This study aims to explore protective effects of Lycium barbarum polysaccharides(LBP)on intestinal damage caused by lipopolysaccharide(LPS)-induced inflammatory bowel disease(IBD)in chicks.Network pharmacology was initially employed to determine the target proteins of wolfberry in the prevention and treatment of IBD.Following this,protein-protein interaction analy-sis,GO and KEGG pathway enrichment analysis,and molecular docking studies were conducted.Subsequently,an animal study was conducted:a total of 100 one-day-old male Hy-line brown lay-ing hens were randomly divided into five groups:a blank control group(CON),an LPS treatment group(LPS),a low-dose LBP group(LPS+LBP 0.25 g/L,L-LBP),a medium-dose LBP group(LPS+LBP 0.5 g/L,M-LBP),and a high-dose LBP group(LPS+LBP 1 g/L,H-LBP).Upon reac-hing 21 days old,duodenal,jejunal,ileal,and cecal tissues were collected to determine SOD and GSH-Px levels.Furthermore,the mRNA expression levels of TNF-α,AKT1,IL-6,IL-1β and TP53 in the intestinal tissues were measured using quantitative real-time PCR.The results demonstrated that network pharmacology identified 45 active ingredients in wolfberry that target 116 key protein sites,including TNF,AKT1 and IL6.The primary objectives focus on signaling pathways including AGE-RAGE,IL-17,TNF,HIF-1,and NF-κB.Molecular docking showed excellent ligand-receptor docking scores,with stable binding facilitated by hydrogen bonds and hydrophobic interactions.Compared to the LPS group,the 0.5 g/L LBP exhibited notably higher levels of SOD and T-AOC.In comparison with the LPS group,the medium and high-dose LBP experimental groups showed notably decreased the mRNA expressions of TNF-α,AKT1,IL-6,and IL-1β,while TP53 mRNA expression was significantly upregulated(P＜0.01).In summary,wolfberry exerts preventive and therapeutic effects on IBD through a multi-component,multi-target,and multi-pathway mecha-nism.

To examine how Lycium barbarum polysaccharide(LBP)impacts reproductive harm caused by perfluorooctanoic acid(PFOA)in male offspring mice.Sixty expectant female rats were randomly allocated into 6 groups,with each group consisting of 10 rats.From 1 to 17 d of gesta-tion,the blank control group was given 0.2 mL deionized water;The PFOA group was given 3.5 mg/kg PFOA;the LBP intervention group were given different doses(40,80,120 mg/kg)of LBP by gavage based on the PFOA group;the control group was given 80mg/kg.At 21 d of age,the offspring mice were weaned,and the offspring male mice were fed normally until 35 d of age,and testicular tissue was taken.HE staining was used to observe the pathological changes of testic-ular tissue sections.Body mass and testicular index were measured.The levels of SOD,MDA,LDH,SHD,GSH-PX and AR in testicular tissue were determined.Serum levels of LH,FSH,Gn-RH and T were determined by ELISA.Differential genes and differential metabolites of testis were analyzed in combination with transcriptome and metabolome.Real-time fluorescence quantitative PCR was used to detect the expression of key genes in fatty acid metabolic pathway.The results showed that LBP could alleviate PFOA-induced decline in body mass and increase testicular index(P＜0.01).LBP could alleviate the necrosis,edema of testicular cells caused by PFOA.LBP can in-crease the contents of SOD,GSH-Px,LDH,SDH and AR in testicular tissue of offspring male mice induced by PFOA,increase the contents of FSH,LH,GnRH and T in serum of offspring male mice,and decrease the content of MDA.Analysis of the transcriptome revealed that 1 388 genes exhibited differential expression between the groups exposed to PFOA and 80 mg/kg LBP,with 696 genes being up-regulated and 692 genes being down-regulated.The differentially ex-pressed genes were predominantly involved in pathways such as fatty acid metabolism,unsaturated fatty acid biosynthesis,cholesterol metabolism,the PPAR signaling pathway,and protein digestion and absorption,with fatty acid metabolism being the most prominent among them.Examination of the metabolome revealed 34 metabolites that were expressed differently between the PFOA group and the 80 mg/kg LBP group.Key metabolic pathways such as fatty acid biosynthesis,unsaturated fatty acid biosynthesis,and steroid hormone biosynthesis were found to be significant.In a joint transcriptome and metabolome analysis,the Differentially expressed genes(DEGs)and Differential expression of metabolites(DEMs)are highly correlated in signaling pathways such as fatty acid bi-osynthesis and unsaturated fatty acid biosynthesis.This study shows that PFOA can cause testicu-lar injury in offspring male mice,and LBP can effectively alleviate the testicular injury caused by PFOA in offspring male mice.Meanwhile,transcriptomic metabolism shows that LBP can effec-tively improve the testicular injury caused by PFOA in offspring male mice through fatty acid bio-synthesis and unsaturated fatty acid biosynthesis signaling pathways.Among them,80 mg/kg LBP has better effect.

