ObjectiveTo investigate the effects of Ditantang on metabolic dysfunction-associated fatty liver disease （MAFLD） in rats by focusing on the regulation of glycogen synthesis mediated by the uridine diphosphate glucose （UDPG）-site-1-protease （S1P）-sterol regulatory element-binding protein （SREBP） axis. MethodsMAFLD was modeled in SD rats by feeding a high-fat diet for 12 weeks. Rats were randomized into a control group， a model group， low-， medium-， and high-dose （2.68， 5.36， and 10.72 g·kg^-1·d^-1， respectively） Ditantang groups， and a positive control （Yishanfu， 0.18 g·kg^-1·d^-1） group. Starting from week 9 of modeling， each treatment group received corresponding drug interventions via gavage. After the experiment， the serum levels of total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， and high-density lipoprotein cholesterol （HDL-C） were measured. The levels of TG， non-esterified fatty acids （NEFA）， glycogen， glucose-6-phosphate （G6P）， glucose-1-phosphate （G1P）， and UDPG in the liver tissue samples were measured by biochemical assay kits. Liver pathological morphology and lipid/glycogen deposition were observed via hematoxylin-eosin （HE） staining， oil red O staining， and Periodic acid-Schiff （PAS） staining. Immunofluorescence assay was conducted to detect the expression and localization of phosphoglucomutase-1 （Pgm1） and UDP-glucose pyrophosphorylase 2 （Ugp2） in the rat liver. Real-time PCR and Western blot were employed to quantify mRNA and protein levels， respectively， of key glycogen synthesis enzymes （Pgm1 and Ugp2）， key lipogenesis-related transcription factor SREBP and its target genes ［acetyl-CoA carboxylase （ACC）， fatty acid synthetase （FASN）， and stearoyl-CoA desaturase （SCD1）］， as well as S1P. ResultsCompared with the control group， the model group exhibited elevated levels of TC， TG， LDL-C in the serum and TG and NEFA in the liver， decreased serum HDL-C level （P<0.01）， reduced hepatic levels of G1P， G6P， UDPG， and glycogen （P<0.01）， appearance of fat vacuoles of varying sizes and abundant red lipid droplets， with prominent lipid deposition and reduced areas of deep glycogen staining in the liver tissue， upregulated mRNA and protein levels of SREBP1， S1P， ACC， FASN， and SCD1 （P<0.01）， and downregulated mRNA and protein levels of Pgm1 and Ugp2 （P<0.01）. Compared with the model group， all doses of Ditantang reduced the levels of TC and TG in the serum and TG and NEFA in the liver， while elevating the serum HDL-C level. Additionally， medium- and high-dose Ditantang reducted the LDL-C level （P<0.05）. Ditantang at all doses increased the hepatic levels of G1P， G6P， UDPG， and glycogen， alleviated hepatic steatosis and lipid deposition， enhanced glycogen storage， downregulated the mRNA and protein levels of SREBP1， S1P， ACC， FASN， and SCD1 （P<0.05）， while upregulating the expression of Pgm1 and Ugp2 （P<0.01）. Immunofluorescence analysis revealed decreased fluorescence intensity of S1P and enhanced fluorescence intensity of Ugp2 （P<0.01）. ConclusionDitantang can regulate glycogen synthesis through the UDPG-S1P-SREBP axis to prevent and treat MAFLD.

OBJECTIVE Analyze the nasal nitric oxide(NNO)of CRS children,and explore the clinical value of NNO in the diagnosis and treatment of CRS in children.METHODS CRS children diagnosed in the outpatient clinic were selected,and were divided into CRS with and without AR according to their allergen results.VAS score and NNO test were performed for them.Healthy children during the same period were selected as the control group.Finally their results were compared and analyzed.RESULTS The NNO of CRS children with and without AR were(193±62)ppb and(138±49)ppb,both lower than the control group's[(243±51)ppb];There were negative correlations between NNO and VAS scores in CRS children without AR before and after treatment;The NNO of CRS children with and without AR were significantly increased after treatment(P<0.05);NNO has high predictive value for diagnosing CRS children without AR(P<0.01).CONCLUSION The levels of NNO in different types of CRS were lower than normal,and CRS children without AR was lower than those with AR.NNO could assist in the diagnosis of CRS,dynamically reflect the severity of nasal inflammation,and help to distinguish the allergic status of CRS.

