ObjectiveTo investigate whether macrophage lipolysis-stimulated lipoprotein receptor （LSR） deficiency affects the progression of metabolic dysfunction-associated steatohepatitis （MASH） by activating the Yes-associated protein （YAP） signaling pathway. MethodsMale wild-type （WT） mice and macrophage-specific Lsr knockout （Lsr^MφKO， KO） mice， with an age of 8 weeks and similar body weights， were selected and fed with a normal diet， a high-fat diet （HFD）， or a high-fat high-cholesterol （HFHC） diet for 30 weeks. HE staining and oil red O staining were used to evaluate liver pathological changes； immunofluorescent staining was used to measure the expression levels of F4/80 and α-smooth muscle actin； RT-qPCR and Western blot were used to measure the levels of markers associated with lipid metabolism， inflammation， and fibrosis. Bone marrow transplantation rescue experiments （WT→KO vs KO→KO groups） were conducted to explore the functional role of LSR in macrophages. At the cellular level， hepatic macrophages were isolated from WT and KO mice to measure the expression levels of YAP signaling pathway-related proteins and their downstream target genes， and in addition， these cells were treated in vitro with verteporfin （VP）， a specific inhibitor of YAP， to verify the regulatory effect of this pathway on the expression of inflammatory factors. The independent samples t-test was used for comparison of normally distributed measurement data between two groups， and the Mann-Whitney U test was used for comparison of non-normally distributed measurement data. ResultsUnder the condition of normal diet， there were no significant differences in hepatic indicators between WT and KO mice. KO mice fed an HFD or HFHC diet showed a significant increase in hepatic lipid droplet accumulation， accompanied by lipid metabolism disorder and significant increases in the levels of indicators associated with inflammation and fibrosis （P<0.05）. Bone marrow transplantation experiments confirmed that compared with the KO→KO group， the WT→KO group had significant alleviation of liver injury （P<0.05）. Mechanistic studies showed that there were significant reductions in the levels of phosphorylated large tumor suppressor kinase 1 （LATS1） and phosphorylated YAP and significant increases in the expression levels of total YAP protein and its downstream target genes in hepatic macrophages of KO mice （P<0.05）. In vitro VP intervention significantly inhibited the expression levels of inflammatory factors in hepatic macrophages isolated from KO mice （P<0.05）. ConclusionMacrophage LSR deficiency activates the YAP signaling pathway by inhibiting LATS1/2 kinase activity and promotes the expression of inflammatory factors， thereby accelerating the progression of liver injury in a mouse model of MASH.

BACKGROUND:Eucommia ulmoides has a certain osteogenic effect,which can promote the proliferation and differentiation of osteoblasts.However,it is unclear whether Eucommia ulmoides has effects on alveolar bone formation and Wnt/β-Catenin signaling pathway. OBJECTIVE:To investigate the mechanism by which Eucommia ulmoides promotes alveolar bone formation in ovariectomized rats based on the Wnt/β-Catenin signaling pathway. METHODS:Sixty female Sprague-Dawley rats were selected and randomly divided into five groups:blank control group,sham-operation group,model group,low-dose group Eucommia ulmoides group,and high-dose Eucommia ulmoides group,with twelve rats in each group.Osteoporosis animal models were constructed by bilateral oophorectomy in the model group and the low-dose and high-dose Eucommia ulmoides groups.The sham-operation group underwent the same method to remove adipose tissue of equal mass around the bilateral ovaries.Three months after surgery,the low-and high-dose Eucommia ulmoides groups were given 2.1 g/kg/d and 4.2 g/kg/d Eucommia ulmoides by gavage,respectively.The sham-operation group and model group were given the same amount of physiological saline by gavage.After 12 weeks of drug intervention,the changes in alveolar bone mass of rats in each group were observed through Micro-CT;hematoxylin-eosin staining was used to observe the pathological structural changes of alveolar bone in rats;enzyme linked immunosorbent assay was used to detect the expression levels of alkaline phosphatase and osteocalcin in the serum of rats;western blot was used to detect the expression levels of β-Catenin and Frizzled9 receptor proteins in the alveolar bone of rats;and real-time fluorescence quantitative PCR was used to detect the expression of osteocalcin,Runt-related transcription factor 2(Runx2),alkaline phosphatase,β-catenin,and frizzled9 mRNAs in alveolar bone tissues of rats. RESULTS AND CONCLUSION:Compared with the blank control group,bone volume