ObjectiveTo investigate whether Shixiaosan can improve neurological function and inhibit ferroptosis in rats with cerebral ischemia-reperfusion injury （CIRI） by regulating the nuclear factor E₂-related factor 2 （Nrf2）/solute carrier family 7 member 11 （SLC7A11）/glutathione peroxidase 4 （GPX4） pathway. MethodsA rat model of CIRI was established using the intraluminal filament method. Briefly， cervical blood vessels were separated， branches of the external carotid artery were ligated， and the common carotid artery and internal carotid artery were clamped. A nylon filament was inserted through the opening of the external carotid artery to the origin of the middle cerebral artery to block blood flow and induce cerebral ischemia. After 60-120 min of ischemia， the filament was withdrawn to restore blood flow， and the external carotid artery incision was ligated. The rats were divided into a CIRI group， a Shixiaosan low-dose （-L） group （intragastric administration of 1.26 g·kg^-1 Shixiaosan）， a Shixiaosan high-dose （-H） group （intragastric administration of 2.52 g·kg^-1 Shixiaosan）， a donepezil hydrochloride tablet （DON） group （intragastric administration of 0.45 mg·kg^-1 DON）， and a Shixiaosan -H + Nrf2 inhibitor （ML385） group （intragastric administration of 2.52 g·kg^-1 Shixiaosan combined with intraperitoneal injection of 30 mg·kg^-1 ML385）. An additional 12 rats underwent cervical artery separation followed by incision suturing and served as the control group. Equal volumes of double-distilled water were administered to the CIRI and control groups. Neurological function impairment was assessed using the modified Garcia JH score. Magnetic resonance imaging was used to determine the cerebral infarct volume ratio. Hematoxylin-eosin （HE） staining and Prussian blue staining were performed to observe neuronal injury and iron accumulation in the ischemic penumbra， respectively. Transmission electron microscopy was used to examine the ultrastructure of neuronal mitochondria in the ischemic penumbra. Commercial kits were used to measure ferrous iron （Fe²⁺）， malondialdehyde （MDA）， reduced glutathione （GSH） content， and reactive oxygen species （ROS） activity in the ischemic penumbra. The BODIPY （581/591） C11 fluorescent probe was used to detect intracellular lipid peroxidation levels. Western blot was performed to detect protein expression levels of Nrf2， SLC7A11， GPX4， transferrin receptor 1 （TFRC）， ferritin heavy chain （FHC）， and ferritin light chain （FLC） in the ischemic penumbra. ResultsCompared with the control group， the CIRI group exhibited neuronal injury in the ischemic penumbra， characterized by reduced neuron numbers， nucleolar shrinkage， and interstitial edema. Marked iron accumulation was observed in the tissue. Neuronal mitochondria showed atrophy and rupture， with reduced mitochondrial cristae and increased membrane density. The cerebral infarct volume ratio， Fe²⁺ content， MDA content， ROS activity， and lipid peroxidation levels were increased， whereas the modified Garcia JH score， GSH content， and protein expression levels of Nrf2， SLC7A11， GPX4， FHC， and FLC were decreased， and TFRC protein expression was increased （P<0.05）. Compared with the CIRI group， the Shixiaosan -L group， Shixiaosan -H group， and DON group showed attenuated neuronal injury in the ischemic penumbra， reduced iron accumulation， alleviated mitochondrial damage， decreased cerebral infarct volume ratio， Fe²⁺ and MDA contents， ROS activity， and lipid peroxidation levels， as well as increased modified Garcia JH scores， GSH content， and protein expression levels of Nrf2， SLC7A11， GPX4， FHC， and FLC， while TFRC protein expression was decreased （P<0.05）. The magnitude of changes in all indicators was greater in the Shixiaosan -H group than in the Shixiaosan -L group （P<0.05）. Compared with the Shixiaosan -H group， all measured indicators in the Shixiaosan -H + ML385 group showed opposite trends （P<0.05）. ConclusionShixiaosan may inhibit ferroptosis and restore neurological function in rats with CIRI by activating the Nrf2/SLC7A11/GPX4 pathway.