To examine how Lycium barbarum polysaccharide(LBP)impacts reproductive harm caused by perfluorooctanoic acid(PFOA)in male offspring mice.Sixty expectant female rats were randomly allocated into 6 groups,with each group consisting of 10 rats.From 1 to 17 d of gesta-tion,the blank control group was given 0.2 mL deionized water;The PFOA group was given 3.5 mg/kg PFOA;the LBP intervention group were given different doses(40,80,120 mg/kg)of LBP by gavage based on the PFOA group;the control group was given 80mg/kg.At 21 d of age,the offspring mice were weaned,and the offspring male mice were fed normally until 35 d of age,and testicular tissue was taken.HE staining was used to observe the pathological changes of testic-ular tissue sections.Body mass and testicular index were measured.The levels of SOD,MDA,LDH,SHD,GSH-PX and AR in testicular tissue were determined.Serum levels of LH,FSH,Gn-RH and T were determined by ELISA.Differential genes and differential metabolites of testis were analyzed in combination with transcriptome and metabolome.Real-time fluorescence quantitative PCR was used to detect the expression of key genes in fatty acid metabolic pathway.The results showed that LBP could alleviate PFOA-induced decline in body mass and increase testicular index(P＜0.01).LBP could alleviate the necrosis,edema of testicular cells caused by PFOA.LBP can in-crease the contents of SOD,GSH-Px,LDH,SDH and AR in testicular tissue of offspring male mice induced by PFOA,increase the contents of FSH,LH,GnRH and T in serum of offspring male mice,and decrease the content of MDA.Analysis of the transcriptome revealed that 1 388 genes exhibited differential expression between the groups exposed to PFOA and 80 mg/kg LBP,with 696 genes being up-regulated and 692 genes being down-regulated.The differentially ex-pressed genes were predominantly involved in pathways such as fatty acid metabolism,unsaturated fatty acid biosynthesis,cholesterol metabolism,the PPAR signaling pathway,and protein digestion and absorption,with fatty acid metabolism being the most prominent among them.Examination of the metabolome revealed 34 metabolites that were expressed differently between the PFOA group and the 80 mg/kg LBP group.Key metabolic pathways such as fatty acid biosynthesis,unsaturated fatty acid biosynthesis,and steroid hormone biosynthesis were found to be significant.In a joint transcriptome and metabolome analysis,the Differentially expressed genes(DEGs)and Differential expression of metabolites(DEMs)are highly correlated in signaling pathways such as fatty acid bi-osynthesis and unsaturated fatty acid biosynthesis.This study shows that PFOA can cause testicu-lar injury in offspring male mice,and LBP can effectively alleviate the testicular injury caused by PFOA in offspring male mice.Meanwhile,transcriptomic metabolism shows that LBP can effec-tively improve the testicular injury caused by PFOA in offspring male mice through fatty acid bio-synthesis and unsaturated fatty acid biosynthesis signaling pathways.Among them,80 mg/kg LBP has better effect.

This study aims to explore protective effects of Lycium barbarum polysaccharides(LBP)on intestinal damage caused by lipopolysaccharide(LPS)-induced inflammatory bowel disease(IBD)in chicks.Network pharmacology was initially employed to determine the target proteins of wolfberry in the prevention and treatment of IBD.Following this,protein-protein interaction analy-sis,GO and KEGG pathway enrichment analysis,and molecular docking studies were conducted.Subsequently,an animal study was conducted:a total of 100 one-day-old male Hy-line brown lay-ing hens were randomly divided into five groups:a blank control group(CON),an LPS treatment group(LPS),a low-dose LBP group(LPS+LBP 0.25 g/L,L-LBP),a medium-dose LBP group(LPS+LBP 0.5 g/L,M-LBP),and a high-dose LBP group(LPS+LBP 1 g/L,H-LBP).Upon reac-hing 21 days old,duodenal,jejunal,ileal,and cecal tissues were collected to determine SOD and GSH-Px levels.Furthermore,the mRNA expression levels of TNF-α,AKT1,IL-6,IL-1β and TP53 in the intestinal tissues were measured using quantitative real-time PCR.The results demonstrated that network pharmacology identified 45 active ingredients in wolfberry that target 116 key protein sites,including TNF,AKT1 and IL6.The primary objectives focus on signaling pathways including AGE-RAGE,IL-17,TNF,HIF-1,and NF-κB.Molecular docking showed excellent ligand-receptor docking scores,with stable binding facilitated by hydrogen bonds and hydrophobic interactions.Compared to the LPS group,the 0.5 g/L LBP exhibited notably higher levels of SOD and T-AOC.In comparison with the LPS group,the medium and high-dose LBP experimental groups showed notably decreased the mRNA expressions of TNF-α,AKT1,IL-6,and IL-1β,while TP53 mRNA expression was significantly upregulated(P＜0.01).In summary,wolfberry exerts preventive and therapeutic effects on IBD through a multi-component,multi-target,and multi-pathway mecha-nism.