fraction,trabecular number,trabecular thickness,and bone mineral density were reduced in the model group(P＜0.05),and trabecular separation was elevated(P＜0.05).Pathological observation showed that the arrangement of trabeculae was disordered and irregular,the trabeculae were thinned or broken,and the marrow cavity was enlarged in the model group,with a significant reduction in bone volume;the level of alkaline phosphatase in the serum was increased(P＜0.05),and the level of osteocalcin was decreased(P＜0.05);mRNA expression of alkaline phosphatase,osteocalcin,Runx2,β-catenin,and frizzled9 were decreased(P＜0.05);protein expression of β-Catenin and Frizzled9 was decreased(P＜0.05).Compared with the model group,the low-and high-dose Eucommia ulmoides groups showed an increase in bone volume fraction,trabecular number,trabecular thickness,and bone mineral density(P＜0.05)and a decrease in trabecular separation(P＜0.05).In the low-and high-dose Eucommia ulmoides groups,bone trabeculae were slightly aligned and thickened,with a significant increase in bone mass.Compared with the model group,the serum level of alkaline phosphatase was reduced(P＜0.05)and the serum level of osteocalcin was elevated(P＜0.05)in the low-and high-dose Eucommia ulmoides groups.Compared with the model group,the mRNA expression of alkaline phosphatase,osteocalcin,Runx2,β-catenin,and frizzled9 were increased in the low-and high-dose Eucommia ulmoides groups(P＜0.05).Compared with the model group,the protein expression of Frizzled9 was increased in the low-dose Eucommia ulmoides group(P＜0.05),while the protein expression of β-Catenin and Frizzled9 was increased in the high-dose Eucommia ulmoides group(P＜0.05).Compared with the low-dose Eucommia ulmoides group,the high-dose Eucommia ulmoides group had a more significant improvement in the above indexes.To conclude,Eucommia ulmoides can effectively promote the alveolar bone formation,and its mechanism of action might be related to the activation of the Wnt/β-catenin signaling pathway.

OBJECTIVE To explore whether pachymic acid （Pac） regulates mitochondrial autophagy mediated by the PTEN- induced kinase 1 （PINK1）/Parkin RBR E3 ubiquitin-protein ligase （Parkin） signaling pathway to alleviate myocardial injury in coronary heart disease （CHD） rats. METHODS SD rats were divided into control （Con） group， CHD group， Pac low-dose group （Pac-L group）， Pac high-dose group （Pac-H group）， Pac-H+PINK1/Parkin signaling pathway inhibitor group （Pac-H+3-MA group）， with 10 rats in each group. Except for the Con group， CHD models were established in the remaining groups of rats. After successful modeling， the rats in each group were intraperitoneally injected with the corresponding drugs or normal saline. After continuous intervention for 4 weeks， the left ventricular ejection fraction （LVEF）， left ventricular end-diastolic volume （LVEDV）， left ventricular end-systolic volume （LVESV）， and mean arterial pressure （MAP） of the rats were detected. The levels of creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， cardiac troponin I （cTnI）， and cardiac troponin T （cTnT） in the serum， as well as the levels of tumor necrosis factor-α （TNF-α）， interleukin-10 （IL-10）， IL-1β， reactive oxygen species （ROS）， malondialdehyde （MDA） in the myocardial tissue， and the activities of catalase （CAT） and superoxide dismutase （SOD）， as well as the expression levels of p62， cleaved caspase-3， Parkin， PINK1 proteins and the ratio of microtubule-associated protein 1 light chain 3 Ⅱ （LC3Ⅱ）/LC3Ⅰ ratio were measured. The morphology of myocardial tissue and mitochondrial autophagic vesicles were observed， and the number of mitochondrial autophagic vesicles per unit area and the rate of cardiomyocyte apoptosis were counted. RESULTS Compared with CHD group， LVEF， MAP， IL-10 levels， CAT and SOD activities， p62， Parkin， PINK1 protein expressions， LC3Ⅱ/LC3Ⅰ ratio， the numbers of mitochondrial autophagic vesicles per unit area in the Pac-L and Pac-H E-mail：hzdpft@163.com groups were increased significantly （P＜0.05）； the levels of LVEDV， LVESV， CK-MB， LDH， cTnI， cTnT， TNF-α， IL-1β， ROS and MDA， cell apoptosis rates， and protein expression of cleaved caspase-3 were all decreased significantly （P＜0.05）； and the changes in various indicators were more pronounced in the Pac-H group （P＜0.05）； both groups showed varying degree of improvement in myocardial histopathological morphology. Compared with the Pac-H group， the aforementioned indicators in rats from the Pac-H+3-MA group were all significantly reversed （P＜0.05）. CONCLUSIONS Pac may promote mitochondrial autophagy in cardiomyocytes of CHD rats by activating the PINK1/ Parkin signaling pathway， thereby reducing inflammatory responses and oxidative stress and improving myocardial injury.

