum levels of FSH， LH， and GnRH， and expression of Kisspeptin， GPR54， and GnRH in the ARC region of the hypothalamus and GnRH-R in pituitary （P0.05， P0.01） and significantly increased wet weight and index of uterus， serum level of E₂， and expression of SIRT1 in the ARC region of the hypothalamus （P0.05， P0.01）. In addition， they showed thickened endometrium， increased number of endometrial glands， and improved glandular atrophy. ConclusionModified Erxian decoction regulates the function of the HPG axis through multi-targets， and its mechanism of action may be related to the up-regulation of the expression of SIRT1 in the ARC region of the hypothalamus， the inhibition of the over-activation of the Kisspeptin/GnRH signaling pathway， the regulation of the expression of GnRH-R in the pituitary， the restoration of secretion balance of gonadotropins， and the elevation of the estrogen level. This study provides an experimental basis for the interpretation of the scientific connotation of modified Erxian decoction in the treatment of perimenopausal syndrome and a theoretical reference for the development of a novel therapeutic strategy based on the SIRT1/Kisspeptin/GnRH pathway.

Objective: To examine the causal relationship between inflammatory cytokines and premature ovarian insufficiency (POI) using bidirectional Mendelian randomization (MR) approach, so as to provide the basis for the prevention and treatment of POI. Methods: The data for 91 inflammatory cytokines were sourced from the IEU OpenGWAS database, comprising 14 824 participants. GWAS data for POI were sourced from the FinnGen database, including 118 484 individuals (among which 254 were POI cases). MR analysis was performed using the inverse variance weighted (IVW) method with inflammatory cytokines as exposure and POI as the outcome for forward MR analysis and POI as the exposure and inflammatory cytokines as outcome for reverse MR analysis. Sensitivity analysis were conducted using Cochran's Q test, MR-Egger regression, and the MR-PRESSO test. Results: Forward MR analysis demonstrated statistically significant associations between POI and interleukin-10 (OR=0.410, 95%CI: 0.233-0.721), interleukin-33 (OR=2.826, 95%CI: 1.228-6.504), C-C motif chemokine ligand 19 (OR=0.583, 95%CI: 0.364-0.932), monocyte chemoattractant protein-3 (OR=0.559, 95%CI: 0.335-0.936), interleukin-18 receptor 1 (OR=1.370, 95%CI: 1.030-1.821), and interleukin-13 (OR=1.990, 95%CI: 1.034-3.832). Reverse MR analysis revealed significant negative associations between POI and 15 inflammatory cytokines, including C-C motif chemokine ligand 23 (OR=0.981, 95%CI: 0.968-0.994) and axin-1 (OR=0.978, 95%CI: 0.963-0.994). Sensitivity analysis showed no evidence of heterogeneity or horizontal pleiotropy (all P>0.05). Conclusion Elevated levels of interleukin-33, interleukin-18 receptor 1 and interleukin-13 were associated with an increased risk of POI, while POI may be associated with decreased levels of 15 inflammatory cytokines including C-C motif chemokine ligand 23 and axin-1.