Objective To investigate the effects of Icariin(ICA)on the proliferation,angiogenesis,and migration of human retinal pigment epithelial(RPE)cells in a high-glucose environment and its mechanism.Methods ARPE-19 cells in good growth state were selected and divided into five groups:control group(Control group),high glucose group(HG group),high glucose+low-dose Icariin group(HG+ICA-L group),high glucose+medium-dose Icariin group(HG+ICA-M group),and high glucose+high-dose Icariin group(HG+ICA-H group).The cells in the control group were cul-tured in a medium containing 5.5 mmol·L-1 glucose.Cells in the HG group were cultured in a medium containing 30.0 mmol·L-1 glucose.The cells in each ICA intervention group were first cultured in a medium containing 30.0 mmol·L-1 glucose,and then 10.0 μmol·L-1,20.0 μmol·L-1 and 40.0 μmol·L-1 ICA were added for culture,respectively.The CCK-8 assay was used to detect cell proliferation activity,the EdU assay was used to detect cell proliferation,the Transwell assay was used to detect cell migration ability,and the Matrigel assay was used to detect in vitro tube formation ability.The expression levels of α-smooth muscle actin(α-SMA),matrix metalloproteinase-2(MMP-2),vascular endothelial growth factor A(VEGFA),epidermal growth factor receptor(EGFR),and proteins related to the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)pathway were detected by Western blot.Results The cell viability and EdU-positive rate of ARPE-19 cells in the HG group were higher than those in the Control group(all P＜0.05).The cell viability and EdU-positive rate in the HG+ICA-L,HG+ICA-M,and HG+ICA-H groups were lower than those in the HG group(all P＜0.05).The number of migrated cells and tubes formed in the HG+ICA-L,HG+ICA-M,and HG+ICA-H groups were less than those in the HG group,and the expression levels of α-SMA,MMP-2,VEGFA,and EGFR proteins were lower than those in the HG group(all P＜0.05).The levels of p-PI3K and p-Akt in the HG+ICA-L,HG+ICA-M,and HG+ICA-H groups were lower than those in the HG group(all P＜0.05).Conclusion ICA inhibits the proliferation,migration,and angiogenesis of ARPE-19 cells stimulated by high glucose by suppressing the activation of the PI3K/Akt pathway.

Recent years have witnessed significant advancements in myopia control research through the application of diffuse optical technology(DOT)spectacle lenses. Myopia has emerged as a global public health challenge, affecting nearly half of the world's population, with childhood and adolescent myopia rates continuing to rise. DOT lenses represent an innovative myopia control intervention based on retinal contrast signal theory. These lenses incorporate micro-light scattering dots distributed across the lens surface to reduce retinal imaging contrast and modulate the influence of visual input on axial elongation, thereby slowing myopia progression. The core mechanism operates through refractive index differences between the lens substrate(1.53)and scattering dots(1.50), which generate optical scattering effects. This design maintains clear vision through a central 5 mm optical zone while effectively reducing contrast signal intensity in the peripheral retina. Large-scale randomized controlled trials, including the CYPRESS study, have demonstrated significant myopia control efficacy in children aged 6-10 years: 12-month follow-up data revealed a 74% reduction in myopia progression and a 50% reduction in axial elongation, with sustained safety and visual quality maintained over 4-year long-term follow-up. However, several aspects of DOT technology remain contentious and require further clinical validation, including its applicability across different age groups, optimal scattering dot density configurations, combined application effects with other myopia control methods, and long-term visual adaptation during extended use. This review systematically examines the theoretical foundations, design characteristics, clinical application progress, and future development directions of DOT technology, providing scientific evidence for clinical myopia prevention and control strategy formulation.

Objective: To explore the regulatory effects of ginkgo biloba extract on airway inflammatory injury and Toll⁃like receptor 4(TLR4)/nucleotide⁃binding oligomerization domain⁃containing 3(NLRP3) pathway in rats with vided into four groups : the normal control group , Methods: Thirty⁃six male SD rats were selected and randomly divided into four groups : the normal control group , the model group , the prednisone treatment group , and the ginkgo biloba extract treatment group , with 9 rats in each group. Except for the normal control group , the COPD rat mod⁃els in the other groups was constructed by intratracheal instillation of lipopolysaccharide (LPS) combined with ciga⁃rette smoke exposure. After successful modeling , the rats were continuously administered drugs for 12 weeks , fol⁃lowed by sampling. The general conditions and respiratory symptoms of the rats were observed. The pathological changes of lung tissues were observed by hematoxylin⁃eosin (HE) staining technique ; the mRNA and protein ex⁃pression levels of TLR4 , tumor necrosis factor⁃α (TNF⁃α ) , interleukin⁃1β (IL⁃1β) and NLRP3 in rat lung tissueswere detected by real⁃time quantitative polymerase chain reaction (RT⁃qPCR) and Western blot. Results: Com⁃pared with the normal control group , the lung tissues of rats in the model group were significantly damaged , and the protein and mRNA expression of TLR4 , TNF⁃α , IL⁃1β , and NLRP3 increased ( P < 0. 05 ) . Compared with the model group , lung tissue damage was reduced in the prednisone group and the ginkgo biloba extract group , and TLR4 , TNF⁃α , IL⁃1β , NLRP3 protein and mRNA expression decreased (P < 0. 05) . Conclusion Ginkgo biloba airway inflammatory response by inhibiting the TLR4/NLRP3 signaling pathway.