ObjectiveTo clarify the neuroprotective effect of black Panacis Quinquefolii Radix（PQR） and explore its active ingredients， with the aim of establishing an activity-oriented quality evaluation method. MethodsTransgenic Tg（HuC∶EGFP） zebrafish was used to establish a neuronal injury model by aluminum chloride immersion. Different doses（10， 20 mg·L^-1） of PQR and black PQR ethanol extracts were administered. The neuroprotective effects of PQR and black PQR were compared by analyzing the fluorescent area and intensity of zebrafish neurons. Based on ultra-performance liquid chromatography（UPLC）， a fingerprint profile of black PQR was established， followed by principal component analysis（PCA） and orthogonal partial least squares-discriminant analysis（OPLS-DA）. Differential components were screened using the criteria of variable importance in the projection（VIP） value>1 and P<0.05. The neuroprotective activity of 14 batches of black PQR was assessed， and Spearman correlation analysis was used to identify saponins related to neuroprotective activity， which were then validated. Based on the above results， active marker components were determined， and an UPLC method was established for their quantitation with clear content limits. ResultsPharmacological efficacy results showed that both PQR and black PQR at different doses could significantly improved neuronal damage in zebrafish. At a dose of 20 mg·L^-1， black PQR demonstrated superior efficacy（P<0.05）. The fingerprint similarities of 14 batches of black PQR were>0.94， with 26 common peaks identified. Through comparison with the reference standards， 8 components were confirmed， including peak 1（ginsenoside Rg₁）， peak 2（ginsenoside Re）， peak 5（ginsenoside Rb₁）， peak 9（ginsenoside Rd）， peak 16［ginsenoside 20（S）-Rg₃］， peak 17［ginsenoside 20（R）-Rg₃］， peak 18（ginsenoside Rk₁）， and peak 19（ginsenoside Rg₅）. The results of PCA and OPLS-DA indicated that there were differences in saponins among black PQR samples from different origins， and 12 differential components were screened. All 14 batches of black PQR exhibited good protective effects on zebrafish neurons， with Shaanxi-produced black PQR showing superior protective effects compared to the other three production regions. Spearman correlation analysis revealed that a total of 11 components， including ginsenosides 20（S）-Rg₃， 20（R）-Rg₃， Rk₁ and Rg₅， showed a significant positive correlation with the neuroprotective effect in zebrafish（P<0.05）. The activity validation results indicated that ginsenosides 20（S）-Rg₃， 20（R）-Rg₃， Rk₁ and Rg₅ were the primary components responsible for the neuroprotective effects of black PQR. Quantitative analysis showed that the content of ginsenoside 20（S）-Rg₃ in 14 batches of black PQR ranged from 0.17% to 0.52%， and the repair rate of neuronal damage ranged from 42.77% to 97.83%. ConclusionBased on the fingerprint and neuronal protective activity， the spectrum-effect related quality control model of black PQR was established， with ginsenoside 20（S）-Rg₃ as the quality control index， and the neuronal damage repair rate≥60% as the evaluation standard， the minimum limit of ginsenoside 20（S）-Rg₃ in black PQR should be≥0.20%.

