Objective To study the mechanism of the protective effect of lycium barbarum polysaccharide on light aging resistance rats by using the metabolic profile and metabolic target analysis technique.Methods Ultraviolet irradiation induced Wistar rats were induced to produce skin photo aging model and 24 rats were randomly divided into three groups, including control goup, model group, Lycium barbarum polysaccharide group (LBP). After modeling for 24 hours, LBP group was conducted with Lycium barbarum polysaccharide solution of 10 mg/kg. Control group and model group were given same volume of stroke-physiological saline solution for 14 days. The biochemical indexes such as rat serum antioxidant activity of related substances and MDA were measured in model group and drug group; the urine metabolomics study was also investigated for the mechanism of lycium barbarum polysaccharide against light aging band.Results Compared with the model group, the LBP group rats total superoxide dismutase activity (301.51 ± 42.56 U/mgvs.93.41 ± 56.31 U/mg), hydroxyproline (8.91 ± 5.78μg/mgvs.4.74 ± 1.54μg/mg) content significantly increased (P<0.05), but the malondialdehyde (8.54 ± 6.41 nmol/mgvs.21.31 ± 6.58 nmol/mg) decreased without any statistics difference (P<0.05). The urine metabonomics results showed that LBP could regulate the skin photoaging of multiple metabolic pathways and key metabolic enzymes in the process, such as peanut four acid, tyrosine, taurine, citric acid and hippuric acid, L-cysteine, inositol, threonine etc.Conclusions In the process of skin photoaging in rats, multiple metabolic pathways in vivo were disordered, and Lycium barbarum polysaccharide could play a protective role by regulating the key metabolic enzymes in the network.

Objective Gas chromatography-mass spectrometer (GC-MS) technology combined with Heuristic evolving latent projections (HELP) method were used to qualitatively analyze the volatile oil of fructus lycii (Lycium barbarumL.)Methods With the best temperature-programmed chromatographic condition, overlapping peaks among the total ion chromatogram were separated. Then an automatic mass spectral deconvolution and identification system (AMDIS) was used to identify volatile components comprehensively. Finally, the pure chromatographic peaks were matched with NIST 05a mass spectra library for giving the precise qualitative result. Results Totally, 29 compounds in fructus lycii (Lycium barbarum L.) were identified accurately.Conclusions Compared with the traditional qualitative analysis method, the new established method which GC-MS technology combined with HELP could get tremendous advantages. It not merely enhanced the accuracy of identification but also solved the bottleneck of handling the inseverable compounds.

Objective To explore the protective effect of olfactory ensheathing cell(OEC)Schwann cell(SC)-extracellular matrix(ECM)-poly(DL-lactide-co-glycolide acid)(PLGA)bridging complex on peripheral target organ and spinal cord neurons after rat sciatic nerve defect.Methods A 15 mm right sciatic nerve defect model was established in SD rats and repaired with OEC-SC-ECM-PLGA bridging complex that contained OEC,SC,ECM and self-made PLGA conduit.At the same time,the study set OEC-ECM-PLGA group,SC-ECM-PLGA group,ECM-PLGA group,PLGA group and nerve autograft control group.At 1,3,6 and 9 weeks after surgery,the gastrocnemius muscle water weight test and motor end-plate test were performed.At the 9th week after surgery,CM-DiI and horseradish peroxidase(HRP)retrograde tracing were performed.Results The gastrocnemius muscle water weight and number of motor end-plate were decreased in all groups after surgery but gradually increased after three weeks except for ECM-PLGA group and PLGA group.At the 9th week,OEC-SC-ECM-PLGA group showed no statistical differences with nerve autograft group in aspects of gastrocnemius muscle water weight,number of motor end-plate and length of motor end-plate major axis(P ＞ 0.05).At the 9th week,CM-DiI and HRP retrograde tracing found that the number of positive neurons in spinal cord in OEC-SC-ECM-PLGA group showed no statistical differences compared with nerve autograft group(P ＞0.05).Conclusions OEC-SC-ECM-PLGA bridging complex can partially protect peripheral target organ and spinal cord neurons after rat sciatic nerve defect.

