RESUMEN
Energy-field-assisted cutting exhibits excellent ability to reduce cutting force and improve machining quality. In this study, a magnetic field was applied in an innovative way to aid in the cutting process, and magnetic-field-assisted scratching experiments of single-crystal copper were carried out. It was found that magnetic-field-assisted scratching increased the actual scratching force due to the additional Lorentz force in the cutting process. However, the friction coefficient of the magnetic-field-assisted scratching was reduced by 19.4% due to the tribological modification effect on tool/chip contact. Meanwhile, magnetic-field-assisted scratching was conducive to decreasing the degree of chip deformation, reducing microburrs on the machined surface, and obtaining a surface roughness reduction of an average of 26.8%. The possible reason for this effect was that the presence of a magnetic field in the cutting process promoted the dislocation slip of metal materials. The results indicated that magnetic-field-assisted cutting improves the machinability in the metal cutting process.
RESUMEN
The present study aimed to investigate the role of ZEB1-antisense RNA 1 (AS1) in diabetic lung (pneumonia with excluded causes other than diabetes). In the present study, the expression of ZEB1-AS1 in plasma was detected by performing reverse transcription-quantitative PCR. A receiver operating characteristic curve was used for diagnostic analysis. Lung cell apoptosis under the treatment of high glucose was analyzed by a cell apoptosis assay. p53 expression in lung cells was detected by performing western blotting. The present data demonstrated that ZEB1-AS1 was downregulated in the plasma of patients with diabetic lung (DL) compared with diabetic patients without complications (~1.6-fold) and healthy controls (~2.4-fold), and downregulation of ZEB1-AS1 distinguished patients with DL from healthy controls. ZEB1-AS1 in lung cells was downregulated by high glucose treatment, and overexpression of ZEB1-AS1 resulted in inhibited lung cancer cell apoptosis and downregulated p53. p53 overexpression attenuated the effects of ZEB1-AS1 overexpression on lung cell apoptosis. In conclusion, the present study demonstrated that ZEB1-AS1 was downregulated in patients with DL and regulates lung cancer cell apoptosis by downregulating p53.
RESUMEN
Acute lung injury (ALI) is a life-threatening condition caused by severe inflammation of lung tissues. We hypothesized that lipopolysaccharide induced acute lung inflammation and injury in mice might be controlled by lonicerin (LCR), a plant flavonoid that impacts immunity, oxidative stress, and cell proliferation. LCR reduced pathological changes including pulmonary edema, elevation of protein in bronchoalveolar lavage, inflammation, pro-inflammatory gene expression, expression of toll-like receptor 4/nuclear factor-kappa B, apoptosis, and significantly reduced mortality. Together, the results suggest that LCR might be a potential and effective candidate for the treatment of ALI that acts by inhibiting inflammation and apoptosis.
Asunto(s)
Lesión Pulmonar Aguda/prevención & control , Apoptosis/efectos de los fármacos , Inflamación/prevención & control , Luteolina/farmacología , Lesión Pulmonar Aguda/inducido químicamente , Lesión Pulmonar Aguda/mortalidad , Animales , Citocinas/genética , Citocinas/metabolismo , Expresión Génica/efectos de los fármacos , Humanos , Inflamación/genética , Inflamación/metabolismo , Lipopolisacáridos , Pulmón/efectos de los fármacos , Pulmón/metabolismo , Pulmón/patología , Masculino , Ratones Endogámicos C57BL , FN-kappa B/metabolismo , Tasa de Supervivencia , Receptor Toll-Like 4/metabolismoRESUMEN
Acute lung injury (ALI) as a serious disease with high mortality has been emphasized as a threat to human health and life. Accumulating studies demonstrated that PM2.5 plays a significant role in metabolic and lung diseases. Histone deacetylases 3 (HDAC3) is an important regulator in control of gene transcription, required in up-regulation of inflammation-related signaling, and has been known as a key hotpot in treating a lot of chronic inflammatory diseases. TGF-ß/Smad signaling pathway has been proven to be of significance in fibrosis development. Our results found that PM2.5 induced lung function injury in WT mice with a inflammatory responses through the activation of TGF-ß/Smad signaling pathways, resulting in lung injury. Of note, HDAC3-deficient mice after PM2.5 administration further promoted TGF-ß/Smad signaling pathways activation. In addition, TLR4, p-NF-κB and p-IκBα indicated that HDAC3 knockout mice have a higher inflammation-related signals expression in lung tissue than WT mice after PM2.5 administration, resulting in pro-inflammatory cytokines releasing. Moreover, in vitro experiment of lung epithelial cells challenged with PM2.5, further indicated that TGF-ß/Smad2/3 was involved in fibrosis development, leading to inflammation response. Also, the activation of TLR4/NF-κB could be observed in PM2.5-induced lung epithelial cells, leading to inflammation infiltration. These results indicate a new therapeutic target to protect against lung injury caused by PM2.5.
