Incorporation mechanism of colloidal TiO2 nanoparticles and their effect on properties of coatings grown on 7075 Al alloy from silicate-based solution using plasma electrolytic oxidation

Plasma electrolytic oxidation (PEO) was applied using a pulsed unipolar waveform to produce Al2O3-TiO2 composite coatings from sol electrolytic solutions containing colloidal TiO2 nanoparticles. The sol solutions were produced by dissolving 1, 3, and 5 g/L of potassium titanyl oxalate (PTO) in a silicate solution. Scanning electron microscopy, energy dispersive spectrometry, X-ray diffraction, and Raman spectroscopy were applied to characterizing the coatings. Corrosion behavior of the coatings was investigated using polarization and impedance techniques. The results indicated that TiO2 enters the coating through all types of micro-discharging and is doped into the alumina phase. The higher level of TiO2 incorporation results in the decrease of surface micro-pores, while the lower incorporation shows a reverse effect. It was revealed that the higher TiO2 content makes a more compact outer layer and increases the inner layer thickness of the coating. Electrochemical measurements revealed that the coating obtained from the solution containing 3 g/L PTO exhibits higher corrosion performance than that obtained in the absence of PTO. The coating produced in the absence of PTO consists of gamma-Al2O3, delta-Al2O3 and amorphous phases, while alpha-Al2O3 is promoted by the presence of PTO

Silicate and Hydroxide Concentration Influencing the Properties of Composite Al2 O3-TiO2 PEO Coatings on AA7075 Alloy

This work evaluates the effect of sodium meta-silicate pentahydrate (SMS) and potassium hydroxide concentrations on properties of Al2O3-TiO2 coatings produced through plasma electrolytic oxidation in a solution containing 3 g L−1 potassium titanyl oxalate, (PTO), using a unipolar waveform with constant current density. The surface and cross-section characteristics of PEO coatings including morphology, elemental distribution, and phase composition were evaluated using FESEM, EDS, and XRD techniques. Voltage-time response indicated the concentration of SMS and KOH had a significant effect on the duration of each stage of the PEO process. More cracks and pores were formed at the higher concentrated solutions that resulted in the incorporation of solution components especially Si into the coating inner parts. Ti is distributed throughout the coatings, but it had a dominant distribution in the Si-rich areas. The coating prepared in the electrolyte containing no silicate consisted of non-stoichiometric γ-Al2O3 and/or amorphous Al2O3 phase. Adding silicate into the coating electrolyte resulted in the appearance of α-Al2O3 besides the dominant phase of γ-Al2O3. The corrosion behaviour of the coatings was investigated using the EIS technique. It was found that the coating prepared in the presence of 3 g L−1 SMS and 2 g L−1 KOH, possessed the highest barrier resistance (~10 MΩ cm2), owing to a more compact outer layer, thicker inner layer along with appropriate dielectric property because this layer lacks the Si element. It was discovered that the incorporation of Ti4+ and especially Si4+ in the coating makes the dielectric loss in the coating

Targeting of cellular redox metabolism for mitigation of radiation injury

Accidental exposure to ionizing radiation is a serious concern to human life. Studies on the mitigation of side effects following exposure to accidental radiation events are ongoing. Recent studies have shown that radiation can activate several signaling pathways, leading to changes in the metabolism of free radicals including reactive oxygen species (ROS) and nitric oxide (NO). Cellular and molecular mechanisms show that radiation can cause disruption of normal reduction/oxidation (redox) system. Mitochondria malfunction following exposure to radiation and mutations in mitochondria DNA (mtDNA) have a key role in chronic oxidative stress. Furthermore, exposure to radiation leads to infiltration of inflammatory cells such as macrophages, lymphocytes and mast cells, which are important sources of ROS and NO. These cells generate free radicals via upregulation of some pro-oxidant enzymes such as NADPH oxidases, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Epigenetic changes also have a key role in a similar way. Other mediators such as mammalian target of rapamycin (mTOR) and peroxisome proliferator-activated receptor (PPAR), which are involved in the normal metabolism of cells have also been shown to regulate cell death following exposure to radiation. These mechanisms are tissue specific. Inhibition or activation of each of these targets can be suggested for mitigation of radiation injury in a specific tissue. In the current paper, we review the cellular and molecular changes in the metabolism of cells and ROS/NO following exposure to radiation. Furthermore, the possible strategies for mitigation of radiation injury through modulation of cellular metabolism in irradiated organs will be discussed. © 2020 Elsevier Inc

Functionalization of Magnetic Nanoparticles by Folate as Potential MRI Contrast Agent for Breast Cancer Diagnostics