ObjectiveTo assess the quality consistency of black Panacis Quinquefolii Radix（bPQR） decoction pieces prepared by atmospheric and pressurized steaming processes based on chromaticity-chemical composition-vasoactive inhibition. The ultimate goal was to screen the pressurized steaming process yielding quality equivalent to atmospheric steaming， and optimize the processing technology of bPQR. MethodsThe bPQR decoction pieces were prepared using both atmospheric and pressurized steaming processes， and the chromaticity values［lightness value（L^*）， red/green chromaticity value（a^*）， yellow/blue chromaticity value（b^*）， total chromaticity value（E^*ab）］ were measured. High performance liquid chromatography（HPLC） was employed to establish fingerprint profiles for the decoction pieces， and cluster analysis was conducted on chromaticity values and the common peak areas in fingerprint profiles to elucidate the quality relationships between the decoction pieces processed by different methods. The optimal atmospheric steaming of bPQR decoction pieces was determined through zebrafish angiogenesis inhibition experiments. The contents of ginsenosides Rg₁， Re， Rb₁， 20（S）-Rg₃， Rk₁ and Rg₅ in the decoction pieces were quantified， and Spearman correlation analysis was employed to investigate the relationship between saponin content， chromaticity， and angiogenesis inhibition activity during the steaming process. By integrating the consistency of chromaticity， saponin components and angiogenesis inhibition activity， pressurized steaming conditions with quality equivalent to the atmospheric pressure method were selected. ResultsCompared with the atmospheric steaming method， pressurized steaming resulted in faster color darkening and higher conversion rates of ginsenosides in bPQR decoction pieces. Moreover， the neovascularization inhibitory activity of bPQR decoction pieces continued to increase with the deepening of processing. Based on the effectiveness and safety， the optimal process for preparing bPQR decoction pieces with neovascularization inhibitory activity was determined to be atmospheric steaming for 21 h. All six ginsenosides tested exhibited strong to extremely strong correlations with both the chromaticity values of the decoction pieces and their neovascularization inhibitory activities. Among them， ginsenosides Rg₁， Re and Rb₁ exhibited positive correlations with chromaticity values and negative correlations with zebrafish angiogenesis inhibition activity. Conversely， ginsenosides 20（S）-Rg₃， Rk₁ and Rg₅ showed negative correlations with chromaticity values and positive correlations with zebrafish angiogenesis inhibition activity. By integrating chromaticity values， cluster analysis results， as well as the results of activity， it was determined that the quality of bPQR decoction pieces steamed under pressurized conditions of 110 ℃（0.045 MPa） for 5 h and 115 ℃（0.07 MPa） for 3 h was highly consistent with that obtained by atmospheric steaming for 21 h. ConclusionThe preparation of bPQR decoction pieces by pressurized steaming has the advantages of short preparation time， low energy consumption， and rapid saponin conversion rate， making it a viable alternative to atmospheric steaming for preparing bPQR decoction pieces. Meanwhile， the evaluation method based on chromaticity-chemical composition-activity can provide a more scientific and effective explanation of change rules in the quality during traditional Chinese medicine processing， and offer a new model for optimizing processing technology and enhancing quality control.

Objective To explore the potential targets and mechanism of Gufang Granules in treating osteoporosis through network pharmacology,molecular dynamics simulations,and in vitro experiment validation.Methods The active components of Gufang Granules were obtained from the TCMSP database and literature,and their related targets were predicted using SwissTargetPrediction database.Core drug targets were selected through protein-protein interaction(PPI)network analysis and machine learning models,and the predictive performance of the models was assessed by drawing receiver operating characteristic(ROC)curves on independent validation datasets.Gene Set Enrichment Analysis(GSEA)was used to analyze the expression and pathways of core targets.Molecular dynamics(MD)simulations were applied to evaluate the structural stability and interactions of the compound-target complexes.Non-cytotoxic concentrations of Gufang Granules containing serum were determined by the CCK-8 assay.RAW264.7 cells were treated with low,medium,and high concentrations of drug containing serum,respectively.The number of osteoclasts was quantified using TRAP staining.The expression levels of relevant genes and proteins were analyzed through qRT-PCR and Western blot methods.Results A total of 251 potential active components and 1 078 related targets of Gufang Granules were identified.The high expressions of core targets SRC and TNF were mainly associated with osteoclast differentiation,MAPK signaling pathway and PI3K/Akt signaling pathway.MD simulations showed that the core active component Glabridin exhibited strong stability and interaction with the SRC and TNF target proteins.The number of TRAP positive cells in all concentration groups of Gufang Granules was significantly reduced compared to the RANKL group(P<0.01,P<0.001).The serum containing Gufang Granules significantly reduced the mRNA expression of NFATc1,CTSK,SRC and TNF-α,and also downregulated the protein expression of NFATc1,CTSK,p-SRC and TNF-α(P<0.05,P<0.01,P<0.001).Conclusion Gufang Granules may inhibit osteoclast differentiation by downregulating the expression of NFATc1,CTSK,p-SRC and TNF-α,thereby slowing the pathological progression of osteoporosis.