ObjectiveTo explore whether the intestinal absorption solution containing Banxia Xiexintang （BXT） can inhibit the invasion and migration of gastric cancer cells by interfering with the stromal cell-derived factor 1 （SDF1）-CXC chemokine receptor 4 （CXCR4） axis in tumor-associated bone marrow mesenchymal stem cells （TA-BMSCs）. MethodsThe intestinal absorption solution containing BXT was prepared， and the optimal intervention concentration and duration for MFC cells were determined through the cell counting kit-8 （CCK-8） assay. A co-culture system was established comprising TA-BMSCs conditioned medium （TA-BMSCs-CM） and gastric cancer MFC cells. The experiment was conducted with a blank control group， a TA-BMSCs-CM group， an SDF1 inhibitor （LY2510924） group， and intervention groups with varying concentrations （55%， 70%， 85%） of the intestinal absorption solution containing BXT. Cell proliferation was assessed by the CCK-8 assay. Horizontal and vertical cell migration were evaluated via scratch and Transwell assays， respectively. Cell invasion was examined by a Transwell assay with Matrigel. Cell apoptosis was detected by flow cytometry. The levels of factors such as SDF1， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA）， as well as the protein levels of macrophage migration inhibitory factor （MIF）， CXCR4， VEGFA， and MMP-9， were quantified by ELISA and Western blot， respectively. ResultsThe CCK-8 assay results indicated that compared with the 24 h intervention， the 48 h interventions with all concentrations of the intestinal absorption solution containing BXT increased the inhibition rate on MFC cells （P<0.01）. The half-maximal inhibitory concentration （IC₅₀） of the intestinal absorption solution containing BXT at the time point of 48 h was 68.51%， and subsequent intervention concentrations were selected as 55%， 70%， and 85%. Compared with the TA-BMSCs-CM group， the intestinal absorption solution containing BXT （particularly at concentrations of 70% 85%） suppressed the proliferation， migration， and invasion of MFC cells， promoted the cell apoptosis （P<0.05， P<0.01）， decreased the levels of SDF1， MMP-9， and VEGFA， and downregulated the protein levels of MIF， CXCR4， VEGFA， and MMP-9 （P<0.05， P<0.01）. The inhibitory effects of the intestinal absorption solution containing BXT were comparable to or superior to those of the SDF1 inhibitor （P<0.01）. ConclusionThe intestinal absorption solution containing BXT can inhibit the invasion and migration of gastric cancer cells by interfering with the SDF1-CXCR4 axis in TA-BMSCs. The underlying mechanism may involve the regulation of the MIF/SDF1/CXCR4 signaling pathway and its downstream effector molecules.

ObjectiveTo observe how Banxia Xiexintang affects programmed cell death 1 ligand 1 （PD-L1） expression induced by exosomes derived from gastric cancer cells in bone marrow mesenchymal stem cells （BMSCs） through the protein kinase B （Akt）/c-myelocytomatosis oncogene （c-Myc） signaling axis， and its effects on the migration of BMSCs and gastric cancer cells. MethodsExosomes were isolated from human gastric cancer NCI-N87 cells and identified by transmission electron microscopy and Western blot. Rat BMSCs were passaged and identified by immunofluorescence staining. A Transwell chamber was used to create a non-contact co-culture system for NCI-N87 exosomes and BMSCs. The experiment was designed with normal， model， Banxia Xiexintang （10% serum containing Banxia Xiexintang）， PD-L1 monoclonal antibody （10% blank serum containing PD-L1 antibody）， and combination （10% serum containing Banxia Xiexintang and 10% blank serum containing PD-L1 antibody） groups. The suspension of BMSCs was added to the upper chamber of each group， with the normal group receiving serum culture medium without exosomes in the lower chamber， and the model group receiving NCI-N87 exosomes. The Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group received 10% serum containing Banxia Xiexintang， 10% blank serum containing PD-L1 monoclonal antibody， and 10% serum containing Banxia Xiexintang and 10% blank serum containing PD-L1 antibody， respectively， in the upper chamber. After 96 h， BMSCs from the upper chamber were collected， and the protein levels of p-Akt， Akt， c-Myc， and PD-L1， as well as the mRNA levels of Akt， c-Myc， and PD-L1， were determined by Western blot and Real-time PCR， respectively. The migration of BMSCs and NCI-N87 was assessed by the Transwell method. ResultsCompared with the normal group， the model group showed increases in protein levels of p-Akt， c-Myc， and PD-L1， as well as mRNA levels of c-Myc and PD-L1 （P<0.05， P<0.01）， and no significant change in the protein and mRNA levels of Akt. Compared with the model group， the Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group showed decreases in protein levels of p-Akt， c-Myc， and PD-L1 （P<0.01）. In addition， they had significant effects on the protein and mRNA levels of Akt. The combination group showed greater reductions in the protein and mRNA levels of c-Myc and PD-L1 than the Banxia Xiexintang group and PD-L1 monoclonal antibody group （P<0.05）. Compared with the normal group， the model group showed increases in the number of migrating NCI-N87 and BMSCs （P<0.05， P<0.01）. Compared with the model group， the Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group showed decreases in the number of migrating NCI-N87 and BMSCs （P<0.05， P<0.01）， with the combination group showing greater reductions in the number of migrating NCI-N87 and BMSCs than the Banxia Xiexintang group and PD-L1 monoclonal antibody group （P<0.01）. ConclusionBanxia Xiexintang can lower the PD-L1 expression induced by gastric cancer cell-derived exosomes in BMSCs induced and inhibit the migration of BMSCs and gastric cancer cells. Moreover， it has a synergistic effect when being used together with PD-L1， possibly related to the regulation of the Akt/c-Myc signaling axis.