Objective To investigate the effects of Icariin(ICA)on the proliferation,angiogenesis,and migration of human retinal pigment epithelial(RPE)cells in a high-glucose environment and its mechanism.Methods ARPE-19 cells in good growth state were selected and divided into five groups:control group(Control group),high glucose group(HG group),high glucose+low-dose Icariin group(HG+ICA-L group),high glucose+medium-dose Icariin group(HG+ICA-M group),and high glucose+high-dose Icariin group(HG+ICA-H group).The cells in the control group were cul-tured in a medium containing 5.5 mmol·L-1 glucose.Cells in the HG group were cultured in a medium containing 30.0 mmol·L-1 glucose.The cells in each ICA intervention group were first cultured in a medium containing 30.0 mmol·L-1 glucose,and then 10.0 μmol·L-1,20.0 μmol·L-1 and 40.0 μmol·L-1 ICA were added for culture,respectively.The CCK-8 assay was used to detect cell proliferation activity,the EdU assay was used to detect cell proliferation,the Transwell assay was used to detect cell migration ability,and the Matrigel assay was used to detect in vitro tube formation ability.The expression levels of α-smooth muscle actin(α-SMA),matrix metalloproteinase-2(MMP-2),vascular endothelial growth factor A(VEGFA),epidermal growth factor receptor(EGFR),and proteins related to the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)pathway were detected by Western blot.Results The cell viability and EdU-positive rate of ARPE-19 cells in the HG group were higher than those in the Control group(all P＜0.05).The cell viability and EdU-positive rate in the HG+ICA-L,HG+ICA-M,and HG+ICA-H groups were lower than those in the HG group(all P＜0.05).The number of migrated cells and tubes formed in the HG+ICA-L,HG+ICA-M,and HG+ICA-H groups were less than those in the HG group,and the expression levels of α-SMA,MMP-2,VEGFA,and EGFR proteins were lower than those in the HG group(all P＜0.05).The levels of p-PI3K and p-Akt in the HG+ICA-L,HG+ICA-M,and HG+ICA-H groups were lower than those in the HG group(all P＜0.05).Conclusion ICA inhibits the proliferation,migration,and angiogenesis of ARPE-19 cells stimulated by high glucose by suppressing the activation of the PI3K/Akt pathway.

In order to investigate the chemical constituents of glycosides in Piper sintenense Hatusima, column chromatographic techniques such as silica gel, ODS, MCI GEL CHP20P, Sephadex LH-20, and semi-preparative high performance liquid chromatography were used to afford nine glycosides from the n-butanol part of the 95% ethanol extract of Piper sintenense Hatusima. Based on the physicochemical properties and NMR data, the above compounds were identified as (2S)-2-hydroxy-1-(4-hydroxy-3-methoxyphenyl)-1-propanone-2-O-β-D-glucopyranoside (1), 2-phenylethyl β-D-glucopyranoside (2), benzyl α-L-arabinopyranosyl-(1''→6')-β-D-glucopyranoside (3), benzyl β-D-xylopyanosyl-(1''→6')-β-D-glucopyranoside (4), phenethyl β-D-apiofuranosyl-(1''→ 2')-β-D-glucopyranoside(5), salidroside (6), phenethanol β-D-xylopyanosyl-(1''→6')-β-D-glucopyranoside (7), (Z)-hexenyl-O-α-L-arabinopyranosyl-(1''→6')-O-β-D-glucopyranoside (8), (Z)-hexenyl-O-β-D-xylopyanosyl-(1''→6')-O-β-D-glucopyranoside (9). Compound 1 was identified as a new compound, and compounds 3-9 were isolated from the genus Piper for the first time.

