ObjectiveTo investigate the therapeutic effect of sitravatinib on carbon tetrachloride （CCl₄）-induced liver fibrosis in mice. MethodsA total of 30 male C57BL/6J mice， aged 8 weeks， were randomly divided into control group， CCl₄ model group， and low- （5 mg/kg）， middle- （10 mg/kg）， and high-dose （20 mg/kg） sitravatinib groups. All mice except those in the control group were given intraperitoneal injection of CCl₄ for 4 consecutive weeks to induce liver fibrosis， and since the first day of modeling， the mice in the low-， middle-， and high-dose sitravatinib groups were given sitravatinib at the corresponding dose by gavage every day. The serum levels of total cholesterol （TC）， triglyceride （TG）， and alanine aminotransferase （ALT） were measured for the mice in each group； hepatic hydroxyproline content was measured； HE staining， Masson staining， and Sirius Red staining were used to observe liver histopathological changes； quantitative real-time PCR and Western blot were used to measure the mRNA and protein expression levels of α-smooth muscle actin （α-SMA） and collagen type I alpha 1 （Col1a1） in liver tissue. The therapeutic effect of sitravatinib was assessed based on the above results. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the control group， the model group had significant increases in the levels of TC， TG， and ALT （all P<0.05）， and there were no significant differences in the levels of TC， TG， and ALT between the model group and the low-， middle-， and high-dose sitravatinib groups （all P>0.05）. Hepatic hydroxyproline content decreased after sitravatinib intervention， with a significant difference between the middle-/high-dose sitravatinib groups and the CCl₄ model group （both P<0.05）. Histopathological staining showed that the sitravatinib treatment groups had a reduction in collagen deposition， along with thinning and fragmentation of fibrous septa， and in the high-dose sitravatinib group， 4 mice had a fibrosis stage of S0—S1 and 2 mice had a fibrosis stage of S2—S3， suggesting a certain degree of alleviation of liver fibrosis degree compared with the CCl₄ model group （mainly S3—S4）. The measurement of related molecules showed that sitravatinib downregulated the mRNA and protein expression levels of α-SMA and Col1a1 （all P<0.05）. ConclusionSitravatinib can effectively alleviate CCl₄-induced liver fibrosis in mice， possibly by inhibiting hepatic stellate cell activation and collagen synthesis.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

OBJECTIVE To clarify the current development status of clinical pharmacist training bases and the pharmacist workforce in China， and to provide evidence for standardizing base construction and promoting the high-quality development of hospital pharmacy. METHODS Questionnaires were distributed to all clinical pharmacist training bases for urgently-needed health professionals and clinical pharmacist training bases under the Chinese Hospital Association that had been approved by the end of 2023 to collect data including base profiles and pharmacist staffing conditions. Expert teams carried out field investigations to verify the collected data. Descriptive statistical analyses were conducted on the quantity， type and regional distribution of training bases， and the influencing factors of pharmacist staffing in the bases were analyzed. RESULTS Field surveys were completed covering 297 training bases across 31 provincial-level administrative regions. Among the base hospitals， 87.88% were Grade A tertiary general hospitals， and 65.32% were located in provincial capitals. The eastern region had the largest number of bases （136， accounting for 45.79%）， followed by the western region （79， 26.60%）. Great disparities existed among provinces in terms of base quantity and hospital scale. The median proportion of pharmaceutical technical personnel in base hospitals was 4.05%， and the median number of clinical pharmacists per 100 hospital beds was 0.53. Both indicators reached the highest in the eastern region （0.57， 4.43%） and the lowest in the northeastern region （0.45， 3.01%）. A total of 3 627 full-time clinical pharmacists were employed in all surveyed bases， among whom 83.68% held clinical pharmacist training certificates， 35.43% possessed senior professional titles， and 78.19% had postgraduate or higher educational background. The total annual training capacity of the surveyed bases was 4 291 trainees， with obvious differences in annual training capacity across regions and provinces. Training specialties covered 19 specialized disciplines plus one general discipline， and no province could deliver training for all 20 specialties simultaneously. Multivariate Logistic regression analysis showed that geographic region exerte d a significant impact on the proportion of pharmaceutical technical personnel （≥4%） （ P ＜0.05）， while the approval time of training bases and hospital scale had significant effects on the number of clinical pharmacists per 100 beds （≥0.6） （ P ＜0.05）. CONCLUSIONS China’s clinical pharmacist training system has basically matured and taken initial shape. The distribution of clinical pharmacist training resources is generally consistent with regional population and economic development levels. However， the allocation of pharmaceutical staff and clinical pharmacists has not yet met national standards and clinical service demands.

