Current trends and future perspectives of stroke management through integrating health care team and nanodrug delivery strategy.

Stroke is accounted as the second-most mortality and adult disability factor in worldwide, while causes the bleeding promptly and lifetime consequences. The employed functional recovery after stroke is highly variable, allowing to deliver proper interventions to the right stroke patient at a specific time. Accordingly, the multidisciplinary nursing team, and the administrated drugs are major key-building-blocks to enhance stroke treatment efficiency. Regarding the healthcare team, adequate continuum of care have been declared as an integral part of the treatment process from the pre-hospital, in-hospital, to acute post-discharge phases. As a curative perspective, drugs administration is also vital in surviving at the early step and reducing the probability of disabilities in later. In this regard, nanotechnology-based medicinal strategy is exorbitantly burgeoning. In this review, we have highlighted the effectiveness of current clinical care considered by nursing teams to treat stroke. Also, the advancement of drugs through synthesis of miniaturized nanodrug formations relating stroke treatment is remarked. Finally, the remained challenges toward standardizing the healthcare team and minimizing the nanodrugs downsides are discussed. The findings ensure that future works on normalizing the healthcare nursing teams integrated with artificial intelligence technology, as well as advancing the operative nanodrugs can provide value-based stroke cares.

CD147 modulates androgen receptor activity through the Akt/Gsk-3ß/ß-catenin/AR pathway in prostate cancer cells.

The androgen signaling pathway serves an important role in the development of prostate cancer. ß-Catenin is an androgen receptor (AR) cofactor and augments AR signaling. Glycogen synthase kinase-3ß (GSK-3ß), a target of phosphorylated serine/threonine protein kinase B (p-Akt), regulates ß-catenin stability. In addition, ß-catenin, a coregulator of AR, physically interacts with AR and enhances AR-mediated target gene transcription. The multifunctional glycoprotein cluster of differentiation (CD) 147 is highly expressed on the cell surface of the majority of cancer cells, and it promotes tumor invasion, metastasis and growth. In the present study, the molecular effects of CD147 on the Akt/GSK-3ß/ß-catenin/AR signaling network were investigated in LNCaP cells. Using short hairpin-mediated RNA knockdown of CD147 in LNCaP cells, it was demonstrated that downregulation of CD147 resulted in inhibitory phosphorylation of GSK-3ß, and then promoted degeneration of ß-catenin and reduced nuclear accumulation of ß-catenin. In addition, immunoprecipitation studies demonstrated that CD147 downregulation decreased the formation of a complex between ß-catenin and AR. It was shown that CD147 knockdown suppressed the expression of the AR target gene prostate-specific antigen and the growth of AR-positive LNCaP cells. Furthermore, inhibition of PI3K/Akt with LY294002 augmented CD147-mediated function. The present study indicates that the PI3K/Akt pathway may facilitate CD147-mediated activation of the AR pathway.

Juglone exerts antitumor effect in ovarian cancer cells.

OBJECTIVES: Juglone is isolated from many species of the Juglandaceae family and used as an anti-viral, anti-bacterial, and anti-tumor therapeutic. Here, we evaluated juglone-induced antitumor effect in ovarian cancer SKOV3 cells. MATERIALS AND METHODS: MTT assay was performed to examine juglone anti-proliferative effect. Cell cycle and apoptosis were studied using flow cytometry in juglone-treated SKOV3 cells. To investigate molecular mechanism of cell cycle and apoptosis, protein expression levels were measured by Western blot analysis of cyclin D1, Bcl-2, Bax, cytochrome c, caspase-9 and caspase-3. To investigate the motility of juglone-treated SKOV3 cell, Matrigel invasion assay was employed to characterize cell invasion. Also, matrix metalloproteinase-2 (MMP-2) expression levels were detected by western blot. RESULTS: Juglone significantly inhibited SKOV3 cell proliferation as shown by G0/G1 phase arrest, and this effect was mediated by inactivation of cyclin D1 protein (P<0.05). Juglone induced apoptosis in SKOV3 cell which was accompanied by caspase-9 and caspase-3 activation (P<0.05). Juglone decreased Bcl-2 levels and increased Bax and cytochrome c (Cyt c) levels (P<0.05). Juglone sufficiently inhibited invasion while evidently decreased MMP-2 expression (P<0.05). CONCLUSION: The results suggest that juglone could probably induce apoptosis through mitochondrial pathway and restrained cell invasiveness by decreasing MMP expression.

Soy isoflavones protect against H2O2-induced injury in human umbilical vein endothelial cells.

The aim of this study was to investigate the effects of soy isoflavones on the injury of human umbilical vein endothelial cells induced by H2O2. EVC­304 cells were preincubated with soy isoflavones for 12 h, and then exposed to 100 µM H2O2 for 1 h. Cell viability was evaluated by a 3­(4,5­di­methylthiazol­2­yl) 2,5­diphenyltetrazolium bromide assay. The apoptosis of EVC­304 cells was detected by Hoechst 33258 and Annexin­V/propidium iodide staining. The oxidative stress­related biochemical parameters were detected and the expression of apoptosis­related proteins was examined by western blot analysis. The results showed that incubation with soy isoflavones caused a significant increase in the viability of EVC­304 cells and a decrease in cell apoptosis induced by H2O2. Soy isoflavones also markedly enhanced the activities of superoxide dismutase and glutathione peroxidase, and reduced the level of malondialdehyde. Western blot analysis results show that soy isoflavones can modulate the activation of nuclear factor­κB and the mitochondria­mediated apoptosis signaling pathway. The results of this study indicated the potential biological relevance of soy isoflavones in the therapy of cardiovascular diseases.