ABSTRACT This study aimed to perform exhaustive bioinformatic analysis by using GSE29221 micro-array maps obtained from healthy controls and Type 2 Diabetes (T2DM) patients. Raw data are downloaded from the Gene Expression Omnibus database and processed by the limma package in R software to identify Differentially Expressed Genes (DEGs). Gene ontology functional analysis and Kyoto Gene Encyclopedia and Genome Pathway analysis are performed to determine the biological functions and pathways of DEGs. A protein interaction network is constructed using the STRING database and Cytoscape software to identify key genes. Finally, immune infiltration analysis is performed using the Cibersort method. This study has implications for understanding the underlying molecular mechanism of T2DM and provides potential targets for further research. GSE GSE2922 microarray micro array TDM T DM (T2DM patients DEGs . (DEGs) genes Finally method research GSE292 (DEGs GSE29 GSE2

Abstract Preeclampsia is associated with the insufficient invasion of trophoblasts. NF-κB is a transcription factor in almost all mammalian cells and has been validated to be upregulated in the maternal circulation and placenta of women with preeclampsia. MiR-518a-5p is also overexpressed in pre-eclamptic placenta. The present study was designed to explore whether NF-κB can transcriptionally activate miR-518a-5p and investigate the influences of miR-518a-5p on the viability, apoptosis, migration, and invasion of HTR8/SVneo trophoblast. In situ hybridization and real time polymerase chain reaction were used to reveal miR-518a-5p expression in placenta tissues and HTR8/SVneo cells, respectively. Cell migration and invasion were detected using Transwell inserts. Our findings indicated that NF-κB p52, p50, and p65 can bind to miR-518a-5p gene promoter. MiR-518a-5p further influences the levels of p50 and p65 but not p52. HTR8/SVneo cell viability and apoptosis were not influenced by miR-518a-5p. However, miR-518a-5p represses the migratory/invasive capacities of HTR8/SVneo cell and decreased gelatinolytic activity of MMP2 and MMP9, which was reversed by an NF-κB inhibitor. To sum up, miR-518a-5p is induced by NF-κB and represses trophoblast cell migration and invasion by the NF-κB pathway. trophoblasts NFκB NF κB preeclampsia MiR518a5p MiRap MiR 518a 5p p preeclamptic pre eclamptic miR518a5p miRap miR HTR8SVneo HTRSVneo HTR8 SVneo HTR respectively inserts p52 p6 promoter p5 miR518a5p. 5p. However migratoryinvasive migratory invasive MMP MMP9 inhibitor up pathway

Abstract The goal of this work was to clarify the mechanism of action of Lactobacillus casei on genipin in triggering glioma apoptosis. DPPH and ABTS free radicals could be successfully eliminated by geniposide, LC-NBRC101979 (Lactobacillus casei), and geniposide + LC-NBRC101979. Geniposide and LC-NBRC101979 had effects that were stronger when combined than when taken alone. Geniposide, LC-NBRC101979, and Geniposide + LC-NBRC101979 did not have any detrimental effects on healthy epithelial cells HBE, but they greatly decreased the growth of U87 glioma cells, according to cell studies. Additionally, the combination of geniposide and LC-NBRC101979 had a stronger inhibitory impact than either drug alone. Results from qPCR revealed that in U87 cells, geniposide, LC-NBRC101979, and eniposide + LC-NBRC101979 could up-regulate caspase-3, COX-2, p53, c-myc, p21 mRNA expression and down-regulate Bcl-2, NF-κB expression. According to the results of the study on the effects of oxidative stress on cells, geniposide, LC-NBRC101979, and geniposide combined with LC-NBRC101979 can decrease the levels of MDA, LDH, and NO in normally damaged epithelial cells caused by oxidative stress and increase the levels of CAT, SOD, GSH-Px, and T-AOC. According to HPLC data, LC-NBRC101979 was able to convert the majority of geniposide into geniposide. It is clear that LC-NBRC101979 may enhance geniposide's inhibitory impact on glioma. apoptosis LCNBRC101979 LCNBRC LC NBRC101979 NBRC LC-NBRC10197 casei, , casei) LCNBRC101979. NBRC101979. alone LCNBRC101979, NBRC101979, HBE U U8 studies Additionally upregulate up regulate caspase3, caspase3 caspase 3, 3 caspase-3 COX2, COX2 COX 2, 2 COX-2 p53 p cmyc, cmyc c myc, myc c-myc p2 downregulate down Bcl2, Bcl2 Bcl Bcl-2 NFκB NF κB MDA LDH CAT SOD GSHPx, GSHPx GSH Px, Px GSH-Px TAOC. TAOC T AOC. AOC T-AOC data geniposides s LCNBRC10197 NBRC10197 LC-NBRC1019 caspase- COX- p5 Bcl- LCNBRC1019 NBRC1019 LC-NBRC101 LCNBRC101 NBRC101 LC-NBRC10 LCNBRC10 NBRC10 LC-NBRC1 LCNBRC1 NBRC1 LC-NBRC