This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

Objective To explore the dietary nutrition status and nutritional intervention strategy of patients with Alzheimer’s disease (AD). Methods Among the 1 332 patients with AD diagnosed at Xijing Hospital from January 2021 to December 2023 were enrolled as the study subjects. The dietary intake data of patients were collected through questionnaire surveys and dietary reviews. During the study period, 30 patients did not complete the intervention due to withdrawal or loss of follow-up. Based on the actual number of people who completed the intervention, AD patients were randomly divided into intervention group (n=651, individualized nutritional intervention strategy) and control group (n=651, routine nutritional intervention), and both groups were intervened for 3 months. The cognitive function (MMSE score and MoCA score), nutritional status (MNA scale, NRS-2002 scale), and quality of life (GQOL-74) of the two groups of AD patients were compared to evaluate the effectiveness of the intervention strategies. Results A total of 1 332 questionnaires were distributed, and 1 302 valid questionnaires were finally recovered, with an effective recovery rate of 97.75% (1 302/1 332). The survey results showed that there were no statistical differences in baseline characteristics and dietary nutrition status between the two groups of AD patients before intervention (P>0.05). After nutritional intervention, the cognitive function, quality of life, and nutritional status of patients in the intervention group were significantly improved. The MMSE score, MoCA score, MNA score, and GQOL-74 score of the intervention group were significantly higher than those of the control group, while the NRS-2002 score was lower than that of the control group (P<0.05). Conclusion Nutritional intervention strategy has a significant effect on improving nutritional status, cognitive function, and quality of life of AD patients.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

AIM: To investigate the effects of agkis-trodon halys venom anti-tumor component (AHVAC-) on the biological behavior of gastric cancer MKN-28 cells. METHODS: Gastric cancer MKN-28 cells were treated with the experimental concentrations (5, 10, 15 μg/mL) of AHAVC- for 24 h. Cell proliferation and toxicity assay (cell counting kit-8, CCK-8) was used to detect the inhibition rates of the cells in different concentrations of AHVAC-. The migration ability of the cells was evaluated by wound-healing and Transwell assay. The apoptosis were observed by laser confocal microscopy with annexin V-mCherry/DAPI double staining, and the apoptosis rates were analyzed by flow cytometry with annexin V-FITC/PI double fluorescence staining. The protein level of Caspease-3 was determined by Western blot. RESULTS: Compared with normal control group, the results of AHVAC- concentration groups showed that with the increase of AHVAC- concentration, the proliferative activity of MN-28 cells decreased gradually (P<0.01), the cell migration ability decreased gradually (P<0.01), and the cell apoptosis rate increased (P<0.05). The expression of apoptosis-related protein Caspease-3 was up-regulated (P<0.01). CONCLUSION: AHVAC- inhibits proliferation and migration of gastric cancer MSN-28 cells and induces apoptosis.

Objective To observe the morphological changes of levator hiatus in patients with gestational diabetes mellitus(GDM)after spontaneous delivery with ultrasonography.Methods A total of 302 pregnant women in the first trimester(6-8 weeks)were prospectively observed,and the parameters of pelvic floor muscle hiatus were measured with ultrasound during the first trimester,also 12 weeks,6 months and 1 year after delivery at resting-state(resting period),anal contraction state(systole period)and Valsalva maneuver(tension period),respectively.Blood glucose was measured at 28 weeks of gestation,GDM was diagnosed,and the pregnant women enrolled were divided into GDM group and non-GDM group.The ultrasonic parameters and postpartum pelvic floor muscle tension were compared between groups.Spearman correlation analysis was used to evaluate the correlations of pelvic floor muscle tension grade and anal levator hiatus parameters in GDM group.Results Totally 153 pregnant women were enrolled and assigned into GDM group(n=51)and non-GDM group(n=102).Transversal diameter of levator hiatus(LH-TD),anteroposterior diameter of levator hiatus(LH-APD)and levator hiatus area(LHA)in different periods 12 weeks postpartum in both groups were higher than those in early pregnancy(all P＜0.05).Six months and 1 year postpartum,in GDM group,LH-APD and LHA in systole period,also LH-TD,LH-APD and LHA in tension period were higher than those in early pregnancy(all P＜0.05),while in non-GDM group,LH-APD and LHA in tension period were higher than those of early pregnancy(all P＜0.05).One year after delivery,LH-APD and LHA in systolic period,as well as LH-TD and LHA in tension period in GDM group were all higher than those in non-GDM group(all P＜0.05),whereas the proportion of pelvic floor muscle tension of grade Ⅱ-Ⅲ was higher,of grade Ⅳ-Ⅴ was lower in GDM group than those in non-GDM group(P＜0.05).One year after delivery,pelvic floor muscle tone grade in GDM group was negatively correlated with LH-TD,LH-APD and LHA in resting,systole and tension period(all P＜0.05).Conclusion The morphology of levator hiatus changed greatly in GDM patients after spontaneous delivery,and rehabilitation training should be carried out early.