Neuraminidase(NA),a glycoprotein on the surface of the influenza virus,plays a crucial role in viral escape and serves as a stable target for drug candidates.Monoclonal antibodies targeting the NA active site can bind to multiple influenza virus subtypes and inhibit the spread of influenza virus through various mechanisms,such as neutralizing,mediating antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotox-icity.In vivo experiments have shown that human monoclonal antibodies targeting the influenza virus NA can ef-fectively exert preventive and therapeutic effects,rescuing mice infected with lethal doses and reducing viral ti-ters in lungs of mice.This article provides a review of the currently reported human monoclonal antibodies targe-ting NA of Influenza A and Influenza B viruses,providing new ideas and prospects for the subsequent development of anti-influenza drugs.

Objective To retrospectively analyze the changes in cerebral blood flow(CBF)of hippocampus before and after radiotherapy(RT)and to explore its relationship with dose for providing a feasible approach for dynamically monitoring hippocampal response after whole brain radiation therapy in patients with brain metastases(BMs).Methods A retrospective analysis was conducted on magnetic resonance(MR)images from 43 BMs patients before and after RT,including T1-weighted imaging(T1WI)and three-dimensional arterial spin labeling(3D-ASL)imaging.Manual segmentation of the hippocampal structures was performed on T1WI to determine hippocampal volume,while CBF within the hippocampus was derived from 3D-ASL images.Patients were categorized into different groups according to the time interval between two MR scans and the dose received by the hippocampus,namely short time interval[<30 d,with an average of(19.74±7.15)d]≤1 Gy,1-30 Gy and≥30 Gy groups;long time interval[>3 months,with an average of(495.50±226.06)d]≤1 Gy,1-30 Gy and≥30 Gy groups.The patterns of changes in hippocampal CBF and volume,as well as the dose-effect relationship following RT were analyzed.Results(1)A total of 86 hippocampi were enrolled,showing reductions of 8.32%in minimum CBF(CBF-min),7.31%in maximum CBF(CBF-max),8.09%in mean CBF(CBF-mean),and 4.11%in hippocampal volume after RT(P<0.05).The decrease rates of CBF-min,CBF-max and CBF-mean were 6.33%,7.01%and 8.23%higher than the reduction rate of hippocampal volume,respectively.(2)With a brief interval between two MR simulation localization scans,hippocampal CBF in the groups receiving≤1 Gy and 1-30 Gy exhibited an increase,with the increase rate positively correlated to the radiation dose absorbed by the hippocampus.Conversely,in the group receiving≥30 Gy,hippocampal CBF decreased.The variations in the rate of hippocampal CBF change across the dose groups were statistically significant,except when comparing≤1 Gy and 1-30 Gy groups(P<0.05).Additionally,the hippocampal volume in all 3 dose groups experienced a slight increase,with the growth rate also positively correlated to the radiation dose received by the hippocampus;however,these differences were not statistically significant(P>0.05).(3)With a long interval between MR simulation localization scans,both hippocampal CBF and volume in all 3 dose groups demonstrated decreasing trends,with the decrease rate positively correlated to the radiation dose received by the hippocampus.Statistically significant differences in the rate of CBF change were noted among the dose groups,except for the comparison between≤1 Gy and 1-30 Gy groups(P<0.05).The reduction rate of hippocampal volume across 3 dose groups was statistically significant(P<0.05).Conclusion The reduction in hippocampal CBF following RT in BMs patients is more sensitive than the reduction in hippocampal volume,exhibiting a pronounced dependence on both time and radiation dose.Consequently,CBF changes should be employed as a standard bioindicator for monitoring the response to hippocampal RT and predicting radiological injuries after whole brain radiotherapy in BMs patients.