Objective To investigate the relationships of serum amyloid A(SAA),eotaxin and pentraxin 3(PTX3)levels with Mycoplasma pneumoniae DNA(MP-DNA)level,lung function and prognosis in children with Mycoplasma pneumoniae pneumonia(MPP).Methods A total of 163 chil-dren with MPP were enrolled in MPP group and divided into good prognosis group(n=109)and poor prognosis group(n=54)based on prognosis;another 124 healthy children with physical examinations in the same period were included as control group.Levels of serum SAA,eotaxin and PTX3 were measured in the children.Multivariable Logistic regression analysis was conducted to explore risk fac-tors for poor prognosis in children with MPP.Results Compared with the control group,the MPP group had significantly increased levels of SAA,eotaxin,PTX3 and MP-DNA positivity(P＜0.01);the MPP group also had significantly lower values of peak expiratory flow(PEF),forced expiratory volume in the first second(FEV1),forced vital capacity(FVC),tidal expiratory flow time to total expiratory time(tPTEF/TE),and tidal volume compared with the control group(P＜0.01).Compared with the good prognosis group,the poor prognosis group had significantly increased MP-DNA level,SAA,eotaxin and PTX3 levels,as well as decreased values of PEF,FEV1,FVC,tPTEF/TE and tidal volume(P＜0.01).Multivariable Logistic regression analysis showed that high MP-DNA lev-el,high SAA,eotaxin and PTX3 levels,low values of PEF,FEV1,FVC,tPTEF/TE and tidal vol-ume were risk factors for poor prognosis in children with MPP(P＜0.01).The SAA,PTX3 and eotaxin levels in children with MPP were positively correlated with their MP-DNA level and negative-ly correlated with lung function indicators(P＜0.05).Conclusion SAA,PTX3 and eotaxin lev-els are positively correlated with MP-DNA level and negatively correlated with lung function indica-tors in children with MPP.SAA,PTX3 and eotaxin levels can be used to assess the prognosis of children with MPP.

Objective:To investigate the anatomical feasibility of the endoscopic transorbital approach (ETOA) to the orbital apex and lateral middle cranial fossa, to identify stable and recognizable surgical landmarks under endoscopic visualization, and to provide morphometric data for preoperative planning and intraoperative navigation.Methods:Stepwise anatomical dissection was performed on five formalin-fixed cadaveric heads and one fresh arterially injected cadaveric specimen to simulate the ETOA using a 0° endoscope. Key structures and their anatomical relationships were observed and recorded. Additionally, high-resolution CT scans of 50 adults were retrospectively analyzed. Three-dimensional reconstructions and measurements were performed using Mimics 17.0 software. Spatial validation was performed using 17 dry skulls to verify the consistency and reliability of osseous anatomical landmarks.Results:Cadaveric dissection identified the meningo-orbital band, superior orbital fissure, optic canal, foramen rotundum, and foramen ovale as reliable surgical landmarks for the ETOA. A topographic map of the surgical region was established based on the endoscopic view. CT measurements revealed the following distances (Mean±SD): the midpoint of the supraorbital rim to the foramen rotundum (57.31±3.59) mm and foramen ovale (71.46±3.42) mm; the lateral orbital rim to the lateral edge of the superior orbital fissure (37.38±2.52) mm; the distance from the superior orbital fissure to the optic canal (9.98±1.49) mm; and the distance from the anterior ethmoidal artery to the optic canal (19.98±2.05) mm. These measurements were consistent with dry skull data, indicating that these osseous landmarks had stable spatial relationships and were suitable for intraoperative localization.Conclusions:The ETOA provides favorable anatomical accessibility and clinical feasibility for lesions involving the orbital apex and lateral skull base. Key osseous structures demonstrate high identifiability and stable spatial relationships, serving as critical references for intraoperative navigation and preoperative pathway planning. The quantitative anatomical framework established in this study provides critical morphometric support for minimally invasive surgery targeting lesions in this region.