Objective:To explore the relationship between dietary pattern and sexual function in people of childbearing age.Methods:This study adopted a cross-sectional method and included all women and men who visited Reproduction Center of Maanshan Maternal and Child Health Hospital, Reproductive Medicine Center of the 901th Hospital of the Joint Logistics Support Force of People's Liberation Army and Reproduction Center of Anhui Wanbei Coal Power Group General Hospital from December 2020 to March 2022. The Female Sexual Function Index (FSFI) and International Index of Erectile Function-15 (IIEF-15) were used to assess sexual function. Factor analysis was used to establish dietary patterns, and multivariate logistic regression was used to analyze the association between dietary patterns and sexual function.Results:A total of 1 290 females and 1 331 males were included in the study, including 1 031 females and 899 males with sexual dysfunction. There were 289 women and 272 men with balanced dietary pattern, 473 women and 395 men with traditional dietary pattern, 272 women and 324 men with processed dietary pattern, and 256 women and 340 men with beverage dietary pattern. After adjusting for confounding factors such as residence and age, it was found that balanced dietary pattern was negatively correated with female sexual desire disorder ( OR=0.904, 95% CI: 0.820-0.995, P=0.039), sexual arousal disorder ( OR=0.840, 95% CI: 0.759-0.929, P=0.001), vaginal lubrication disorder ( OR=0.833, 95% CI: 0.710-0.979, P=0.026), orgasmic disorder ( OR=0.764, 95% CI: 0.680-0.858, P<0.001), low sexual satisfaction ( OR=0.887, 95% CI: 0.796-0.987, P=0.028), sexual dysfunction ( OR=0.805, 95% CI: 0.714-0.907, P<0.001), and male orgasmic disorder ( OR=0.859, 95% CI: 0.763-0.967, P=0.012). The traditional dietary pattern was negatively correlated with female sexual desire disorder ( OR=0.879, 95% CI: 0.786-0.983, P=0.024), sexual arousal disorder ( OR=0.884, 95% CI: 0.784-0.995, P=0.042), male erectile disorder ( OR=0.736, 95% CI: 0.634-0.855, P<0.001), sexual desire disorder ( OR=0.753, 95% CI: 0.648-0.876, P<0.001), and sexual dysfunction ( OR=0.769, 95% CI: 0.653-0.907, P=0.020). The processed dietary pattern was positively correlated with erectile disorder ( OR=1.162, 95% CI: 1.049-1.287, P=0.004), orgasmic dysfunction ( OR=1.207, 95% CI: 1.091-1.337, P<0.001), sexual desire disorder ( OR=1.199, 95% CI: 1.081-1.330, P=0.001) and sexual dysfunction ( OR=1.134, 95% CI: 1.020-1.261, P=0.002). Beverage dietary pattern was not associated with sexual dysfunction in men and women (all P>0.05). Conclusion:Balanced, traditional dietary patterns were related to the reduce risk of sexual dysfunction in both women and men of childbearing age, while processed dietary patterns were related to the increased risk of sexual dysfunction in men of childbearing age.

Purpose: Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin. Materials and Methods: We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1. Results: Our study reveals Gal-1 expression was significantly associated with poor outcomes.Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/ Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects. Conclusions These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.

Inhibiting the death receptor 3(DR3)signaling pathway in group 3 innate lymphoid cells(ILC3s)pre-sents a promising approach for promoting mucosal repair in individuals with ulcerative colitis(UC).Paeoniflorin,a prominent component of Paeonia lactiflora Pall.,has demonstrated the ability to restore barrier function in UC mice,but the precise mechanism remains unclear.In this study,we aimed to delve into whether paeoniflorin may promote intestinal mucosal repair in chronic colitis by inhibiting DR3 signaling in ILC3s.C57BL/6 mice were subjected to random allocation into 7 distinct groups,namely the control group,the 2％dextran sodium sulfate(DSS)group,the paeoniflorin groups(25,50,and 100 mg/kg),the anti-tumor necrosis factor-like ligand 1A(anti-TL1A)antibody group,and the IgG group.We detected the expression of DR3 signaling pathway proteins and the proportion of ILC3s in the mouse colon using Western blot and flow cytometry,respectively.Meanwhile,DR3-overexpressing MNK-3 cells and 2％ DSS-induced Rag1-/-mice were used for verification.The results showed that paeoniflorin alleviated DSS-induced chronic colitis and repaired the intestinal mucosal barrier.Simultaneously,paeoniflorin inhibited the DR3 signaling pathway in ILC3s and regulated the content of cytokines(interleukin-17A,granulocyte-macrophage colony stimulating factor,and interleukin-22).Alternatively,paeoniflorin directly inhibited the DR3 signaling pathway in ILC3s to repair mucosal damage indepen-dently of the adaptive immune system.We additionally confirmed that paeoniflorin-conditioned me-dium(CM)restored the expression of tight junctions in Caco-2 cells via coculture.In conclusion,paeoniflorin ameliorates chronic colitis by enhancing the intestinal barrier in an ILC3-dependent manner,and its mechanism is associated with the inhibition of the DR3 signaling pathway.