Objective To investigate the role of sulfydral redox agent in the modulation of insulin secretion and the potential mechanism. Methods Insulin secretion was evaluated in INS-1 cells after treatment with different concentrations of glucose and sulfydral redox agents by a standard insulin radio immunoassay. Results Glucose concentration-dependently potentiates insulin secretion was observed in INS-1 cells. DTBNP and DTDP could not only significantly increase glucose-stimulated insulin secretion (GSIS), but also increase insulin secretion in nifedipine-pretreated cells, which could be abrogated by DTT. Importantly, pharmacological ablation of L-type calcium channels by nifedipine and/or ablation of K ATP channelby diazoxide both could potentiate glucose-induced insulin secretory. Conclusions Sulfydral redox agent could regulates GSIS. DTBNP and DTDP may increase insulin secretion via regulating the activities of KATP, L-type CaV channel and IP3 receptor.

OBJECTIVETo observe the changes of the mechanical pain threshold in the rat model of autoimmune prostatitis, explore the mechanism of autoimmune prostatitis pain and offer some animal experimental evidence for the drug therapy of the condition.

METHODSTwenty male Wistar rats weighing 180 - 220 g were divided into a model and a control group. The autoimmune prostatitis model was established by subcutaneous injection of an extract of male rat prostate glands (RPG) at 60 mg/ml in Freund's complete adjuvant (FCA) and pertussis-diphtheria-tetanus vaccine at 0 and 30 days, respectively. Mechanical tactile hyperalgesia was measured once a week using Von Frey Filaments from the beginning of the study. At 8 weeks after modeling, the rats were sacrificed and the prostate tissues harvested for observation of histomorphological changes by HE staining.

RESULTSHE staining revealed different degrees of benign prostatitis in the model rats. Compared with the controls, the mechanical pain threshold in the model rats was significantly decreased with the increased time of modeling, from (65.52 +/- 6.27) g at 0 week to (23.67 +/- 4.09) g at 8 weeks (P < 0.01). Statistically significant differences were found in the variation trend at different time points between the two groups (P < 0.01).

CONCLUSIONAutoimmune prostatitis models were successfully established in rats and hyperalgesia was induced after modeling.

Animals ; Autoimmune Diseases ; physiopathology ; Disease Models, Animal ; Male ; Pain Threshold ; physiology ; Prostatitis ; immunology ; physiopathology ; Rats ; Rats, Wistar

Objective:To explore potential signaling pathways and genes related to vitiligo progression by using bioinformatics methods.Methods:A vitiligo genechip dataset GSE75819 was downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were screened between lesional and non-lesional skin tissues from 15 Indian patients with vitiligo with the dataset GSE75819 by using LMFit and eBayes functions in R LIMma package. The Kyoto Encyclopedia of Genes and Genomes (KEGG) -based pathway analysis, Gene Ontology (GO) analysis and Gene Set Enrichment Analysis (GSEA) were carried out to identify enriched pathways and functions of the DEGs. Protein-protein interaction networks were established to screen hub genes from the DEGs. In addition, lesional and non-lesional skin tissue specimens were obtained from 8 patients of Han nationality with vitiligo vulgaris in Hospital of Xinjiang Traditional Uyghur Medicine between January and June in 2019, and real-time quantitative PCR was performed to verify the expression of the top 10 up- or down-regulated DEGs.Results:Compared with the 15 non-lesional skin tissues, a total of 148 DEGs were identified in the 15 lesional skin tissues. Among these DEGs, KRT9, CXCL10, C8ORF59, TPSAB1 and RPL26 were the top 5 up-regulated genes, and SILV, RPPH1, TYRP1, MLANA and LOC401115 were the top 5 down-regulated genes, which were all verified by real-time quantitative PCR in the lesional and non-lesional skin tissues from the 8 patients of Han nationality with vitiligo. GO analysis showed that the DEGs were chiefly enriched in translational initiation, cellular response to lipopolysaccharide, ribosomes, ribosomal subunits and structural constituents of ribosomes. KEGG analysis showed that the DEGs were chiefly enriched in tyrosine metabolism, peroxisome proliferator-activated receptor signaling pathway, oxidative phosphorylation and Toll-like receptor signaling pathway. Four hub genes, including UPF3B, SNRPG, MRPL13 and RPL26L1, were screened out by protein-protein interaction analysis.Conclusion:KRT9, CXCL10, C8ORF59, TPSAB1, RPL26, SILV, RPPH1, TYRP1, MLANA and LOC401115 genes may serve as potential diagnostic molecular markers and therapeutic targets for vitiligo.