Objective To investigate the effects of Zuogui Jiangtang Tongmai Prescription on short-chain fatty acids(SCFAs)and G protein-coupled receptor 109A(GPR109A)in diabetic atherosclerotic mice;To explore its mechanism of improving diabetic atherosclerosis.Methods ApoE-/-mice were fed with high sugar and high fat diet and intraperitoneal injection of streptozotocin to establish atherosclerosis model of diabetes.After modeling,the mice were randomly divided into the model group,Western medicine group(metformin hydrochloride+atorvastatin),and Zuogui Jiangtang Tongmai Prescription low-,medium-and high-dosage groups(19,38,76 g/kg);and the other C57BL/6J mice were set as the control group,with 6 mice in each group.Each group was given solution for gavage,once a day for 4 weeks.Blood glucose of the mice were detected,HE staining was used to observe the morphology of the aorta,TG,TC,LDL-C and HDL-C contents were detected by fully automated biochemistry analyzers,ELISA was used to detect the contents of serum HbA1c,fasting insulin(FINS),interleukin(IL)-1β,IL-6 and tumor necrosis factor(TNF)-α,gas chromatography was used to detect the content of intestinal SCFAs,and RT qPCR and Western blot were used to detect the mRNA and protein expressions of GPR109A in ileal tissue and nuclear factor(NF)-κB p65 in aortic tissue,respectively.Results Compared with the control group,obvious plaques and inflammatory cells infiltration were seen in the aorta of the model group,the blood glucose and serum HbA1c,TG,TC,LDL-C,IL-1β,IL-6 and TNF-α contents increased(P<0.01),FINS and HDL-C content decreased(P<0.01),intestinal acetate,propionate,butyric acid,isobutyric acid and isovaleric acid contents decreased(P<0.01),GPR109A mRNA and protein expression in ileal tissue decreased,NF-κB p65 mRNA and protein expression in aortic tissue increased(P<0.01).Compared with the model group,the aortic plaque area and inflammatory cells infiltration were significantly improved in each drug intervention group,the blood glucose and serum HbA1c,TG,TC,LDL-C,IL-1β,IL-6 and TNF-α contents decreased(P<0.05,P<0.01);the FINS and HDL-C content increased(P<0.05,P<0.01),intestinal acetic,propionic,butyric acid,isobutyric acid and isovaleric acid contents increased(P<0.05,P<0.01),GPR109A mRNA and protein expression in ileal tissue increased and NF-κB p65 mRNA and protein expression in ileal tissue decreased decreased(P<0.05,P<0.01).Conclusion Zuogui Jiangtang Tongmai Prescription can improve glucolipid metabolism and inflammatory response in diabetic atherosclerotic mice,which may be related to regulating SCFAs/GPR109A pathway.

Objective:To investigate the effect and mechanism of Jiedu Xiaoying Patch in rats with Hashimoto's thyroiditis (HT).Methods:Totally 32 rats were randomly divided into a blank group of 8 rats and a model group of 24 rats. The HT rat model was prepared by freely drinking 0.064% sodium iodide solution in the modeling module. 24 successfully modeled rats were randomly divided into model group, selenium yeast group, and patch group, with 8 rats in each group. Starting from the 9th week, the application group applied Jiedu Xiaoying Patch to the surface projection area of the thyroid gland in the neck of rats for 6 hours, once a day, for a total of 6 weeks; the selenium yeast group was orally administered with 21 μg/ml selenium yeast solution at a dose of 0.5 ml/100 g, while the blank group, model group, and patch group were orally administered with equal volumes of physiological saline solution once a day for a total of 6 weeks. The levels of TGAb,TPOAb, Sema 5A, and IL-17A in rat serum were detected by ELISA. The changes of thyroid tissue was observed with HE staining. The relative expression levels of plexin-A1 and plexin-B3 were determined through RT-PCR.Results:Compared with the model group, the levels of TPOAb, TGAb, Sema 5A, and IL-17A decreased ( P<0.05), and the expressions of plexin-A1 and plexin-B3 decreased in the selenium yeast group and the patch group ( P<0.05). The thyroid follicles in the model group were severely damaged, with a large number of lymphocytes infiltrating the interstices; the thyroid follicular structure of the selenium yeast group was relatively intact, and lymphocyte infiltration was reduced compared to the model group. The thyroid follicular structure of the patch group was basically intact, with a small amount of lymphocyte infiltration observed. Conclusion:Jiedu Xiaoying Patch can significantly reduce the levels of TPOAb and TGAb in HT rats. The mechanism may be related to reducing the content of Sema 5A, inhibiting the expressions of receptors plexin-A1 and plexin-B3, reducing the production of inflammatory cytokines such as IL-17A, and inhibiting immune and inflammatory responses.