ObjectiveTo investigate the mechanism by which Xianglian Huazhuo prescription （XLHZ） ameliorates chronic atrophic gastritis （CAG） through regulating glycolysis via the microRNA-34b-5p （miR-34b-5p）/6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 1 （PFKFB1） signaling pathway. MethodsBioinformatic screening was performed to identify the target genes of miR-34b-5p. In the animal experiments， a mouse model of CAG was established through a combination of N-methyl-N′-nitro-N-nitrosoguanidine （MNNG）， ranitidine， and irregular feeding. The mice were randomized into the following groups： normal， model， Morodan group （2 g·kg^-1）， and high-， medium-， and low-dose XLHZ groups（7.2，3.8，1.9 g·kg^-1）. In the cell experiments， GES-1 cells were treated with MNNG for the modeling of CAG and grouped as follows： GES-1， MNNG+GES-1， MNNG+GES-1+XLHZ（10%）， MNNG+GES-1+miR-34b-5p mimics， MNNG+GES-1+miR-34b-5p inhibitor， MNNG+GES-1+PFKFB1 inhibitor， and MNNG+GES-1+PFKFB1 mimics+XLHZ（10%）. The general conditions of mice were observed. Real-time PCR was adopted to measure the expression levels of miRNA-34b-5p and PFKFB1 mRNA in the gastric mucosa of mice in each group. Dual luciferase reporter gene was used to verify the targeting interaction between miR-34b-5p and PFKFB1 in GES-1 cells exposed to MNNG. The cell-counting kit-8 （CCK-8） was used to screen the drug-containing serum concentration. Real-time PCR was employed to verify the transfection efficiency. Fluorescent probes were used to detect the expression and nuclear translocation of hypoxia-inducible factor-1α （HIF-1α） in each group of cells. The protein levels of HIF-1α， hexokinase 2 （HK2）， PFKFB1， phosphofructokinase 1 （PFK1）， and lactate dehydrogenase （LDHA） in the gastric mucosa of mice were determined by Western blot. The levels of glucose consumption and lactate in the serum and cells were measured by biochemical methods. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the content of adenosine triphosphate （ATP） in the gastric mucosa tissue and cells. ResultsThe animal experiments showed that compared with the normal group， the model group exhibited symptoms including mental fatigue， lethargy， sparse and dull fur， a tendency to curl up， sluggish responses， reduced food and water intake， and slow body weight gain. In addition， the model group showed decreased expression of miRNA-34b-5p （P<0.01）， increased mRNA level of PFKFB1 （P<0.01）， upregulated protein levels of HIF-1α， HK2， PFKFB1， PFK1， and LDHA （P<0.01）， and increased glucose consumption， lactate content， and ATP content （P<0.01）. Compared with the model group， the XLHZ group and Morodan group showed improved mental state， gradually improved fur， increased activity， food and water intake， and body weight. HE showed that each treatment group exhibited well arranged and increased gastric mucosal glands， reduced inflammatory cells， and recovered gastric pits. Transmission electron microscopy showed that the size of mitochondria in each treatment group returned to normal， with no obvious irregular shape， complete and clear cristae， and uniform matrix. Furthermore， each treatment group showed increased expression of miRNA-34b-5p （P<0.05）， reduced mRNA level of PFKFB1 （P<0.05）， downregulated protein levels of HIF-1α， HK2， PFKFB1， PFK1， and LDHA （P<0.05）， and decreased glucose consumption， lactic acid， and ATP （P<0.05）. The cell experiments showed that the expression and nuclear translocation of HIF-1α were reduced in all groups after treatment （P<0.05）. The cell transfection efficiency was satisfactory （P<0.05）. miR-34b-5p exhibited an effect comparable to that of XLHZ， effectively inhibiting glycolysis， whereas PFKFB1 promoted glycolysis and reversed the protective effect of XLHZ in CAG mice （P<0.05）. ConclusionXLHZ could regulate the miR-34b-5p/PFKFB1 axis to inhibit glycolysis， thereby ameliorating MNNG-induced gastric mucosal atrophy.