Lung transplantation is currently the only effective treatment for end-stage lung disease. However, the field of lung transplantation still faces numerous challenges, including donor shortage, primary graft dysfunction, rejection, infection and others. In 2025, scholars worldwide have made remarkable progress in clinical research on lung transplantation. This article systematically reviews the cutting-edge developments in clinical research on lung transplantation in 2025, focusing on the application of novel evaluation tools in donor lung screening, optimization of lung perfusion techniques, exploration of extracorporeal membrane oxygenation and robot-assisted minimally invasive surgery, as well as mechanistic research and intervention strategies for primary graft dysfunction, acute kidney injury and chronic lung allograft dysfunction. Meanwhile, hot topics such as the management of special populations, prevention and control of postoperative infections, and improvement of quality of life are summarized. This review aims to conclude the important annual research findings and provide references for the clinical practice and research development of lung transplantation in China.

OBJECTIVE To clarify the current development status of clinical pharmacist training bases and the pharmacist workforce in China， and to provide evidence for standardizing base construction and promoting the high-quality development of hospital pharmacy. METHODS Questionnaires were distributed to all clinical pharmacist training bases for urgently-needed health professionals and clinical pharmacist training bases under the Chinese Hospital Association that had been approved by the end of 2023 to collect data including base profiles and pharmacist staffing conditions. Expert teams carried out field investigations to verify the collected data. Descriptive statistical analyses were conducted on the quantity， type and regional distribution of training bases， and the influencing factors of pharmacist staffing in the bases were analyzed. RESULTS Field surveys were completed covering 297 training bases across 31 provincial-level administrative regions. Among the base hospitals， 87.88% were Grade A tertiary general hospitals， and 65.32% were located in provincial capitals. The eastern region had the largest number of bases （136， accounting for 45.79%）， followed by the western region （79， 26.60%）. Great disparities existed among provinces in terms of base quantity and hospital scale. The median proportion of pharmaceutical technical personnel in base hospitals was 4.05%， and the median number of clinical pharmacists per 100 hospital beds was 0.53. Both indicators reached the highest in the eastern region （0.57， 4.43%） and the lowest in the northeastern region （0.45， 3.01%）. A total of 3 627 full-time clinical pharmacists were employed in all surveyed bases， among whom 83.68% held clinical pharmacist training certificates， 35.43% possessed senior professional titles， and 78.19% had postgraduate or higher educational background. The total annual training capacity of the surveyed bases was 4 291 trainees， with obvious differences in annual training capacity across regions and provinces. Training specialties covered 19 specialized disciplines plus one general discipline， and no province could deliver training for all 20 specialties simultaneously. Multivariate Logistic regression analysis showed that geographic region exerte d a significant impact on the proportion of pharmaceutical technical personnel （≥4%） （ P ＜0.05）， while the approval time of training bases and hospital scale had significant effects on the number of clinical pharmacists per 100 beds （≥0.6） （ P ＜0.05）. CONCLUSIONS China’s clinical pharmacist training system has basically matured and taken initial shape. The distribution of clinical pharmacist training resources is generally consistent with regional population and economic development levels. However， the allocation of pharmaceutical staff and clinical pharmacists has not yet met national standards and clinical service demands.

