Sleep deprivation (SD) has a profound impact on the central nervous system, resulting in an array of mood disorders, including depression and anxiety. Despite this, the dynamic alterations in neuronal activity during sleep deprivation have not been extensively investigated. While some researchers propose that sleep deprivation diminishes neuronal activity, thereby leading to depression. Others argue that short-term sleep deprivation enhances neuronal activity and dendritic spine density, potentially yielding antidepressant effects. In this study, a two-photon microscope was utilized to examine the calcium transients of anterior cingulate cortex (ACC) neurons in awake SD mice in vivo at 24-hour intervals. It was observed that SD reduced the frequency and amplitude of Ca2+ transients while increasing the proportions of inactive neurons. Following the cessation of sleep deprivation, neuronal calcium transients demonstrated a gradual recovery. Moreover, whole-cell patch-clamp recordings revealed a significant decrease in the frequency of spontaneous excitatory post-synaptic current (sEPSC) after SD. The investigation also assessed several oxidative stress parameters, finding that sleep deprivation substantially elevated the level of malondialdehyde (MDA), while simultaneously decreasing the expression of Nuclear Factor erythroid 2-Related Factor 2 (Nrf2) and activities of Superoxide dismutase (SOD) in the ACC. Importantly, the administration of gallic acid (GA) notably mitigated the decline of calcium transients in ACC neurons. GA was also shown to alleviate oxidative stress in the brain and improve cognitive impairment caused by sleep deprivation. These findings indicate that the calcium transients of ACC neurons experience a continuous decline during sleep deprivation, a process that is reversible. GA may serve as a potential candidate agent for the prevention and treatment of cognitive impairment induced by sleep deprivation.

OBJECTIVE To study the mechanism of Qingre huashi decoction in the treatment of gastric cancer by intervening in miRNA-155 and inhibiting Wnt/β-catenin signaling pathway. METHODS Thirty nude mice were randomly divided into model group， control group （0.004 g/kg cisplatin+0.02 g/kg fluorouracil）， overexpression group， Qingre huashi prescription low-dose， medium-dose and high-dose groups （2.71， 5.43， 10.86 g/kg）， with 5 mice in each group. The overexpression group was inoculated with miRNA-155 AGS cell line， and the other groups were inoculated with AGS cells to induce tumor-bearing gastric cancer model. The control group was given relevant medicine intraperitoneally， and other groups were given relevant medicine or normal saline intragastrically， once a day， for 3 consecutive weeks. The weight of tumor tissue in nude mice was determined； the pathological morphology of tumor tissue was observed； the miRNA-155 expression， mRNA and protein expressions of Wnt7， β-catenin and T- cell factor-4（TCF-4） in tumor tissue were detected. RESULTS Compared with the model group， the tumor weights of nude mice in the control group， the overexpression group and Qingre huashi decoction high-dose group were significantly reduced （P＜0.05）； mRNA and protein expressions of Wnt7， β -catenin and TCF-4 were significantly decreased （P＜0.05）， while miRNA-155 expression was increased significantly （P＜0.05）. Tumor cells exhibited varying degrees of loose arrangement， shallow nuclear staining， and necrotic foci. CONCLUSIONS Qingre huashi decoction can inhibit the protein and mRNA expressions of Wnt7， β-catenin and TCF-4 in Wnt/β-catenin signaling pathway by up-regulating miRNA-155， thus inhibiting the tumor growth of tumor-bearing nude mice.

Objective To construct a new type of glucosamine/DNA composite nanostructure(NTGlcN)assembled without magnesium,verify whether or not glucosamine can mediate the assembly of DNA nanotubes(NT)and assess its effect on the function of Raw264.7 cells.Methods Utilizing the gradient annealing method with 3 DNA single strands Y1,Y2,and Y3,glucosamine(GlcN)was employed to mediate the assembly of DNA NT,resulting in the formation of glucosamine/DNA composite nanostructures.Atomic force microscopy(AFM)was used to observe the surface structure of the nanomaterial and dynamic light scattering(DLS)was used to measure its size.RAW264.7 cells were used in cell experiments.The cytotoxicity of GlcN and NTGlcN was assessed using CCK-8 assay.Flow cytometry and laser confocal microscopy were employed to investigate the cellular uptake efficiency of the nanostructures.The effects of NTGlcN and NTMg(Mg2+-assembled of DNA NT)on the expression levels of inflammatory cytokines(IL-1β,IL-6)in macrophages induced by lipopolysaccharides(LPS)were evaluated using RT-qPCR.Results GlcN successfully mediated the synthesis of NTGlcN,which exhibited good stability.AFM characterization results revealed that NTGlcN formed tubular particles that were uniformly distributed on the surface of mica.DLS measurements indicated that the diameter of NTGlcN was approximately 15.26±3.86 nm.Cell experiments demonstrated that,compared to NTMg,macrophages exhibited a higher cellular uptake efficiency for NTGlcN,with a higher cell survival rate following treatment with NTGlcN(P＜0.05).After NTGlcN treatment,the expression of inflammatory cytokines in LPS-induced macrophages was reduced(P＜0.05).Conclusion The glucosamine/DNA composite nanostructures have been successfully developed,possessing excellent stability,biocompatibility and cell uptake efficiency.NTGlcN is capable of reducing the cytotoxicity of GlcN and can suppress cellular inflammatory responses by decreasing the expression of inflammatory cytokines in RAW264.7 cells.

MTUS1 (microtubule-associated tumor suppressor 1) has been identified that can function as a tumor suppressor gene in many malignant tumors. However, the function and mechanisms underlying the regulation of MTUS1 are unclear. In the present study, we reported that miR-19a and miR-19b (miR-19a/b) promote proliferation and migration of lung cancer cells by targeting MTUS1. First, MTUS1 was proved to function as a tumor suppressor in lung cancer and was linked to cell proliferation and migration promotion. Second, an inverse correlation between miR-19a/b expression and MTUS1 mRNA/protein expression was noted in human lung cancer tissues. Third, MTUS1 was appraised as a direct target of miR-19a/b by bioinformatics analysis. Fourth, direct MTUS1 regulation by miR-19a/b in lung cancer cells was experimentally affirmed by cell transfection assay and luciferase reporter assay. Finally, miR-19a/b were shown to cooperatively repress MTUS1 expression and synergistically regulate MTUS1 expression to promote lung cancer cell proliferation and migration. In conclusion, our findings have provided the first clues regarding the roles of miR-19a/b, which appear to function as oncomirs in lung cancer by downregulating MTUS1.
A549 Cells ; Cell Movement ; Cell Proliferation ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms ; genetics ; metabolism ; pathology ; Male ; MicroRNAs ; genetics ; metabolism ; RNA, Neoplasm ; genetics ; metabolism ; Tumor Suppressor Proteins ; biosynthesis ; genetics