Objective:To select the animal model more consistent with the pathophysiology of abdominal compartment syndrome (ACS) through the comparative study of the methods of multiple water sacs superimposed compression and gas perfusion.Methods:Ten experimental pigs were randomly divided into two groups ( n = 5): the "constant volume model" (constant volume model group) and the "constant pressure model" (constant pressure model group) of intra-abdominal hypertension. The models were prepared by the method of water sac superposition and pressurization, and artificial pneumoperitoneum respectively. The abdominal pressures of both groups were 25 mmHg (1 mmHg = 0.133 kPa) and observed for 4 hours. The pressure was measured once an hour for 4 hours and the pressure-time curves of the two groups were drawn respectively. The experimental animals were sacrificed 4 hours after modeling. The heart and lung were harvested, and the histopathological changes were observed by hematoxylin-eosin (HE) staining. Results:Two groups of experimental pigs were successfully modeled. The abdominal pressure gradually increased at 0, 1, 2, 3, 4 hours after operation in the constant volume model group (mmHg: 25.0±0, 27.1±0.2, 29.4±0.1, 30.9±0.2, 33.1±0.1), and there was a positive correlation between the abdominal pressure and time (functional equation: Y1 = 25.102 0+1.996 0 X1; R2 = 0.996 2, P = 0.000 1). The abdominal pressure value in the constant pressure model group at 0, 1, 2, 3, 4 hours were maintained 25 mmHg, and there was no linear correlation between the abdominal pressure and time (functional equation: Y2 = 25). HE staining showed that in the constant volume model group, the myocardial fibers were accompanied with hyaline degeneration, significantly reduced transverse lines, part of myocardial fiber atrophy, and visible nuclear aggregation; hemorrhage, chronic inflammatory cell infiltration and inflammatory exudation were found in the lung tissues. In the constant pressure model group, partial atrophy of myocardial fiber, partial hypertrophy, focal hyaline degeneration, disappearance of local striae, hyaline degeneration of myocardial fiber, dilation and congestion of intermyocardial artery were observed. Slight hyperplasia of alveolar epithelium in some areas, heart failure cells, dilation and congestion of bronchi and trachea artery, a large number of red blood cells and uniform light staining substances in lumen were found. Conclusion:After the model was made by the method of multiple water sacs, the pressure of the abdominal cavity continued to increase with the development of the disease, which was in line with the clinical pathological changes of ACS, and was more suitable for making the animal model of the intra-abdominal hypertension.

OBJECTIVE: To investigate the inhibitory effects of silencing migration-inducing gene-7 (Mig-7) on vasculogenic mimicry formation, migration and invasion of human glioma cells and whether MEK/ERK signaling pathway mediates these effects. METHODS: Human glioma U251 cells were infected by lentiviral vectors carrying a small interfering RNA targeting Mig-7 gene (sh-Mig-) or a negative control shRNA (sh-NC), and real-time quantitative PCR was used to detect the expression level of Mig- mRNA in the cells. Three-dimensional culture and Transwell chamber invasion assay were used to observe the effect of Mig- gene silencing on vasculogenic mimicry formation and invasion ability of the U251 cells. Western blotting was performed to detect the changes in the protein expression levels of MEK/ERK in the infected cells. RESULTS: We successfully obtained a U251 cell line with stable low expression of Mig- gene using RNA interference technique. Compared with the cells infected with sh-NC lentivirus and the non- infected cells, U251 cells infected with the lentiviral vector carrying sh-Mig- showed significantly decreased expression level of Mig- ( < 0.01) with obviously lowered vasculogenic mimicry formation and invasion abilities ( < 0.05). Mig- silencing also significantly lowered the expressions of MEK and ERK proteins in U251 cells ( < 0.05). CONCLUSIONS Silencing of Mig-7 gene inhibits vasculogenic mimicry formation and invasion of U251 cells possibly by suppressing MEK/ERK signaling, suggesting the important role of Mig-7 gene in vasculogenic mimicry formation and invasion of human glioma cells.
Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Gene Silencing ; Glioma ; genetics ; pathology ; Humans ; Neoplasm Proteins ; metabolism ; RNA, Small Interfering ; Signal Transduction

OBJECTIVE:To enhance the competitive edge of Chinese pharmaceutical enterprises.METHODS:Patents problems confronted by Chinese pharmaceutical enterprises were analyzed in terms of the research and development and patent protection of the original new drugs,the administrative protection and patent protection of drugs,patent documentation in?formation,patent strategy and patent talents,etc.RESULTS&CONCLUSION:Chinese pharmaceutical enterprises should highlight the patent problems and apply patent strategy to achieve competitive advantage.