ObjectiveTo explore whether the intestinal absorption solution containing Banxia Xiexintang （BXT） can inhibit the invasion and migration of gastric cancer cells by interfering with the stromal cell-derived factor 1 （SDF1）-CXC chemokine receptor 4 （CXCR4） axis in tumor-associated bone marrow mesenchymal stem cells （TA-BMSCs）. MethodsThe intestinal absorption solution containing BXT was prepared， and the optimal intervention concentration and duration for MFC cells were determined through the cell counting kit-8 （CCK-8） assay. A co-culture system was established comprising TA-BMSCs conditioned medium （TA-BMSCs-CM） and gastric cancer MFC cells. The experiment was conducted with a blank control group， a TA-BMSCs-CM group， an SDF1 inhibitor （LY2510924） group， and intervention groups with varying concentrations （55%， 70%， 85%） of the intestinal absorption solution containing BXT. Cell proliferation was assessed by the CCK-8 assay. Horizontal and vertical cell migration were evaluated via scratch and Transwell assays， respectively. Cell invasion was examined by a Transwell assay with Matrigel. Cell apoptosis was detected by flow cytometry. The levels of factors such as SDF1， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA）， as well as the protein levels of macrophage migration inhibitory factor （MIF）， CXCR4， VEGFA， and MMP-9， were quantified by ELISA and Western blot， respectively. ResultsThe CCK-8 assay results indicated that compared with the 24 h intervention， the 48 h interventions with all concentrations of the intestinal absorption solution containing BXT increased the inhibition rate on MFC cells （P<0.01）. The half-maximal inhibitory concentration （IC₅₀） of the intestinal absorption solution containing BXT at the time point of 48 h was 68.51%， and subsequent intervention concentrations were selected as 55%， 70%， and 85%. Compared with the TA-BMSCs-CM group， the intestinal absorption solution containing BXT （particularly at concentrations of 70% 85%） suppressed the proliferation， migration， and invasion of MFC cells， promoted the cell apoptosis （P<0.05， P<0.01）， decreased the levels of SDF1， MMP-9， and VEGFA， and downregulated the protein levels of MIF， CXCR4， VEGFA， and MMP-9 （P<0.05， P<0.01）. The inhibitory effects of the intestinal absorption solution containing BXT were comparable to or superior to those of the SDF1 inhibitor （P<0.01）. ConclusionThe intestinal absorption solution containing BXT can inhibit the invasion and migration of gastric cancer cells by interfering with the SDF1-CXCR4 axis in TA-BMSCs. The underlying mechanism may involve the regulation of the MIF/SDF1/CXCR4 signaling pathway and its downstream effector molecules.