Objective:To explore the mechanism by which Pien Tze Huang improves liver Kupffer cell damage induced by lipopolysaccharide (LPS) by regulating the expression of miR-155.Methods:LPS induced liver Kupffer cells to establish a cell injury model to simulate septic liver injury. RT-qPCR was used to detect the expression of miR-155 in damaged cells, and RT-qPCR, Western Blot, ELISA and flow cytometry were used to evaluate the inflammatory response and apoptosis of damaged cells. Then we treated LPS-induced Kupffer cells with Pien Tze Huang at different concentrations (0 mg/L, 5 mg/L, 10 mg/L and 15 mg/L), and detected the expression of miR-155 in the cells, the inflammatory response of the cells and Apoptosis rate. MiR-155 was silenced in the cell injury model, and RT-qPCR, Western Blot, ELISA and flow cytometry were used to evaluate the effect of miR-155 on inflammatory response and apoptosis of model cells. Overexpression of miR-155 in damaged cells treated with Pien Tze Huang was used to detect changes in cellular inflammatory response and apoptosis. Data are expressed in the form of mean ± standard deviation, and each group of data is analyzed using t test or one-way analysis of variance.Results:In the LPS-induced liver Kupffer cell injury model, the expression of miR-155 was significantly increased ( P<0.05), the expression levels of pro-inflammatory factors IL-6 and TNF-α were significantly increased, and the anti-inflammatory factor IL-10 was significantly increased. was inhibited ( P<0.05), and the cell apoptosis rate was significantly increased ( P<0.05). After Pien Tze Huang treatment, the expression of miR-155 in damaged liver cells was inhibited ( P<0.05), the levels of cellular inflammatory factors IL-6 and TNF-α were inhibited, and the expression of anti-inflammatory factor IL-10 was promoted ( P<0.05). Inhibit cell apoptosis ( P<0.05). Silencing miR-155 reduced the inflammatory response and apoptosis rate of cells ( P<0.05). Overexpression of miR-155 can reverse the effect of Pien Tze Huang on liver cell injury ( P<0.05). Conclusions:In the model of LPS-induced liver Kupffer cell injury, Pien Tze Huang can inhibite the inflammatory response and apoptosis of cells by inhibiting the expression of miR-155.

Gingival mesenchymal stem cells(GMSCs)are a population of mesenchymal stem cells found in the lamina propria of gingi-val tissue and can be isolated not only from healthy gingival tissue but also from hyperplastic or even inflamed gingival tissue.GMSCs have become a hot topic of research in oral disease treatment because of their abundant sources,easy availability,unique immunomod-ulatory properties and multi-directional differentiation potential.GMSCs have been used in the treatment of periodontitis,gingival reces-sion,oral cancer,mandibular defects,peripheral nerve injury repair and so on.To prevent and treat oral diseases,this study will re-view the recent progress of research on the application of GMSCs in oral diseases.