The main ingredients of Ophiopogonjaponicas include steroidal saponins,flavonoids,polysaccharides,and so on,but the research on polysaccharides is relatively less.This particle will mainly review the chemical composition,analytical methods,and pharmacological effects of Ophiopogon polysaccharides.The Ophiopogon polysaccharides contain a variety of substances,such as MDG-1,Md-1,Md-2,OJP-1,etc;The main analysis methods were sulfuric acid method,phenol-sulfuric acid method,3,5-dinitrosalicylic acid (DNS) colorimetric method,and near-infrared spectroscopy combined with partial least squares regression method.Ophiopogon polysaccharides can effectively improve the cardiovascular system diseases,with antihypoxia,anti-inflammatory,antitumor,anti-oxidation,and other pharmacological effects.

Objective To investigate the expression level of antisense transcript of pseudogene, general transcription factor Ⅱi psedugen23 ( GTF2IP23), in breast cancer and its effect on the host gene general transcription factorⅡi (GTF2I).Methods The expressions of GTF2IP23 and GTF2I were detected in 40 cases of invasive breast cancer tumors and their counterparts by using quantitative real?time polymerase chain reaction (qRT?PCR).The effects of GTF2IP23 on the expression of GTF2I gene and cell proliferation and migration were analyzed by overexpression of GTF2IP23 in breast cancer cells. Results The expression of GTF2IP23 mRNA in breast cancer tissues was significantly higher than that in adjacent tissues ( P＜0.001), while the expression of GTF2I mRNA was significantly lower than that in adjacent tissues ( P＝0.007). The expression of GTF2IP23 was negatively correlated with GTF2I ( r＝－0.335, P＝0.025).The expression of GTF2IP23 in breast cancer cells was significantly higher than in normal breast cells ( P＜0.01), while GTF2I expression in breast cancer cells was significantly lower than that in normal breast cells (P＜0.01). Overexpression of GTF2IP23 in ZR?75?30 cells significantly reduced the expression of GTF2I (P＝0.034) and enhanced cell proliferation (P＝0.017) and migration (P＝0.026) capacity. Conclusions GTF2IP23 is distinctly upregulated in breast cancer, it inhibits the expression of real gene GTF2I and promotes the proliferation of breast cancer cells.

Objective To investigate the expression level of antisense transcript of pseudogene, general transcription factor Ⅱi psedugen23 ( GTF2IP23), in breast cancer and its effect on the host gene general transcription factorⅡi (GTF2I).Methods The expressions of GTF2IP23 and GTF2I were detected in 40 cases of invasive breast cancer tumors and their counterparts by using quantitative real?time polymerase chain reaction (qRT?PCR).The effects of GTF2IP23 on the expression of GTF2I gene and cell proliferation and migration were analyzed by overexpression of GTF2IP23 in breast cancer cells. Results The expression of GTF2IP23 mRNA in breast cancer tissues was significantly higher than that in adjacent tissues ( P＜0.001), while the expression of GTF2I mRNA was significantly lower than that in adjacent tissues ( P＝0.007). The expression of GTF2IP23 was negatively correlated with GTF2I ( r＝－0.335, P＝0.025).The expression of GTF2IP23 in breast cancer cells was significantly higher than in normal breast cells ( P＜0.01), while GTF2I expression in breast cancer cells was significantly lower than that in normal breast cells (P＜0.01). Overexpression of GTF2IP23 in ZR?75?30 cells significantly reduced the expression of GTF2I (P＝0.034) and enhanced cell proliferation (P＝0.017) and migration (P＝0.026) capacity. Conclusions GTF2IP23 is distinctly upregulated in breast cancer, it inhibits the expression of real gene GTF2I and promotes the proliferation of breast cancer cells.

The disorder of group 3 innate lymphoid cells(ILC3)subgroup,such as the predominance of NCR-ILC3 but the deple-tion of NCR+ILC3,is unfavorable to damaged intestinal barrier repair,which leads to the prolongations and obstinacy of ulcerative colitis(UC).Our previous studies had shown that luteolin promoted NCRILC3 differentitating into NCR+ILC3 to improving the de-pletion of NCR+ILC3 in UC mice,while the mechanism is unclear.This article aimed to explore the underlying mechanism of luteolin enhancing the proportion NCR+ILC3.UC mice model was established with 2％DSS and Notch signaling was blocked,then luteolin was used to intervene.The results showed that the effect of luteolin on ameliorating disease symptoms in UC mice,including inhibit-ing the weight loss,reducing the pathological damage of colon mucosa,etc.,was diminished with blocking Notch signaling pathway.In addition,luteolin increased the proportion of NCR+ILC3,NCR+MNK3 and IL-22+ILC3,decreased intestinal permeability,pro-moted mucin secretion,and promoted ZO-1 and Occludin expression,the above effect of luteolin was neutralized by Notch inhibitor LY-411575.Luteolin activated the abnormally blocked Notch signaling pathway in UC mice.And molecular docking predicted the af-finity of luteolin for RBPJ to be-7.5 kcal·mol-1 in mouse,respectively;the affinity of luteolin for Notchl and RBPJ was respectively scored to be-6.4 kcal·mol-1 and-7.7 kcal·mol-1 homo sapiens.These results proved that luteolin is positive for enhancing the propor-tion of NCR+ILC3 via Notch signaling,and it provides a basis for targeting NCR+ILC3 for restoring intestinal barrier function to alle-viating ulcerative colitis.