ObjectiveTo observe how Banxia Xiexintang affects programmed cell death 1 ligand 1 （PD-L1） expression induced by exosomes derived from gastric cancer cells in bone marrow mesenchymal stem cells （BMSCs） through the protein kinase B （Akt）/c-myelocytomatosis oncogene （c-Myc） signaling axis， and its effects on the migration of BMSCs and gastric cancer cells. MethodsExosomes were isolated from human gastric cancer NCI-N87 cells and identified by transmission electron microscopy and Western blot. Rat BMSCs were passaged and identified by immunofluorescence staining. A Transwell chamber was used to create a non-contact co-culture system for NCI-N87 exosomes and BMSCs. The experiment was designed with normal， model， Banxia Xiexintang （10% serum containing Banxia Xiexintang）， PD-L1 monoclonal antibody （10% blank serum containing PD-L1 antibody）， and combination （10% serum containing Banxia Xiexintang and 10% blank serum containing PD-L1 antibody） groups. The suspension of BMSCs was added to the upper chamber of each group， with the normal group receiving serum culture medium without exosomes in the lower chamber， and the model group receiving NCI-N87 exosomes. The Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group received 10% serum containing Banxia Xiexintang， 10% blank serum containing PD-L1 monoclonal antibody， and 10% serum containing Banxia Xiexintang and 10% blank serum containing PD-L1 antibody， respectively， in the upper chamber. After 96 h， BMSCs from the upper chamber were collected， and the protein levels of p-Akt， Akt， c-Myc， and PD-L1， as well as the mRNA levels of Akt， c-Myc， and PD-L1， were determined by Western blot and Real-time PCR， respectively. The migration of BMSCs and NCI-N87 was assessed by the Transwell method. ResultsCompared with the normal group， the model group showed increases in protein levels of p-Akt， c-Myc， and PD-L1， as well as mRNA levels of c-Myc and PD-L1 （P<0.05， P<0.01）， and no significant change in the protein and mRNA levels of Akt. Compared with the model group， the Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group showed decreases in protein levels of p-Akt， c-Myc， and PD-L1 （P<0.01）. In addition， they had significant effects on the protein and mRNA levels of Akt. The combination group showed greater reductions in the protein and mRNA levels of c-Myc and PD-L1 than the Banxia Xiexintang group and PD-L1 monoclonal antibody group （P<0.05）. Compared with the normal group， the model group showed increases in the number of migrating NCI-N87 and BMSCs （P<0.05， P<0.01）. Compared with the model group， the Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group showed decreases in the number of migrating NCI-N87 and BMSCs （P<0.05， P<0.01）， with the combination group showing greater reductions in the number of migrating NCI-N87 and BMSCs than the Banxia Xiexintang group and PD-L1 monoclonal antibody group （P<0.01）. ConclusionBanxia Xiexintang can lower the PD-L1 expression induced by gastric cancer cell-derived exosomes in BMSCs induced and inhibit the migration of BMSCs and gastric cancer cells. Moreover， it has a synergistic effect when being used together with PD-L1， possibly related to the regulation of the Akt/c-Myc signaling axis.

Objective To evaluate the application value of the MR three-dimensional double inversion recovery(3D DIR)sequence in the diagnosis of optic neuritis(ON).Methods A retrospective analysis was conducted on MRI images from 40 patients with sus-pected ON.All patients underwent conventional T2 WI fat suppression(FS)and 3D DIR sequences.The lesion detection rate and diag-nostic accuracy of the intraorbital,intracanalicular,and intracranial segments of the optic nerve were compared between the two sequences,respectively.The receiver operating characteristic(ROC)curves were used to assess the diagnostic performance,and the intraclass correlation coefficient(ICC)were used to analyze interobserver consistency.Imaging assessments were independently performed by two senior and two junior radiologists.Results The sensitivity(SEN),specificity(SPE),and accuracy(ACC)in lesion detection of 3D DIR sequence were significantly better than those of conventional T2 WI FS sequence[odds ratio(OR)221 vs 104,P＜0.001].Notably,3D DIR sequence exhibited superior performance in detecting lesions in the intraorbital segment[area under the curve(AUC)0.915,OR=102]and intracanalicular segment(AUC 0.858,OR=51)compared with conventional T2WI FS sequence.Additionally,3D DIR sequence significantly improved diagnostic consistency among junior radiologists(ICC value increased from 0.469 to 0.655),bring-ing their diagnostic performance closer to that of senior radiologists(AUC improved to 0.883,ACC reached 90.1％).Conclusion The 3D DIR sequence has outstanding diagnostic efficacy in detecting ON lesions,significantly improving ACC and interobserver consistency,thereby offering strong support for the precise diagnosis of ON.