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.

ObjectiveTo investigate the mechanism by which Xianglian Huazhuo prescription （XLHZ） ameliorates chronic atrophic gastritis （CAG） through regulating glycolysis via the microRNA-34b-5p （miR-34b-5p）/6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 1 （PFKFB1） signaling pathway. MethodsBioinformatic screening was performed to identify the target genes of miR-34b-5p. In the animal experiments， a mouse model of CAG was established through a combination of N-methyl-N′-nitro-N-nitrosoguanidine （MNNG）， ranitidine， and irregular feeding. The mice were randomized into the following groups： normal， model， Morodan group （2 g·kg^-1）， and high-， medium-， and low-dose XLHZ groups（7.2，3.8，1.9 g·kg^-1）. In the cell experiments， GES-1 cells were treated with MNNG for the modeling of CAG and grouped as follows： GES-1， MNNG+GES-1， MNNG+GES-1+XLHZ（10%）， MNNG+GES-1+miR-34b-5p mimics， MNNG+GES-1+miR-34b-5p inhibitor， MNNG+GES-1+PFKFB1 inhibitor， and MNNG+GES-1+PFKFB1 mimics+XLHZ（10%）. The general conditions of mice were observed. Real-time PCR was adopted to measure the expression levels of miRNA-34b-5p and PFKFB1 mRNA in the gastric mucosa of mice in each group. Dual luciferase reporter gene was used to verify the targeting interaction between miR-34b-5p and PFKFB1 in GES-1 cells exposed to MNNG. The cell-counting kit-8 （CCK-8） was used to screen the drug-containing serum concentration. Real-time PCR was employed to verify the transfection efficiency. Fluorescent probes were used to detect the expression and nuclear translocation of hypoxia-inducible factor-1α （HIF-1α） in each group of cells. The protein levels of HIF-1α， hexokinase 2 （HK2）， PFKFB1， phosphofructokinase 1 （PFK1）， and lactate dehydrogenase （LDHA） in the gastric mucosa of mice were determined by Western blot. The levels of glucose consumption and lactate in the serum and cells were measured by biochemical methods. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the content of adenosine triphosphate （ATP） in the gastric mucosa tissue and cells. ResultsThe animal experiments showed that compared with the normal group， the model group exhibited symptoms including mental fatigue， lethargy， sparse and dull fur， a tendency to curl up， sluggish responses， reduced food and water intake， and slow body weight gain. In addition， the model group showed decreased expression of miRNA-34b-5p （P<0.01）， increased mRNA level of PFKFB1 （P<0.01）， upregulated protein levels of HIF-1α， HK2， PFKFB1， PFK1， and LDHA （P<0.01）， and increased glucose consumption， lactate content， and ATP content （P<0.01）. Compared with the model group， the XLHZ group and Morodan group showed improved mental state， gradually improved fur， increased activity， food and water intake， and body weight. HE showed that each treatment group exhibited well arranged and increased gastric mucosal glands， reduced inflammatory cells， and recovered gastric pits. Transmission electron microscopy showed that the size of mitochondria in each treatment group returned to normal， with no obvious irregular shape， complete and clear cristae， and uniform matrix. Furthermore， each treatment group showed increased expression of miRNA-34b-5p （P<0.05）， reduced mRNA level of PFKFB1 （P<0.05）， downregulated protein levels of HIF-1α， HK2， PFKFB1， PFK1， and LDHA （P<0.05）， and decreased glucose consumption， lactic acid， and ATP （P<0.05）. The cell experiments showed that the expression and nuclear translocation of HIF-1α were reduced in all groups after treatment （P<0.05）. The cell transfection efficiency was satisfactory （P<0.05）. miR-34b-5p exhibited an effect comparable to that of XLHZ， effectively inhibiting glycolysis， whereas PFKFB1 promoted glycolysis and reversed the protective effect of XLHZ in CAG mice （P<0.05）. ConclusionXLHZ could regulate the miR-34b-5p/PFKFB1 axis to inhibit glycolysis， thereby ameliorating MNNG-induced gastric mucosal atrophy.