Objective To explore the value of probe-based confocal laser endomicroscopy(pCLE)in the differential diagnosis of fundic gland polyps.Methods A total of 63 patients who underwent conventional white light image(WLI)and suggested with gastric polyps in our gastroenterology endoscopy center during June and December 2023 were enrolled,and their clinical data,WLI,narrow band images(NBI),pCLE images and postoperative histopathological findings were collected.The characteristics of fundic gland polyps under pCLE were statistically verified,and the sensitivity,specificity,accuracy and consistency of different endoscopic diagnoses were calculated respectively.Results Under pCLE,fundic gland polyps were mainly manifested as elongated gastric pit opening,"hand-in-hand"gastric pit opening,well-arranged blood vessels around the pit opening,and no luciferin oozing.The sensitivity,specificity,accuracy of WLI were 72.73％,75.00％,73.13％and 0.343 for fundic gland polyps,and 81.82％,71.43％,71.64％and 0.354 for hyperplastic polyps,respectively.While,the above values of NBI were 87.27％,83.33％,86.57％and 0.673 for fundic gland polyps,and 81.82％,85.71％,85.07％and 0.554 for hyperplastic polyps;and those of pCLE were 92.73％,91.67％,92.53％and 0.769 for fundic gland polyps,and 90.91％,94.64％,94.03％and 0.797 for hyperplastic polyps pCLE had better sensitivity,specificity and accuracy than WLI and NBI,and had the results consistent with histopathological findings.Conclusion pCLE can be used in the differential diagnosis of fundic gland polyps.

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.

Objective: To investigate the expression level of antisense transcript of pseudogene, general transcription factor Ⅱi psedugen23 (GTF2IP23), in breast cancer and its effect on the host gene general transcription factor Ⅱi (GTF2I). Methods: The expressions of GTF2IP23 and GTF2I were detected in 40 cases of invasive breast cancer tumors and their counterparts by using quantitative real-time polymerase chain reaction (qRT-PCR). The effects of GTF2IP23 on the expression of GTF2I gene and cell proliferation and migration were analyzed by overexpression of GTF2IP23 in breast cancer cells. Results: The expression of GTF2IP23 mRNA in breast cancer tissues was significantly higher than that in adjacent tissues (P<0.001), while the expression of GTF2I mRNA was significantly lower than that in adjacent tissues (P=0.007). The expression of GTF2IP23 was negatively correlated with GTF2I (r=-0.335, P=0.025). The expression of GTF2IP23 in breast cancer cells was significantly higher than in normal breast cells (P<0.01), while GTF2I expression in breast cancer cells was significantly lower than that in normal breast cells (P<0.01). Overexpression of GTF2IP23 in ZR-75-30 cells significantly reduced the expression of GTF2I (P=0.034) and enhanced cell proliferation (P=0.017) and migration (P=0.026) capacity. Conclusions GTF2IP23 is distinctly upregulated in breast cancer, it inhibits the expression of real gene GTF2I and promotes the proliferation of breast cancer cells.

