Cerebral ischemic injury and treatment are important topics in neurological science. In the present study, an in vitro model of cerebral ischemia was established by subjecting primary cultures of hippocampal neuronal cells to oxygen-glucose deprivation followed by reperfusion (OGD/R), in order to evaluate the possible neuroprotective role of syringic acid (SA). The results of 3-(4,5-dimethylthiazol‑2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays showed that pre-treatment with SA (0.1, 1, 10, and 20 µM) attenuated OGD/R-induced neuronal injury in a dose-dependent manner, with evidence of increased cell viability and decreased LDH leakage. In addition, oxidative stress markers were evaluated using commercial kits, and the results demonstrated that OGD/R exposure induced distinct oxidative stress, accompanied by elevated levels of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) production, and reduced activity of the antioxidant enzyme superoxide dismutase (SOD), which were dose-dependently restored by pre-treatment with SA. In addition, the concentration of intracellular free calcium [Ca2+]i and mitochondrial membrane potential (MMP or Δψm) were determined in order to evaluate the degree of neuronal damage by performing flow cytometric analysis and observing the cells under a fluorescence microscope, respectively. We demonstrated that pre-treatment with SA inhibited elevations in [Ca2+]i, whereas it increased the MMP dose-dependently following exposure to OGD/R. Western blot analysis revealed that OGD/R promoted cell apoptosis with concomitant increases in Bax and caspase-3 expression, and reduced Bcl-2 expression, which was reversed by pre‑treatment with SA in a dose-dependent manner. Moreover, these effects were mediated through the JNK and p38 pathways, as pre‑treatment with SA inhibited the OGD/R-induced increase in phosphorylated (p-)JNK and p-p38 expression. Taken together, these results suggested that SA exerted strong neuroprotective effects in hippocampal neuronal cells, which may be attributed to the attenuation of OGD/R-induced cell injury through the JNK and p38 signaling pathways.

Glioblastoma (GBM) is a devastating and highly aggressive tumor, which is apoptosis resistant and difficult to cure. Recently, long noncoding RNAs have been shown to play a pivotal role in GBM progression. Evidence has suggested that retinal noncoding RNA3 (RNCR3) is a GBM-associated noncoding RNA and is under-expressed in GBM. However, the function and mechanism of RNCR3 on GBM cell growth and apoptosis are still uncertain. In the current study, we found that the level of RNCR3 is decreased in U87, U251, U373, and A172 GBM cell lines when compared with the normal human astrocytes. Elevating long noncoding RNA RNCR3 expression markedly inhibits U87 and U251 cell survival and proliferation. Further studies indicated that RNCR3 overexpression promotes U87 and U251 cell apoptosis and activity caspase-3/7. Moreover, we found that RNCR3 overexpression promotes Krüppel-like factor 16 (KLF16) expression through inhibiting the level of miR-185-5p. We demonstrated that KLF16 is a direct target of miR-185-5p. An increased miR-185-5p level by a miR-185-5p mimic or decreased KLF16 by KLF16 small interfering RNA both reversed the function of RNCR3 overexpression on GBM cell growth and apoptosis. In summary, this study focuses on investigating the key molecular mechanisms of RNCR3 involved in GBM cell growth and apoptosis. Our data indicated that RNCR3 overexpression inhibits cell growth and induces its apoptosis through the miR-185-5p/KLF16 axis.

Emerging evidence has suggested that aberrantly expressed microRNAs (miRNAs) are associated with glioma development and progression. The aberrant expression of miR-409-3p has been reported in several human cancers. However, little is known about the function of miR-409-3p in gliomas. The aim of this study was to investigate the specific role and molecular mechanism of miR-409-3p in gliomas. In the present study, we found that miR-409-3p was downregulated in glioma tissue and cell lines. Overexpression of miR-409-3p inhibited glioma cell invasion and proliferation, whereas suppression of miR-409-3p promoted glioma cell invasion and proliferation. High-mobility group nucleosome-binding domain 5 (HMGN5), a well-known oncogene in gliomas, was identified as a functional target of miR-409-3p using bioinformatics, dual-luciferase reporter assay, real-time quantitative polymerase chain reaction, and Western blot analysis. Furthermore, miR-409-3p was found to regulate the expression of matrix metalloproteinase 2 and cyclin D1. Restoration of HMGN5 expression significantly reversed the inhibitory effects of miR-409-3p overexpression on glioma cell invasion and proliferation. Taken together, our results suggest that miR-409-3p inhibits glioma cell invasion and proliferation by targeting HMGN5, representing a potential therapeutic target for glioma.

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Using ultra-high performance concrete (UHPC) as the pavement layer on the orthotropic steel deck (OSD) can greatly enhance the rigidity to solve the fatigue cracking of the steel deck and the resulting damage to the pavement layer. However, the thin UHPC layer limits the extensive use of the short stud connector. In this study, three types of interfaces were designed by introducing different additives into the epoxy matrix, and the shear properties of each interface and short stud connector were compared. Then, the influence of short stud connectors and optimized interface on the composite bridge deck’s bending property was analyzed through the composite bridge deck’s bending test. Moreover, the mechanical behavior of the interface in the composite bridge deck is discussed based on the finite element model. The results show that the ultimate load of the composite bridge deck with the optimized interface is reduced by 21.5% compared with that of the composite bridge deck with the short stud connector. However, the composite bridge deck with the optimized interface has higher bending stiffness before failure and is less affected by cyclic loading. Moreover, the composite bridge deck with the optimized interface is unsuitable for cyclic loading conditions when the defect area reaches 30%. Finally, the numerical simulation of the composite bridge deck with the optimized interface is successfully realized based on the cohesive zone model, and the applicability of the interface in the composite bridge deck is verified.