In recent years, the intrinsic magnetic properties of magnetic nanoparticles (MNPs) have made them one of the most promising candidates for magnetic resonance imaging (MRI). This study aims to evaluate the effect of different coating agents (with and without targeting agents) on the magnetic property of MNPs. In detail, iron oxide nanoparticles (IONPs) were prepared by the polyol method. The nanoparticles were then divided into two groups, one of which was coated with silica (SiO2) and hyperbranched polyglycerol (HPG) (SPION@SiO2@HPG); the other was covered by HPG alone (SPION@HPG). In the following section, folic acid (FA), as a targeting agent, was attached on the surface of nanoparticles. Physicochemical properties of nanostructures were characterized using Fourier transform infrared spectroscopy (FT-IR), transmission electron microscopy (TEM), and a vibrating sample magnetometer (VSM). TEM results showed that SPION@HPG was monodispersed with the average size of about 20 nm, while SPION@SiO2@HPG had a size of about 25 nm. Moreover, HPG coated nanoparticles had much lower magnetic saturation than the silica coated ones. The MR signal intensity of the nanostructures showed a relation between increasing the nanoparticle concentrations inside the MCF-7 cells and decreasing the signal related to the T2 relaxation time. The comparison of coating showed that SPION@SiO2@HPG (with/without a targeting agent) had significantly higher r2 value in comparison to Fe3O4@HPG. Based on the results of this study, the Fe3O4@SiO2@HPG-FA nanoparticles have shown the best magnetic properties, and can be considered promising contrast agents for magnetic resonance imaging applications. © 2020 by the authors. Licensee MDPI, Basel

Apigenin as Tumor Suppressor in Cancers: Biotherapeutic Activity, Nanodelivery, and Mechanisms With Emphasis on Pancreatic Cancer

Pancreatic cancer is the most lethal malignancy of the gastrointestinal tract. Due to its propensity for early local and distant spread, affected patients possess extremely poor prognosis. Currently applied treatments are not effective enough to eradicate all cancer cells, and minimize their migration. Besides, these treatments are associated with adverse effects on normal cells and organs. These therapies are not able to increase the overall survival rate of patients; hence, finding novel adjuvants or alternatives is so essential. Up to now, medicinal herbs were utilized for therapeutic goals. Herbal-based medicine, as traditional biotherapeutics, were employed for cancer treatment. Of them, apigenin, as a bioactive flavonoid that possesses numerous biological properties (e.g., anti-inflammatory and anti-oxidant effects), has shown substantial anticancer activity. It seems that apigenin is capable of suppressing the proliferation of cancer cells via the induction of cell cycle arrest and apoptosis. Besides, apigenin inhibits metastasis via down-regulation of matrix metalloproteinases and the Akt signaling pathway. In pancreatic cancer cells, apigenin sensitizes cells in chemotherapy, and affects molecular pathways such as the hypoxia inducible factor (HIF), vascular endothelial growth factor (VEGF), and glucose transporter-1 (GLUT-1). Herein, the biotherapeutic activity of apigenin and its mechanisms toward cancer cells are presented in the current review to shed some light on anti-tumor activity of apigenin in different cancers, with an emphasis on pancreatic cancer. © Copyright © 2020 Ashrafizadeh, Bakhoda, Bahmanpour, Ilkhani, Zarrabi, Makvandi, Khan, Mazaheri, Darvish and Mirzaei

The ER Stress/UPR axis in chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis

Cellular protein homeostasis in the lungs is constantly disrupted by recurrent exposure to various external and internal stressors, which may cause considerable protein secretion pressure on the endoplasmic reticulum (ER), resulting in the survival and differentiation of these cell types to meet the increased functional demands. Cells are able to induce a highly conserved adaptive mechanism, known as the unfolded protein response (UPR), to manage such stresses. UPR dysregulation and ER stress are involved in numerous human illnesses, such as metabolic syndrome, fibrotic diseases, and neurodegeneration, and cancer. Therefore, effective and specific compounds targeting the UPR pathway are being considered as potential therapies. This review focuses on the impact of both external and internal stressors on the ER in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) and discusses the role of the UPR signaling pathway activation in the control of cellular damage and specifically highlights the potential involvement of non-coding RNAs in COPD. Summaries of pathogenic mechanisms associated with the ER stress/UPR axis contributing to IPF and COPD, and promising pharmacological intervention strategies, are also presented

Elucidating role of reactive oxygen species (Ros) in cisplatin chemotherapy: A focus on molecular pathways and possible therapeutic strategies

The failure of chemotherapy is a major challenge nowadays, and in order to ensure effective treatment of cancer patients, it is of great importance to reveal the molecular pathways and mechanisms involved in chemoresistance. Cisplatin (CP) is a platinum-containing drug with anti-tumor activity against different cancers in both pre-clinical and clinical studies. However, drug resistance has restricted its potential in the treatment of cancer patients. CP can promote levels of free radicals, particularly reactive oxygen species (ROS) to induce cell death. Due to the double-edged sword role of ROS in cancer as a pro-survival or pro-death mechanism, ROS can result in CP resistance. In the present review, association of ROS with CP sensitivity/resistance is discussed, and in particular, how molecular pathways, both upstream and downstream targets, can affect the response of cancer cells to CP chemotherapy. Furthermore, anti-tumor compounds, such as curcumin, emodin, chloroquine that regulate ROS and related molecular pathways in increasing CP sensitivity are described. Nanoparticles can provide co-delivery of CP with anti-tumor agents and by mediating photodynamic therapy, and induce ROS overgeneration to trigger CP sensitivity. Genetic tools, such as small interfering RNA (siRNA) can down-regulate molecular pathways such as HIF-1α and Nrf2 to promote ROS levels, leading to CP sensitivity. Considering the relationship between ROS and CP chemotherapy, and translating these findings to clinic can pave the way for effective treatment of cancer patients. © 2021 by the authors. Licensee MDPI, Basel, Switzerland