Cisatracurium inhibits the growth and induces apoptosis of ovarian cancer cells by promoting lincRNA-p21.

As a common muscle relaxant, cisatracurium has shown good antitumor effect on some tumors. Recent studies reported that cisatracurium could inhibit the progression of colon cancer by upregulating tumor suppressor gene p53. However, its role in ovarian cancer and its regulatory effect on p53 and p53 downstream targeting gene long intergenic noncoding RNA p21 (lincRNA-p21) is still unknown. Quantitative Real-time Polymerase Chain Reaction (qRT-PCR) was used to assess the expression of p53, lincRNA-p21 and miR-181b. Cell viability and proliferation were detected by CCK-8 assay and Edu staining, respectively. Wound-healing and Transwell assays were performed to determine the abilities of cell migration and invasion. Apoptosis was evaluated by TUNEL staining. Luciferase reporter assay was conducted to detect the relationship between lincRNA-p21 and miR-181b. As a result, cisatracurium could increase the expressions of p53 and lincRNA-p21 of ovarian cancer cell line (OVCAR-3) in a dose-dependent manner. In addition, cisatracurium significantly inhibited the proliferation, migration and invasion of OVACR-3 cells, and induced apoptosis. However, these above changes in biological function can be attenuated by lincRNA-p21 knockdown. Next, lincRNA-p21 could directly target miR-181b and negatively regulate its expression by luciferase reporter assay. In conclusion, cisatracurium inhibited the progression of OVCAR-3 cells through upregulation of lincRNA-p21 expression activated by p53 inhibiting miR-181b expression. The experimental results provide a new research idea for the application of cisatracurium in ovarian cancer.

Fucoidan inhibits LPS-induced acute lung injury in mice through regulating GSK-3ß-Nrf2 signaling pathway.

The purpose of this study was to investigate the protective effects of fucoidan on Lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. The mice were divided into the control, LPS, and LPS + fucoidan (20, 40, or 80 mg/kg) groups. LPS was given by intracheal instillation and fucoidan was given 1 h before LPS treatment. Myeloperoxidase (MPO) activity, malondialdehyde (MDA), superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione (GSH) contents, and inflammatory cytokine production were detected. The results showed that LPS-induced TNF-α, IL-1ß, and IL-6 production, lung wet/dry (W/D) ratio, ROS, MDA content, and MPO activity were suppressed by fucoidan. The levels of SOD and GSH were increased by fucoidan. Meanwhile, LPS-induced nuclear factor kappa-B (NF-κB) activation was dose-dependently attenuated by fucoidan. Furthermore, fucoidan increased the expression of nuclear factor erythroid-2 related factor 2 (Nrf2), Glycogen synthase kinase3ß (GSK-3ß), and heme oxygenase (HO-1). In vitro, the results demonstrated that fucoidan or GSK-3ß inhibitor significantly inhibited LPS-induced TNF-α production in A549 cells. And the inhibition of fucoidan on TNF-α production was blocked by Nrf2 siRNA. This study showed fucoidan protected mice against LPS-induced ALI through inhibiting inflammatory and oxidative responses via regulating GSK-3ß-Nrf2 signaling pathway.

Ameliorative effect of sevoflurane on endoplasmic reticulum stress mediates cardioprotection against ischemia-reperfusion injury 1.

We aimed to investigate whether the cardioprotection of sevoflurane against ischemia-reperfusion (IR) injury is via inhibiting endoplasmic reticulum stress. The rat in vivo model of myocardial IR injury was induced by ligation of the left anterior descending coronary artery. Sevoflurane significantly ameliorated the reduced cardiac function, increased infarct size, and elevated troponin I level and lactate dehydrogenase activity in plasma induced by IR injury. Sevoflurane suppressed the IR-induced myocardial apoptosis. The increased protein levels of glucose-regulated protein 78 and C/EBP homologous protein (CHOP) after myocardial IR were significantly reduced by sevoflurane. The protein levels of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK), phosphorylated eukaryotic initiation factor 2 (eIF2α), and activating transcription factor 4 (ATF4) were significantly increased in rats with IR and attenuated by sevoflurane treatment. The phosphorylation of Akt was further activated by sevoflurane. The cardioprotection of sevoflurane could be blocked by wortmannin, a PI3K/Akt inhibitor. Our results suggest that the cardioprotection of sevoflurane against IR injury might be mediated by suppressing PERK/eIF2a/ATF4/CHOP signaling via activating the Akt pathway, which helps in understanding the novel mechanism of the cardioprotection of sevoflurane.

A novel circular RNA, hsa_circ_0046701, promotes carcinogenesis by increasing the expression of miR-142-3p target ITGB8 in glioma.