Objective To observe the therapeutic effect of Qiwei Tangmaishu capsules on type 2 diabetes mice,and explore the mechanisms of its treatment of type 2 diabetes based on network pharmacology.Methods TCMSP,ETCM databases were used to query all components and of Qiwei Tangmaishu capsules and their targets.OMIM and DrugBank databases were used to search for targets of type 2 diabetes.The targets of type 2 diabetes and Qiwei Tangmaishu capsules were intersected by Venny 2.1.0.to perform GO and KEGG pathway enrichment analysis on those intersecting targets using the Metascape website.Then,a mouse model of type 2 diabetes was established,and Qiwei Tangmaishu capsules were given to low,medium,and high dose groups(234,468,and 936 mg/kg,respectively),and metformin(MET)group(200 mg/kg)for 2 weeks.The weight of each mouse was measured before and after treatment,and fasting blood glucose was also measured.After the 2 weeks,fasting insulin was measured;ELISA was used to detect levels of inflammatory factors IL-1β,TNF-α,IL-6,TLR4,and NF-κB in serum;Hematoxylin eosin staining was used to observe the morphology of pancreatic islets;and Caspase 3 and INS immunofluorescence were used to detect apoptosis of pancreatic islet cells and the number of pancreatic beta cells.Western Blot assay was used to detect the expression levels of pancreatic tissue proteins such as p-Akt,Akt,p-PI3K,PI3K,Bax,Bcl2.Results 1260 active ingredient targets were identified in Qiwei Tangmaishu capsules;1205 targets of type 2 diabetes were found.Of these,312 targets were intersected by Venny,with core targets involving Akt1,TNF,IL-6,TLR4,among others.Enrichment analysis identified 240 KEGG pathways,among which"insulin resistance""PI3K/Akt signaling pathway"were the key pathways enriched.The animal experiment result showed that compared with the model group,the intervention of Qiwei Tangmaishu capsules and metformin significantly improved blood glucose and insulin resistance;the content of inflammatory factors in serum decreased,and the apoptosis rate of pancreatic islet cells significantly decreased;the number of pancreatic beta cells significantly increased;the expression of pro-apoptotic protein Bax decreased,the expression of anti-apoptotic protein Bcl2 significantly increased,and the expression of p-PI3K and p-Akt was upregulated.Conclusions Qiwei Tangmaishu capsules can significantly reduce blood glucose levels,restore insulin sensitivity,and reduce islet cell apoptosis in type 2 diabetic mice.The mechanism may be related to the activation of the PI3K/Akt signaling pathway.

[Purpose]To analyze the lifetime risk of developing and dying from lung cancer at global and regional levels.[Methods]Data of lung cancer incidence and mortality were obtained from GLOBOCAN 2022 and the population and all-cause mortality data were obtained from the United Nations.The lifetime risk of developing and dying from lung cancer globally and across different regions was estimated by multiple primary adjustment method.[Results]The global lifetime risk of developing lung cancer was 3.59％[95％confidence interval(CI):3.58％～3.59％],ranking third among all cancer types.There were significant gender and regional differences in lifetime risk values.The risk for male was 4.43％(95％CI:4.42％～4.44％),which was higher than that for female(2.71％,95％CI:2.70％～2.72％),with a male-to-female ratio of 1.63.Among regions with varying human development index(HDI)levels,the risk increased with HDI levels,in very high HDI re-gions risk was 5.36％(95％CI:5.34％～5.37％),while in low HDI regions the risk was 0.34％(95％CI:0.33％～0.34％).Among the 20 global regions,East Asia had the highest lifetime risk of 7.53％(95％CI:7.52％～7.55％),while West Africa had the lowest risk of 0.16％(95％CI:0.16％～0.17％).The global lifetime risk of dying from lung cancer was 2.78％(95％CI:2.78％～2.78％),ranking the first among all cancer types.There were significant sex and regional differ-ences in lifetime death risk values.The risk for male was 3.64％(95％CI:3.63％～3.64％),which was higher than that for female(1.89％,95％CI:1.89％～1.90％),with a male-to-female ratio of 1.93.Among regions with varying HDI levels,the risk increased with HDI levels,in very high HDI re-gions the risk was 3.98％(95％CI:3.97％～3.99％),while in low HDI regions the risk was 0.31％(95％CI:0.31％～0.31％).Among the 20 global regions,the Federated States of Micronesia/Poly-nesia had the highest death risk of 5.80％(95％CI:4.98％～6.62％),while West Africa had the lowest risk of 0.15％(95％CI:0.15％～0.16％).The lifetime risk of developing and dying from lung cancer in China was 7.54％(95％CI:7.52％～7.56％)and 5.88％(95％CI:5.87％～5.90％),respec-tively,both ranking the first among all cancer types.[Conclusion]The lifetime risk of developing and dying from lung cancer remains high globally and across different regions,with a particularly heavy burden in high-HDI areas.In China,both the lifetime risk of developing and dying from lung cancer are higher than the global average.This highlights the need for continued enhance-ment of comprehensive prevention and control measures,including addressing lung cancer-related risk factors,as well as improving screening,early diagnosis,and treatment efforts to reduce the lung cancer burden.