OBJECTIVE To investigate the current status of quality management in clinical pharmacist training bases in China， and to provide references for the standardized development and improvement of these bases. METHODS A combined approach of questionnaire survey and on-site investigation was adopted， targeting the healthcare highly sought-after talent （clinical pharmacist） training bases in 31 provinces of China as well as the clinical pharmacist training bases affiliated with the Chinese Hospital Association. A training quality management evaluation index system consisting of 25 tertiary indicators was established. Investigations were conducted from two dimensions： structural quality of training and quality management of training processes. Data were statistically analyzed using descriptive statistical methods. RESULTS On-site investigations were completed for 297 clinical pharmacist training bases across the 31 provinces， among which 284 were affiliated with the Chinese Hospital Association and 271 were healthcare highly sought-after talent （clinical pharmacist） training bases. In terms of structural quality， the core indicator compliance rate for hospital-level training systems exceeded 80%， the rate of special fund utilization for designated purposes reached 80.13%， and the overall compliance rate for software and hardware facilities surpassed 88%. A total of 1 348 preceptors were employed across the training bases， among whom those with senior professional titles and full-time specialist clinical pharmacists as lead preceptors accounted for 62.91% and 94.36%， respectively. Regarding process quality， the compliance rate for “establishment of clinical practice teaching groups in accordance with regulations during clinical department rotations” was 85.19%， and 79.80% and 76.09% of the bases were found to implement strict confidentiality in theoretical examinations and meet the required scale of assessment cases， respectively. However， formal documents of corresponding training management regulations were formulated in only 57.91% of the bases， and the completeness and standardization rate of training manual completion was merely 47.47%. In addition， considerable disparities in quality management levels were observed among provinces， with issues in training process quality being particularly prominent. CONCLUSIONS The management system， hardware facilities， and preceptor staffing of clinical pharmacist training bases in China are relatively well-established， yet notable variations in quality management exist among training bases across different provinces.

The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) is higher among individuals with inflammatory bowel disease (IBD) than in the general population. Emerging evidence indicates that the development of MASLD in patients with IBD may occur independently of traditional metabolic risk factors, suggesting a unique pathophysiological mechanism distinct from conventional MASLD pathways. Bile acids (BAs), which act as critical signaling molecules in enterohepatic circulation, play an essential role in maintaining gastrointestinal homeostasis through bidirectional gut–liver axis communication. These molecules are increasingly recognized as pivotal regulators in the progression of both MASLD and IBD. While previous studies have characterized the dynamics of BA in blood or fecal samples under both conditions, a comprehensive understanding of their metabolic profiles and the associated interactions within the gut–liver axis is still lacking. This review synthesizes current evidence from studies employing BA metabolomics to investigate IBD and MASLD. By focusing on BA signatures, we summarize conserved alterations between these two conditions and their potential mechanisms of disease progression. Our review advances understanding of BA-mediated pathways in IBD and MASLD, providing a foundation for assessing their roles in contributing to the pathogenesis of MASLD in patients with IBD.