In the present study, we identified a novel circular RNA (circRNA), hsa_circ_0046701, in glioma cells. We measured the expression of hsa_circ_0046701 using qRT-PCR in glioma tissues and cell lines, and explored its functions using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, colony formation, and Transwell assays. Luciferase reporter assays were performed to validate the correlation between microRNA miR-142-3p and hsa_circ_0046701 or integrin subunit beta 8 (ITGB8). The results showed that hsa_circ_0046701 was significantly upregulated in glioma tissues and cell lines, and knockdown of hsa_circ_0046701 inhibited cell proliferation and invasion. Luciferase reporter assays indicated that hsa_circ_0046701 functions as a sponge for miR-142-3p and regulates the expression of ITGB8. Subsequently, functional assays revealed that silencing of hsa_circ_0046701 could upregulate miR-142-3p, resulting in downregulation of ITGB8. The results demonstrated that the hsa_circ_0046701/miR-142-3p/ITGB8 axis might play critical regulatory roles in the pathogenesis and development of glioma.

Risk factors of intracranial hemorrhage after brain AVM interventional therapy and its effects on prognosis.

OBJECTIVE: This study is to investigate risk factors of intracranial hemorrhage and their effects on prognosis in patients with brain intracranial arteriovenous malformation (AVM) after interventional therapy. METHODS: A total of 80 cases of brain AVM patients were admitted to our hospital and received interventional embolism treatment from December 2011 to July 2014. The patients all were confirmed by digital subtraction angiography. Risk factors of intracranial hemorrhage after interventional therapy were analyzed by multivariate analysis. The factors included age, sex, AVM diameter, vein drainage types, embolism area, etc. Meanwhile, the patients were followed up for 60 months after interventional embolism therapy, so as to assess the impact of related risk factors on prognosis. RESULTS: By logistic regression analysis, it was found that age, AVM diameter, AVM combined with aneurysm, embolism area and venous drainage types were related risk factors those could lead to intracranial hemorrhage. Meanwhile, it was identified by receiver operating characteristic curve that embolism area, AVM diameter and AVM combined with aneurysm were risk factors had considerable influence on prognosis while the diagnosis significance of age and venous drainage types was poor (P > 0.05). The survival curves of embolism area and AVM diameter on prognosis had been identified by Kaplan-Meier analysis and it showed that embolism area < 50% and AVM diameter ≥ 3 cm had a better prognosis than embolism area ≥ 50% and AVM diameter < 3 cm (P < 0.05). CONCLUSIONS: A series of risk factors were related to intracranial hemorrhage and some of them had considerable influence on prognosis, which, could help to reduce the risk of intracranial hemorrhage and improve long-term survival rate.

Thoracoscopic tracheal resection and reconstruction for adenoid cystic carcinoma.

We describe a novel technique of thoracoscopic circumferential tracheal resection and end-to-end anastomosis. A 60-year-old woman presented with wheezing and progressive dyspnea. Computed tomography scan revealed a mass at the lower trachea, and a nitinol mesh stent was implanted by bronchoscopy. After 2 weeks, a complete thoracoscopic tracheal resection and reconstruction was performed. The postoperative course was uneventful. The final pathologic examination confirmed the diagnosis of primary adenoid cystic carcinoma of the trachea.

Targeted suppression of chaperone-mediated autophagy by miR-320a promotes α-synuclein aggregation.

Chaperone-mediated autophagy (CMA) is involved in wild-type α-synuclein degradation in Parkinson's disease (PD), and LAMP2A and Hsc 70 have recently been indicated to be deregulated by microRNAs. To recognize the regularory role of miR-320a in CMA and the possible role in α-synuclein degradation, in the present study, we examined the targeting and regulating role of miR-320 in Hsc 70 expression. We first constructed an α-synuclein-overexpressed human neuroblastoma cell line, SH-SY5Y-Syn(+), stably over-expressing wild-type α-synuclein and sensitive to an autophagy inhibitor, which exerted no effect on the expression of LAMP2A and Hsc 70. Then we evaluated the influence on the CMA by miR-320a in the SH-SY5Y-Syn(+) cells. It was shown that miR-320a mimics transfection of specifically targeted Hsc 70 and reduced its expression at both mRNA and protein levels, however, the other key CMA molecule, LAMP2A was not regulated by miR-320a. Further, the reduced Hsc 70 attenuated the α-synuclein degradation in the SH-SY5Y-Syn(+) cells, and induced a significantly high level of α-synuclein accumulation. In conclusion, we demonstrate that miR-320a specifically targeted the 3' UTR of Hsc 70, decreased Hsc 70 expression at both protein and mRNA levels in α-synuclein-over-expressed SH-SY5Y cells, and resulted in significant α-synuclein intracellular accumulation. These results imply that miR-320a might be implicated in the α-synuclein aggravation in PD.

[Hydrothermo-assisted functionalization, FTIR, Raman and XPS spectra characterization of carbon nanotubes].

The chemical functionalization process of carbon nanotubes(CNTs) by hydrothermal treatments was investigated systematically under various reaction conditions, including different reagents, treatment time, and temperature. The treated samples were characterized by the FTIR, XPS and Raman spectroscopy. The results revealed that the hydrothermal technology is an effective method for the functionalization of CNTs and the control of the resulting chemical groups.