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.

OBJECTIVETo explore the mechanism of paraquat (PQ) poisoning and to observe the changes in inflammatory cytokines in PQ-exposed rats treated in different ways.

METHODSFifty 8-week-old clean male Wistar rats were randomly divided into high-dose curcumin plus conventional treatment group, low-dose curcumin plus conventional treatment group, high-dose curcumin group, PQ poisoning group, and blank control group. On days 1, 3, 5, 7, 14, and 21 after PQ exposure, serum levels of transforming growth factor-β₁(TGF-β₁) , tumor necrosis factor-α (TNF-α) , and interleukin-6 (IL-6) were measured. The pathological changes in lung tissue were evaluated by HE staining.

RESULTSCompared with the blank control group, the high-dose curcumin plus conventional treatment group, low-dose curcumin plus conventional treatment group, high-dose curcumin group, and PQ poisoning group had significantly increased serum levels of TGF-β₁, TNF-α, and IL-6 (P<0.05) , and the three cytokines in each group reached peak levels on day 14 after exposure. Compared with the PQ poisoning group, the high-dose curcumin group had significantly reduced serum levels of TGF-β₁, TNF-α, and IL-6 (P<0.05). On day 21 after exposure, there were no significant differences in serum levels of TGF-β₁, TNF-α, and IL-6 between the high-dose curcumin plus conventional treatment group and the low-dose curcumin plus conventional treatment group (P>0.05). The HE staining revealed alveolar inflammatory changes on days 1~7 and massive pulmonary fibrosis on days 14~21 in the high-dose curcumin plus conventional treatment group, low-dose curcumin plus conventional treatment group, high-dose curcumin group, and PQ poisoning group, but the above changes were milder in the high-dose curcumin group than in the PQ poisoning group.

CONCLUSIONFor rats with PQ poisoning, curcumin can significantly reduce inflammatory response and pathological changes in lung tissue and inhibit and delay the development and progression of body injury.

Animals ; Curcumin ; pharmacology ; Cytokines ; blood ; Interleukin-6 ; blood ; Lung ; pathology ; Male ; Paraquat ; poisoning ; Pulmonary Fibrosis ; pathology ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Transforming Growth Factor beta1 ; blood ; Tumor Necrosis Factor-alpha ; blood