Asunto(s)
Histona Desacetilasas/metabolismo , Lesión Pulmonar/inducido químicamente , FN-kappa B/metabolismo , Proteína Smad2/metabolismo , Proteína smad3/metabolismo , Factor de Crecimiento Transformador beta/metabolismo , Animales , Eliminación de Gen , Regulación de la Expresión Génica/fisiología , Histona Desacetilasas/genética , Lesión Pulmonar/metabolismo , Ratones , FN-kappa B/genética , Tamaño de la Partícula , Material Particulado/química , Material Particulado/toxicidad , Proteína Smad2/genética , Proteína smad3/genética , Factor de Crecimiento Transformador beta/genéticaRESUMEN
Valproic acid (VPA) has been suggested to be a histone deacetylase inhibitor (HDACI). Our present study revealed that VPA at 1 mm, which had no effect on cell proliferation, can significantly increase the sensitivity of non-small cell lung cancer (NSCLC) cells to cisplatin (DDP). VPA treatment markedly decreased the mRNA and protein levels of ABCA1, while had no significant effect on ABCA3, ABCA7 or ABCB10. Luciferase reporter assays showed that VPA can decrease the ABCA1 promoter activity in both A549 and H358 cells. VPA treatment also decreased the phosphorylation of SP1, which can bind to -100 and -166 bp in the promoter of ABCA1. While the phosphorylation of c-Fos and c-Jun were not changed in VPA treated NSCLC cells. Over expression of HDAC2 attenuated VPA induced down regulation of ABCA1 mRNA expression and promoter activities. Over expression of HDAC2 also attenuated VPA induced DDP sensitivity of NSCLC cells. These data revealed that VPA can increase the DDP sensitivity of NSCLC cells via down regulation of ABCA1 through HDAC2/SP1 signals. It suggested that combination of VPA and anticancer drugs such as DDP might be great helpful for treatment of NSCLC patients.
Asunto(s)
Transportador 1 de Casete de Unión a ATP/genética , Carcinoma de Pulmón de Células no Pequeñas/patología , Cisplatino/farmacología , Regulación hacia Abajo/efectos de los fármacos , Histona Desacetilasa 2/metabolismo , Neoplasias Pulmonares/patología , Ácido Valproico/farmacología , Antineoplásicos/farmacología , Apoptosis/efectos de los fármacos , Línea Celular Tumoral , Sinergismo Farmacológico , Histona Desacetilasa 2/genética , Humanos , Factor de Transcripción Sp1/metabolismo , Transcripción Genética/efectos de los fármacosRESUMEN
Human urinary bladder cancer (UBC) is the fourth most common cancer and the eighth most common cause of cancer death in the USA. High mobility group box 3 (HMGB3), a member of a family of proteins containing one or more high mobility group DNA binding motifs, was reported to be overexpressed in a variety of human cancers. However, the expression and role of HMGB3 in human UBC remains unclear. Here, we found that UBC patients had upregulated HMGB at both mRNA and protein levels. Immunochemistry (IHC) evaluation of HMGB3 expression in 113 UBC clinical specimens showed that high expression of HMGB3 had positive correlation with UBC tumor size (P = 0.019), tumor WHO grade (P = 0.031), stage (P = 0.028), and lymph node metastasis (P = 0.017). Moreover, patients with higher HMGB3 expression showed a poorer overall survival rate than those with relatively low HMGB3 (P = 0.0079, log-rank test). Multivariate analysis revealed that HMGB3 expression is an independent prognostic marker. The UBC cancer cell proliferation and migration ability were measured by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and wound healing assays, respectively. RNA interference of HMGB3 in UBC cell lines inhibited cancer cell growth and migration, along with the downregulation of PCNA and MMP2 protein levels. In sum, our data suggests HMGB3 may serve as an important oncoprotein and indicate that overexpression of HMGB3 in UBC could be used as a potential prognostic marker.