Objective:To investigate the effect of transforming growth factor beta 1 (TGF-β1) on the biological activity of infantile hemangioma (IH) -derived endothelial cells (HemECs) .Methods:Three proliferating IH tissues and three involuting IH tissues were collected from IH patients receiving surgical resection at the Department of Pediatric Surgery, West China Hospital, Sichuan University from February to August 2021. Primary HemECs were isolated from proliferating IH tissues, and human umbilical vein endothelial cells (HUVECs) served as the control. The TGF-β1 expression levels in tissues and cells were detected by immunohistochemical study and Western blot analysis. Cell counting kit-8 (CCK8) assay was performed to assess the effect of 0 (control group) - 100 ng/ml TGF-β1 on HemEC proliferation. HemECs were treated with 5 ng/ml TGF-β1 or without (control group), and after several hours of treatment, Transwell assay was performed to evaluate cell migration ability, and immunofluorescence assay to assess the changes in the expression of endothelial markers (platelet-endothelial cell adhesion molecule-1 [CD31], vascular endothelial cadherin [VE-cadherin]) and mesenchymal markers (α-smooth muscle actin [α-SMA], collagen type Ⅰ α 1 [COL1A1]). Comparisons between groups were conducted by t test or one-way analysis of variance. Results:Immunohistochemical study showed that proliferating IH tissues were stained positively for TGF-β1, which was expressed relatively abundantly; the percentages of TGF-β1-positive signal area were higher in the proliferating IH tissues (24.68% ± 3.74%) than in the involuting IH tissues (almost no expression). Western blot analysis revealed that the relative expression level of TGF-β1 was significantly higher in HemECs (1.08 ± 0.13) than in HUVECs (0.30 ± 0.04, t = 9.93, P < 0.001). CCK8 assay showed increased proliferative activity of HemECs in the 3.125-, 6.25-, 12.5-, 25-, 50- and 75-ng/ml TGF-β1 groups compared with the control group (all P < 0.05), and no significant difference was found between the 100-ng/ml TGF-β1 group and the control group ( P > 0.05). Transwell assay revealed an increased number of migratory HemECs in the 5-ng/ml TGF-β1 group (127 ± 6) compared with the control group (103 ± 9; t = 5.32, P < 0.01). Immunofluorescence assay showed significantly decreased fluorescence intensity of endothelial markers CD31 and VE-cadherin in the 5-ng/ml TGF-β1 group (5.441 ± 1.254, 5.073 ± 0.412, respectively) compared with the control group (9.518 ± 1.728,7.671 ± 0.921, t = 3.31, 4.46, P = 0.030, 0.011, respectively), and significantly increased fluorescence intensity of mesenchymal markers α-SMA and COL1A1 in the 5-ng/ml TGF-β1 group (8.074 ± 0.846, 5.885 ± 0.216, respectively) compared with the control group (0.393 ± 0.342, 0.295 ± 0.125, t = 14.58, 38.76, P < 0.001, < 0.000 1, respectively) . Conclusion:TGF-β1 was relatively highly expressed in the proliferating IH tissues and HemECs, and could promote the proliferation, migration and endothelial-to-mesenchymal transition of HemECs.

Malignant pleural effusion(MPE)is a common complication in patients with advanced malignant tumors,which not only significantly reduces their quality of life but also shortens their survival duration.Despite the widespread use of traditional treatment methods such as thoracentesis and pleurodesis,their efficacy is limited accompanied by high recurrence rates.Therefore,exploring novel therapeutic strategies becomes particularly urgent.In recent years,immunotherapy has attracted extensive attention for its potential in cancer treatment.This article systematically reviews the roles of CD4+T cell subsets,including regulatory T cells(Treg),T helper cell(Th)17,Th9,and Th22 cells,within the immunosuppressive microenvironment of MPE.These cell subsets are involved in the formation of the immunosuppressive state of MPE through various mechanisms and play key roles in the occurrence and development of the disease.In addition,the article discusses in detail the role of immune checkpoint molecules,such as programmed death protein 1(PD-1),PD-1 ligand(PD-L1),and cytotoxic T-lymphocyte-associated protein 4(CTLA-4),in the immune evasion of MPE.The abnormal expressions of these molecules provide opportunity for tumor cells to evade immune system surveillance.At the same time,this article also summarizes the application prospects of novel immunotherapy strategies,such as adoptive cell therapy(ACT)and chimeric antigen receptor T cell(CAR-T)therapy,in the treatment of MPE.These innovative therapies offer possibilities for improving the prognosis of MPE patients through activating and enhancing the anti-tumor immune response.