Background Hexavalent chromium [Cr(VI)] exposure can cause structural disruption of intestinal flora and functional impairment. Vitamin C (VC) is one of the essential micronutrients, which plays an important role in promoting the growth of intestinal probiotics, improving the intestinal barrier, and maintaining the homeostasis of intestinal flora. However, the regulatory effect of VC on the intestinal flora disorders caused by Cr(VI) exposure remains to be investigated. Objective To investigate the effect of VC on intestinal flora disruption in mice due to Cr(VI) exposure. Methods Thirty-two SPF-grade C57BL/6 mice were acclimatized and fed for 3 d and randomly divided into control (Con), VC, potassium dichromate [K₂Cr₂O₇, Cr(VI)], and VC+K₂Cr₂O₇ [VC+Cr(VI)] groups. At 8:00 a.m. on day 4, the Con group (double-distilled water given by gavage and injected intraperitoneally), the VC group (VC given by gavage and double-distilled water injected intraperitoneally), the Cr(VI) group (double-distilled water given by gavage and K₂Cr₂O₇ solution injected intraperitoneally), and the VC+Cr(VI) group (VC given by gavage and K₂Cr₂O₇ solution injected intraperitoneally) were treated. The dose of VC was 200 mg·kg⁻¹, and the dose of K₂Cr₂O₇ was 1.25 mg·kg⁻¹. The mice were treated for 45 consecutive days and then executed, the contents of the colon were sampled in sterile freezing tubes, and three replicates were collected from each group. After labeling, the samples were immediately put into liquid nitrogen for rapid freezing. After all the samples were collected, they were transferred to a -80 ℃ ultra-low temperature refrigerator for storage. Samples of colon contents were analyzed for intestinal flora structure by high-throughput sequencing and bioinformatics software. Results The Cr(VI) exposure resulted in reduced body weight gain values in mice compared to the Con group. Pathological changes occurred in the ileal tissue of mice, with significant inflammatory cell infiltration in the Cr(VI) group and reduced inflammatory cell infiltration in the VC+Cr(VI) group. The number of operational taxonomic units (OTUs) of intestinal flora was altered in the Cr(VI) group of mice. In the α diversity analysis, the mean Sobs index in the Cr(VI) group was 240.333±67.796, the Chao index was 258.173±64.813, and the Ace index was 259.481±66.891, which were significantly lower than those in the Con group (P<0.05), the PD whole tree index in the Cr(VI) group was 27.863±2.399, which was significantly higher than that in the Con group (P<0.05), and the VC intervention significantly reversed the changes of the above indexes due to Cr(VI) exposure (P<0.05). In the β diversity analysis, the principal coordinates analysis (PCoA) results showed a significant separation between the Cr(VI) group and the Con group, and after the VC intervention, there was a retraction of the separation trend and the difference was reduced. The multi-sample similarity dendrogram results showed that the control and the VC groups clustered together first, then with the VC+Cr(VI) group, and finally with the Cr(VI) group. The abundances of Bacteroidetes, Saccharibacteria, and Tenericutes in the intestine of mice in the Cr(VI) group were decreased, and the abundance of Firmicutes was increased; the abundances of Lactobacillus, Alistipes, Bacteroides, and Ruminiclostridium were also increased. Included among these, Bacteroides showed a significantly higher abundance compared to the control mice (P<0.05). Changes in the abundances of phyla and genera of the above mentioned gut microorganisms were reversed after the VC intervention. Conclusion Cr(VI) exposure can lead to intestinal damage and disorganization of the intestinal flora structure in mice, while VC intervention can ameliorate the above changes to a certain extent and normalize the intestinal flora structure.

Objective: To analyze the Oxford classification (MESTC) and the International Study of Kidney Disease in Children (ISKDC) classification for evaluating the clinical manifestations, histological lesion and short-term prognosis of children with Henoch-Schönlein purpura nephritis (HSPN). Methods: According to the Oxford classification and ISKDC classification, the histological lesions of children with HSPN diagnosed by renal biopsy from Beijing Children's Hospital affiliated to Capital Medical University from January 2018 to December 2018 were re-evaluated. The renal biopsy specimens of the selected subjects were scored according to the Oxford classification and the ISKDC classification. According to whether the first symptom was combined with renal performance, MESTC score and ISKDC classification, children were grouped. The differences in clinicopathological manifestations between the groups were compared. Correlation between MESTC and ISKDC grades was analyzed by nonparametric test rank correlation. Kaplan-Meier survival curve and Log-rank test were used to compare the difference of proteinuria remission rate between the two groups. Univariate and multivariate Cox regression equations were used to analyze the influencing factors of the proteinuria remission rate. Results: A total of 78 children with HSPN were enrolled. There were 37 male patients (47.4%) with age of (10.4±2.9) years. When the patients were divided according to MESTC scores and ISKDC classification, the results showed that the proportion of children with nephrotic-range proteinuria in the group of endocapillary hypercellularity (E1, P=0.008), segmental glomerulosclerosis (S1, P=0.015) and ISKDCⅢ(P=0.041) was higher than that of E0, S0 and ISKDCⅡ groups. The proportion of children with E1 (P=0.015), crescents (C1&C2, P=0.025) or ISKDCⅢ(P=0.017) that had been treated with high-dose methylprednisolone was higher. The result of Kaplan-Meier survival curve showed more difficult for proteinuria remission in children with C2 are than C0&C1 group (P=0.026), while no difference were found when children were grouped by M, E, S, T and ISKDC. Multivariate Cox regression analysis showed that the C2 (HR=0.143, 95%CI 0.020-1.046, P=0.055) might be a risk factor for proteinuria remission, while the P value was close to 0.05. Conclusions Children with HSPN scored as ISKDCⅢ, E1 and S1 are more likely to show nephrotic-range proteinuria. C2 may indicate that patients are more difficult to achieve proteinuria remission.