Astaxanthin (ATX) has been proven to ameliorate early brain injury (EBI) after experimental subarachnoid hemorrhage (SAH) by modulating cerebral oxidative stress. This study was performed to assess the effect of ATX on the Nrf2-ARE pathway and to explore the underlying molecular mechanisms of antioxidant properties of ATX in EBI after SAH. A total of 96 male SD rats were randomly divided into four groups. Autologous blood was injected into the prechiasmatic cistern of the rat to induce an experimental SAH model. Rats in each group were sacrificed at 24 h after SAH. Expressions of Nrf2 and heme oxygenase-1 (HO-1) were measured by Western blot and immunohistochemistry analysis. The mRNA levels of HO-1, NAD (P) H: quinone oxidoreductase 1 (NQO-1), and glutathione S-transferase-α1 (GST-α1) were determined by real-time polymerase chain reaction (PCR). It was observed that administration of ATX post-SAH could up-regulate the cortical expression of these agents, mediated in the Nrf2-ARE pathway at both pretranscriptional and posttranscriptional levels. Meanwhile, oxidative damage was reduced. Furthermore, ATX treatment significantly attenuated brain edema, blood–brain barrier (BBB) disruption, cellular apoptosis, and neurological dysfunction in SAH models. This study demonstrated that ATX treatment alleviated EBI in SAH model, possibly through activating the Nrf2-ARE pathway by inducing antioxidant and detoxifying enzymes.

Background:Appropriate expression and regulation of the transcriptome, which mainly comprise of mRNAs and lncRNAs, are important for all biological and cellular processes including the physiological activities of bone microvascular endothelial cells (BMECs). Through an intricate intracellular signaling systems, the transcriptome regulates the pharmacological response of the cells. Although studies have elucidated the impact of glucocorticoids (GCs) cell-specific gene expression signatures, it remains necessary to comprehensively characterize the impact of lncRNAs to transcriptional changes.Methods:BMECs were divided into two groups. One was treated with GCs and the other left untreated as a paired control. Differential expression was analyzed with GeneSpring software V12.0 (Agilent, Santa Clara, CA, USA) and hierarchical clustering was conducted using Cluster 3.0 software. The Gene Ontology (GO) analysis was performed with Molecular Annotation System provided by CapitalBio Corporation.Results:Our results highlight the involvement of genes implicated in development, differentiation and apoptosis following GC stimulation. Elucidation of differential gene expression emphasizes the importance of regulatory gene networks induced by GCs. We identified 73 up-regulated and 166 down-regulated long noncoding RNAs, the expression of 107 of which significantly correlated with 172 mRNAs induced by hydrocortisone.Conclusions:Transcriptome analysis of BMECs from human samples was performed to identify specific gene networks induced by GCs. Our results identified complex RNA crosstalk underlying the pathogenesis of steroid-induced necrosis of femoral head.

BackgroundThe purpose of this study was to investigate splanchnic hemodynamic changes and determine an optimal cutoff value for risk factors of portal venous system thrombosis (PVST) after splenectomy with periesophagogastric devascularization (SPD) in cirrhotic patients with esophageal and gastric variceal bleeding (EGVB) and portal hypertension (PH).Material/MethodsData on patients who underwent SPD were collected retrospectively from January 2013 to December 2017. Color Doppler ultrasound was performed to detect hemodynamic changes of the hepatic artery, splenic artery, splenic vein, and portal vein in included patients (n=60) and healthy volunteers (n=30). Outcomes were compared between preoperative and postoperative biochemical indicators. The cutoff values for hemodynamics were identified using receiver operating characteristic (ROC) curve analysis, and univariate and multivariate analyses of risk factors of PVST were performed.ResultsIn our series, hemodynamic indexes of splenic artery, spleen vein, and portal vein in the study group were significantly higher than that of the control group (P<0.05). Multivariate analysis revealed that the portal vein flow and the internal diameter of the portal vein were significantly correlated with PVST. The ROC analysis revealed that the cutoff points for portal vein flow and internal diameter of the splenic vein and portal vein were ≥1822.32 ml/min, ≥1.37 cm, and ≥1.56 cm, respectively.ConclusionsSPD is an effective treatment in cirrhotic patients with concomitant EGVB and PH by increasing hepatic artery flow and decreasing portal vein flow. High portal vein flow and wider diameters of the portal vein and splenic vein are important markers of PVST.

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