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https://www.selleckchem.com/products/ag-221-enasidenib.html The expression levels of miR-335-5p and JNK3 were significantly inversely correlated. Further, dual Luciferase assay verified the relationship between miR-335-5p and JNK3. Overexpression of miR-335-5p obviously decreased the protein levels of JNK3 and Aβ and inhibited apoptosis in SH-SY5Y/APPswe cells, whereas the inhibition of miR-335-5p obtained the opposite results. Moreover, the overexpression of miR-335-5p remarkably improved cognitive abilities of APP/PS1 mice. CONCLUSION The results revealed that the increased JNK3 expression, negatively regulated by miR-335-5p, maybe a potential mechanism that contributes to Aβ accumulation and AD progression, indicating a novel approach for AD treatment. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Neonatal pneumonia is a common disease in the neonatal period with a high incidence and death. This study aimed to investigate the molecular mechanism and effect of microRNA (miR)-429 in neonatal pneumonia. METHODS The peripheral blood was collected from neonatal pneumonia and healthy patients, respectively. Human lung fibroblast WI-38 cells were treated with lipopolysaccharide (LPS) to establish neonatal pneumonia cell model. Then, the miR-429 expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR). In addition, the relationship between miR-429 and kruppel-like factor 4 (KLF4) was confirmed by dual luciferase reporter assay. Cell viability, the level of interleukin 6 (IL-6), IL-1β and tumor necrosis factor α (TNF-α) and apoptosis were measured by Cell Counting Kit-8 (CCK-8), enzyme linked immunosorbent assay (ELISA) and flow cytometry. Meanwhile, apoptosis and nuclear factor kappa-B (NF-κB) pathway related proteins expression were analyzed by western blot. RESULTS MiR-429 expression level was increased in neonatal peripheral blood and LPS-stimulated WI-38 cells. Then, miR-429 ove

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