ObjectiveTo construct a competing endogenous RNA （ceRNA） network involving long non-coding RNA NOTCH1 （lncRNA NOTCH1） and investigate whether Xianglian Huazhuo prescription （XLHZ） ameliorates gastric mucosal injury via regulating ferroptosis through the lncRNA NOTCH1/microRNA-138-5p （miR-138-5p）/silent information regulator 1 （SIRT1） axis. MethodsLncRNA sequencing and bioinformatics tools were used to construct the ceRNA network involving lncRNA NOTCH1. In the animal experiments， a chronic atrophic gastritis （CAG） model was induced by N-methyl-N'-nitro-N-nitrosoguanidine （MNNG） in mice. Mice were randomized into normal， model， Morodan （2.0 g·kg^-1）， and high-， medium-， and low-dose （7.6， 3.8， 1.9 g·kg^-1， respectively） XLHZ groups （n=10）. Transmission electron microscopy was adopted to assess gastric pathology. Real-time PCR was employed to measure the mRNA levels of lncRNA NOTCH1， miR-138-5p， SIRT1， nuclear factor erythroid 2-related factor 2 （Nrf2）， and glutathione peroxidase 4 （GPX4）. Western blot was adopted to quantify the protein levels of SIRT1， Nrf2， and GPX4 in the gastric tissue. In the cell experiment， dual-luciferase assay was employed to verify the targeting among lncRNA NOTCH1， miR-138-5p， and SIRT1. MNNG was used to treat GES-1 cells for disease modeling. The effects of NOTCH1 mimics on the expression of lncRNA NOTCH1， miR-138-5p， and SIRT1， as well as the effects of miR-138-5p inhibitor on the expression of miR-138-5p and SIRT1， were observed. The rescue experiment with XLHZ was designed with five groups： GES-1， GES-1+MNNG （Model）， Model+XLHZ， Model+NOTCH1 inhibitor+XLHZ， and Model+NOTCH1 inhibitor+miR-138-5p mimics+XLHZ. Real-time PCR and immunofluorescence assay were employed to measure the mRNA levels of lncRNA NOTCH1， miR-138-5p， SIRT1， Nrf2， and GPX4 and the Fe²⁺ content， respectively， in GES-1 cells. ResultsThe modeled mice showed mitochondrial damage with shrinkage and cristae loss， downregulated mRNA/protein levels of lncRNA NOTCH1， SIRT1， Nrf2， GPX4， and upregulated expression of miR-138-5p （P<0.01）. Compared with the model group， drug treatments reduced mitochondrial structural damage and the membrane density decreased， partially recovered the crista structure， downregulated the expression of miR-138-5p， and upregulated the mRNA and protein levels of lncRNA NOTCH1， SIRT1， Nrf2， and GPX4 （P<0.05， P<0.01）. In the cell experiments， the dual-luciferase assays confirmed lncRNA NOTCH1 bound to miR-138-5p and miR-138-5p bound to SIRT1， both suppressing luciferase activity （P<0.05， P<0.01）. Compared with the blank control group， the model group showed decreased expression of lncRNA NOTCH1， SIRT1， Nrf2， GPX4， increased expression of miR-138-5p， and enhanced Fe²⁺ fluorescence （P<0.01）. NOTCH1 mimics or miR-138-5p inhibitor reversed these changes （P<0.05， P<0.01）. Rescue experiments showed that NOTCH1 inhibitor reversed XLHZ-induced miR-138-5p decrease and SIRT1 increase （P<0.01）， while miR-138-5p overexpression suppressed SIRT1 expression （P<0.05， P<0.01）. The results confirmed that lncRNA NOTCH1 negatively regulated miR-138-5p， which in turn negatively regulated SIRT1. ConclusionXLHZ effectively alleviates gastric mucosal injury and curbs CAG progression by inhibiting ferroptosis through modulation of the lncRNA NOTCH1/miR-138-5p/SIRT1 axis.