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.

Objective Guided by"Medical Record Management Quality Control Indicators(2021 Edition)"(hereafter regarded as Medical Record Quality Indicators),this study aims to evaluate the quality of inpatient hospice medical records at a tertiary hospital in Guangzhou.Methods A total of 1,071 inpatient hospice medical records from the year 2023 in a tertiary gen-eral hospital in Guangzhou were selected for evaluation.The evaluation focused on three aspects:documentation compliance of documentation of critical examinations(including CT/MRI,pathology,and pathogen examinations),the compliance rate of treat-ment behavior records(encompassing antibiotic usage,chemotherapy or radiotherapy or targeted or immunotherapy for malignant tumors,and surgical records),and the incidence of unreasonable duplication within medical record.Results The compliance rate for major examination records ranged from 47.7％to 100.0％,with the lowest compliance rate(47.7％)observed in docu-mentation of pathogen culture analysis.Treatment behavior documentation compliance varied from 49.1％to 100.0％,with the lowest compliance rate of 49.1％observed in the recording of antibiotic usage.Rates of inappropriate duplication ranged from 1.0％to duplication(63.1％),with the highest rate of 63.1％occurring when initial progress notes replicated admission histo-ries without synthesis(63.1％).Conclusion The Medical Record Management Quality Control Indicators serves as an effective tool for evaluating the dimensions of medical record quality and offers a systematic framework for enhancing documentation integri-ty within hospitals.

Objective Guided by"Medical Record Management Quality Control Indicators(2021 Edition)"(hereafter regarded as Medical Record Quality Indicators),this study aims to evaluate the quality of inpatient hospice medical records at a tertiary hospital in Guangzhou.Methods A total of 1,071 inpatient hospice medical records from the year 2023 in a tertiary gen-eral hospital in Guangzhou were selected for evaluation.The evaluation focused on three aspects:documentation compliance of documentation of critical examinations(including CT/MRI,pathology,and pathogen examinations),the compliance rate of treat-ment behavior records(encompassing antibiotic usage,chemotherapy or radiotherapy or targeted or immunotherapy for malignant tumors,and surgical records),and the incidence of unreasonable duplication within medical record.Results The compliance rate for major examination records ranged from 47.7％to 100.0％,with the lowest compliance rate(47.7％)observed in docu-mentation of pathogen culture analysis.Treatment behavior documentation compliance varied from 49.1％to 100.0％,with the lowest compliance rate of 49.1％observed in the recording of antibiotic usage.Rates of inappropriate duplication ranged from 1.0％to duplication(63.1％),with the highest rate of 63.1％occurring when initial progress notes replicated admission histo-ries without synthesis(63.1％).Conclusion The Medical Record Management Quality Control Indicators serves as an effective tool for evaluating the dimensions of medical record quality and offers a systematic framework for enhancing documentation integri-ty within hospitals.

AIM: To study the possible molecular mechanism of beta-amyloid peptide_ 1-40 -induced apoptosis in rat cortical neurons. METHODS: 40 mg/L beta-amyloid peptide_ 1-40 (A?_ 1-40 ) was used to induce apoptosis in cultured rat cortical neurons. The level of CDK4, phosphorylated pRB were detected by flow cytometry and immunoblotting; RT-PCR was used to examine the mRNA expression of E2F1 while fluorescent spectrofluorometer was used to measure caspase-3 activity. All of the above study was designed to observe whether the level of CDK4, phosphorylated pRB and E2F1 mRNA expression could be affected by A?_ 1-40 . RESULTS: (1)The level of CDK4, phosphorylated pRB increased markedly 2-4 hours after treatment with A?_ 1-40 , and caspase-3 activity elevated remarkably 12-24 hours after treatment with A?_ 1-40 ; (2) E2F1 mRNA expression was upregulated 3 hours after incubation with A?_ 1-40 . CONCLUSION: A?_ 1-40 may induce apoptosis in rat cortical neurons in a manner dependent on CDK4-pRB-E2F1 pathway.