Objective:To identify the hub differentially expressed genes(DEGs)of glomerular pathological changes and potential pathways in molecular process of type 2 diabetic nephropathy(DN)based on bioinformatics technology.Methods:The differentially expressed genes of Gene Expression Omnibus(GEO)dataset GSE96804 in DN and normal kidney tissues were analyzed by R 3.6.2 software. DEGs were further assessed by Gene Ontology(GO)function enrichment analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG)signal pathway analysis. Subsequently, the hub genes and their associated pathways were analyzed using String 11.0 and Cytoscape 3.7.2 software.Results:A total of 168 DEGs were obtained in the dataset. Among them, seven hub genes were identified, including ALB, FN1, EGF, PTGS2, PLG, KDR, and LOX. Three hub genes, ALB, EGF, PLG, exerted a direct action on glomerulus. GO enrichment analysis of DEGs was mainly manifested in extracellular matrix organization, extracellular structure organization, platelet degranulation and other biological processes, extracellular matrix, secretory granule lumen, platelet alpha granule and other cell components, chaperone binding, copper ion binding, antioxidant activity, and other molecular functions. DEGs mainly regulated metabolic process, which was related to fatty acid degradation signal pathway, exogenous substance metabolism related to CYP enzyme and drug metabolism signal pathway.Conclusion:A bioinformatics analysis of DN from the perspective of glomerulopathy is helpful to understand the potential molecular mechanism of DN and provide reference for further validation.

Objective:To develop a questionnaire for compliance with the management standard of nosocomial infection control in hemodialysis rooms (centers), and to evaluate the reliability and validity.Methods:Based on the Knowledge, Attitude/Belief, Practice (KAP) survey model, the initial questionnaire was formed by using literature review, the brainstorming and expert consultation. And the final questionnaire was developed by preliminary investigation and the formal investigation, and the reliability and validity test was carried out.Results:The questionnaire consisted of 3 subscales of knowledge, attitude and practice, totaling 40 items. The S-CVI was 0.953, 0.979, 0.943 respectively and that of each item was above 0.867. In the exploratory factor analysis, 3, 1 and 3 common factors were extracted and the cumulative contribution rate was 47.178%, 68.313% and 62.271% respectively. The Cronbach α coefficient was 0.906 for the total questionnaire and 0.641, 0.958 and 0.864 for 3 subscales. The retest reliability was 0.954 for the total questionnaire and 0.694, 0.893 and 0.708 for 3 subscales.Conclusions:The questionnaire had high reliability and validity, which can be used as an effective evaluation tool for the standard to investigate the compliance of medical staffs in hemodialysis rooms.

Neurogenesis decline in hippocampal dentate gyrus (DG) participates in stress-induced depressive-like behaviors, but the underlying mechanism remains poorly understood. Here, we observed low-expression of NOD-like receptor family pyrin domain containing 6 (NLRP6) in hippocampus of stress-stimulated mice, being consistent with high corticosterone level. NLRP6 was found to be abundantly expressed in neural stem cells (NSCs) of DG. Both Nlrp6 knockout (Nlrp6^-/-) and NSC-conditional Nlrp6 knockout (Nlrp6CKO) mice were susceptible to stress, being more likely to develop depressive-like behaviors. Interestingly, NLRP6 was required for NSC proliferation in sustaining hippocampal neurogenesis and reinforcing stress resilience during growing up. Nlrp6 deficiency promoted esophageal cancer-related gene 4 (ECRG4) expression and caused mitochondrial dysfunction. Corticosterone as a stress factor significantly down-regulated NLRP6 expression, damaged mitochondrial function and suppressed cell proliferation in NSCs, which were blocked by Nlrp6 overexpression. ECRG4 knockdown reversed corticosterone-induced NSC mitochondrial function and cell proliferation disorders. Pioglitazone, a well-known clinical drug, up-regulated NLRP6 expression to inhibit ECRG4 expression in its protection against corticosterone-induced NSC mitochondrial dysfunction and proliferation restriction. In conclusion, this study demonstrates that NLRP6 is essential to maintain mitochondrial homeostasis and proliferation in NSCs, and identifies NLRP6 as a promising therapeutic target for hippocampal neurogenesis decline linked to depression.