Objective To observe the therapeutic effect of Qiwei Tangmaishu capsules on type 2 diabetes mice,and explore the mechanisms of its treatment of type 2 diabetes based on network pharmacology.Methods TCMSP,ETCM databases were used to query all components and of Qiwei Tangmaishu capsules and their targets.OMIM and DrugBank databases were used to search for targets of type 2 diabetes.The targets of type 2 diabetes and Qiwei Tangmaishu capsules were intersected by Venny 2.1.0.to perform GO and KEGG pathway enrichment analysis on those intersecting targets using the Metascape website.Then,a mouse model of type 2 diabetes was established,and Qiwei Tangmaishu capsules were given to low,medium,and high dose groups(234,468,and 936 mg/kg,respectively),and metformin(MET)group(200 mg/kg)for 2 weeks.The weight of each mouse was measured before and after treatment,and fasting blood glucose was also measured.After the 2 weeks,fasting insulin was measured;ELISA was used to detect levels of inflammatory factors IL-1β,TNF-α,IL-6,TLR4,and NF-κB in serum;Hematoxylin eosin staining was used to observe the morphology of pancreatic islets;and Caspase 3 and INS immunofluorescence were used to detect apoptosis of pancreatic islet cells and the number of pancreatic beta cells.Western Blot assay was used to detect the expression levels of pancreatic tissue proteins such as p-Akt,Akt,p-PI3K,PI3K,Bax,Bcl2.Results 1260 active ingredient targets were identified in Qiwei Tangmaishu capsules;1205 targets of type 2 diabetes were found.Of these,312 targets were intersected by Venny,with core targets involving Akt1,TNF,IL-6,TLR4,among others.Enrichment analysis identified 240 KEGG pathways,among which"insulin resistance""PI3K/Akt signaling pathway"were the key pathways enriched.The animal experiment result showed that compared with the model group,the intervention of Qiwei Tangmaishu capsules and metformin significantly improved blood glucose and insulin resistance;the content of inflammatory factors in serum decreased,and the apoptosis rate of pancreatic islet cells significantly decreased;the number of pancreatic beta cells significantly increased;the expression of pro-apoptotic protein Bax decreased,the expression of anti-apoptotic protein Bcl2 significantly increased,and the expression of p-PI3K and p-Akt was upregulated.Conclusions Qiwei Tangmaishu capsules can significantly reduce blood glucose levels,restore insulin sensitivity,and reduce islet cell apoptosis in type 2 diabetic mice.The mechanism may be related to the activation of the PI3K/Akt signaling pathway.

Breast milk is the optimal natural food for newborns. However， some newborns cannot receive maternal breast milk due to reasons such as mother-infant separation or insufficient lactation. The establishment of human milk banks （HMB） can effectively address these issues， thereby increasing the breastfeeding rate among hospitalized newborns and improving their quality of survival. However， HMB in China is still in the development and improvement stage. Its implementation involves a series of ethical issues， such as informed consent， privacy protection， economic incentives， quality and safety， and fair resource distribution， which hinder HMB’s widespread promotion. Therefore， discussing the ethical dilemmas faced by the widespread establishment of HMB in China’s hospitals and analyzing coping strategies are crucial for improving the breastfeeding rate of newborns. This paper deeply analyzed and sorted out the ethical issues and challenges currently faced by HMB in China， and proposed corresponding strategies， including “ensuring informed consent and voluntary participation of both donors and recipients，” “protecting the privacy of donors and recipients，” “establishing an ethics-based moral incentive and social support system，” “strictly controlling quality and safety issues”， and “developing fair and rational policies，” aiming to provide a reference solution for addressing ethical concerns in the establishment and operation of HMB.