ObjectiveTo explore the mechanism of Xianglian Huazhuo prescription （XLHZ） in ameliorating chronic atrophic gastritis （CAG） by regulating lysosomal iron metabolism. MethodsIn the animal experiments， a mouse model of CAG was established through a combined modeling approach， including free drinking of N-methyl-N′-nitro-N-nitrosoguanidine （MNNG， 100 mg·L^-1）， gavage of ranitidine （8 g·L^-1）， and irregular feeding. Mice were randomly assigned into the normal， model， Morodan （2.0 g·kg^-1）， and high-， medium-， and low-dose （7.2， 3.8， 1.9 g·kg^-1， respectively） XLHZ groups. In the cell experiments， GES-1 cells were treated with MNNG to construct a cell model of CAG， and cells were allocated into the GES-1， GES-1+MNNG （Model）， and Model+XLHZ groups. The general physical conditions of mice in each group were observed. Hematoxylin-eosin （HE） staining was used to detect the pathological morphology of the gastric mucosa. Transmission electron microscopy was employed to observe the ultrastructure of gastric mucosal cells. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the serum levels of interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and interleukin-10 （IL-10） in the serum. Western blot was used to determine the protein levels of lysosome-associated membrane protein 1 （LAMP1）， nuclear receptor coactivator 4 （NCOA4）， ferritin heavy chain 1 （FTH1）， six-transmembrane epithelial antigen of prostate 3 （Steap3）， and transient receptor potential mucolipin 1 （TRPML1） in the gastric tissue. Immunohistochemistry was employed to detect the positive expression of glutathione peroxidase 4 （GPX4） and 8-hydroxy-2′-deoxyguanosine （8-OHdG） in the gastric tissue. Fluorescent probe method was used to detect the levels of Fe²⁺ and reactive oxygen species （ROS）. Immunofluorescence assay was applied to observe the co-localization of FTH1 and LAMP1. ResultsThe animal experiments showed that compared with the normal group， the model group exhibited poor mental status and hair condition， accompanied by decreased locomotor activity， food and water intake， and even reduced body weight. HE staining results showed that the gastric mucosal epithelium of model mice presented poor continuity， significantly decreased mucosal thickness， irregular gastric fovea morphology with widened spacing， dilated glandular cavities， reduced and disarranged glands with obvious atrophy， and extensive inflammatory cell infiltration. Transmission electron microscopy revealed that the mitochondria were markedly shrunken with condensed and deeply stained matrix， drastically reduced and irregularly arranged cristae， and even vacuolization， and the outer mitochondrial membrane shrank and ruptured. In addition， the model group showed elevated serum levels of IL-6 and IL-1β （P<0.01）， declined serum level of IL-10 （P<0.01）， upregulated protein levels of LAMP1， NCOA4， Steap3， and TRPML1 （P<0.01）， downregulated protein level of FTH1 （P<0.01） in the gastric tissue， reduced positive expression of GPX4 （P<0.01）， and increased positive expression of 8-OHdG （P<0.01）. Compared with the model group， all the treatment groups showed improved mental state and hair appearance， increased locomotor activity， food and water intake， as well as gradual body weight gain in mice. HE staining demonstrated that the gastric mucosal epithelium of mice in each treatment group was continuous and intact， with normalized gastric fovea morphology， narrowed glandular cavities， increased and neatly arranged glands， and alleviated inflammatory cell infiltration. Transmission electron microscopy results showed that the mitochondria in mice from each treatment group possessed intact structures with recovered normal volume， increased and regularly arranged cristae， and homogeneous density of the mitochondrial membrane. The mice treated with high and medium doses of XLHZ exhibited declined serum levels of IL-6 and IL-1β （P<0.01） and elevated serum level of IL-10 （P<0.01）. Low-dose XLHZ reduced serum IL-1β level in mice （P<0.05）. The expression levels of LAMP1， NCOA4， Steap3 and TRPML1 protein in gastric tissue of mice in XLHZ high- and medium-dose groups were decreased （P<0.05， P<0.01）， and the expression level of FTH1 protein was increased （P<0.05， P<0.01）. The positive expression of GPX4 in the gastric tissue was increased in the high- and medium-dose XLHZ groups （P<0.05， P<0.01）， and that of 8-OHdG was decreased in all treatment groups （P<0.01）. The cell experiments showed that compared with the GES-1 group， the fluorescence intensities of Fe²⁺ and ROS， as well as the co-localization of FTH1 and LAMP1， were significantly increased in the GES-1 + MNNG group （P<0.01）. Compared with the GES-1 + MNNG group， the fluorescence intensities of Fe²⁺ and ROS were markedly decreased in the Model + XLHZ group （P<0.01）， while the co-localization of FTH1 and LAMP1 was reduced （P<0.05）. ConclusionXLHZ can effectively regulate lysosomal iron metabolism and ameliorate gastric mucosal and cellular injury induced by CAG.