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Stem cell transplantation has indicated great promise for cell therapy in a wide range of diseases, but poor and insufficient viability of cells within damaged tissues has limited its potential therapeutic effects. 17 β-Estradiol (E2) is a steroid hormone that plays an important role in expression of many genes and regulating proliferation, viability, and intracellular redox status in different cell types. In this study, we aimed to assess the effect of E2 on bone marrow-derived mesenchymal stem cells (BM-MSCs). Apoptosis was induced by serum deprivation (SD), and cells were exposed to E2 in the presence or absence of serum for varying periods of time, after which cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Expression of proapoptotic and antiapoptotic proteins after exposure to E2 was examined by Western blotting. The ability of E2 to prevent reactive oxygen species (ROS) production was also measured. The results indicated that E2 significantly enhanced the viability of the cells and protected BM-MSCs against SD-induced overproduction of ROS. It could reduce lipid peroxidation, total antioxidant power, and also Bax/Bcl-2 ratio as well as expression of caspase-3. Taken together, our data support that E2 treatment protects BM-MSCs against SD-induced damage by regulating ROS production and upregulation of antiapoptotic/proapoptotic proteins ratio. [ABSTRACT FROM AUTHOR]

Ni aluminide diffusion coatings on the surface of γ-TiAl alloy were produced by electroplating a Ni layer followed by a single step high activity aluminising carried out in ArzH2 atmosphere with a mixture of Al, NH4Cl and Al2O3 powders at 1000°C for 5 h. The effect of initial thickness for Ni layer on microstructure of produced Ni aluminide coating was highlighted. The thickness of initial Ni layer was changed to 4-20μm. In the case of the Ni layer with thickness of 4 μm, only a little amount of NiAl phase was formed in a TiAl3 matrix. However, the microstructure of coating, in the case of the Ni layer with thickness of 8 μm, consisted of an outer layer of two phases (NiAl+TiAl3), an intermediate layer of TiAl3 and an interdiffusion layer. For thicker initial Ni layers (16 and 20 mm), beside the latter coating microstructure, a continuous surface layer of NiAl phase was observed. Isothermal oxidation tests on these aluminide coatings reveal that the oxidation resistance of the aluminide coatings increases with increase in initial thickness of Ni layer. [ABSTRACT FROM AUTHOR]

Wear resistance of electrodeposited tertiary alumina/carbon nanotube/nanodiamond nanocomposite using pulsed current has been studied in Ni-W binary alloy matrix. Electroplating process was performed in citrate based Ni-W bath, and the nanostructure of obtained compound layer was examined by AFM. The effects of process variables, i.e. tungsten concentration in electrolyte, treatment time, frequency and duty cycle, were experimentally studied. Statistical methods were used in order to provide the minimised wear rate. Finally, the contribution percentage of different effective factors was calculated and confirmation run revealed the validity of obtained results. Nanocomposite layers with higher density of nanoparticles will show better tribological properties. [ABSTRACT FROM AUTHOR]

Electrodeposition of nickel based tertiary Al2O3/Y2O3/CNT nanocomposites by using pulsed current has been studied in this investigation. The coating process has been performed in a nickel sulphate bath and the nanostructure of the obtained compound layer was examined with high precision figure analysis of SEM nanographs. The effects of process variables, i.e. Y2O3 concentration, treatment time, current density and temperature of electrolyte have been experimentally studied. Statistical methods were used to achieve the minimum corrosion rate and average size of nanoparticles. Finally the contribution percentage of different effective factors was revealed and a confirmation experiment has shown the validity of the obtained results. In addition, it has been revealed that by changing the size of nanoparticles, the corrosion properties of coatings will change significantly with this trend. Atomic force microscopy and transmission electron microscopy analyses have confirmed the smooth surface and average size of nanoparticles in the optimal coating. [ABSTRACT FROM AUTHOR]

Spinal cord injury (SCI) is a severely debilitating problem leading to substantial decrease in the quality of life. After spinal cord injury, inflammation and oxidative stress plays a key role in initiating the secondary injury cascades leading to progressive tissue degradation and extreme functional deficits. Given that the primary mechanical injuries to spinal cord are rarely repaired, the pharmacological interventions may improve the neurological outcomes caused by secondary injury. Astaxanthin (AST) is considered as a xanthophyll carotenoid with potent antioxidant and anti-inflammatory properties, which has various pharmacological activities. In the present study, we aimed to firstly assess the protective effect of AST, and then to define the AST mechanism of action on a rat model of SCI. Based on the results of von Frey test, AST treatment significantly alleviated the SCI-induced neuropathic pain compared with the control groups (P < 0.05). The expression analysis by western blot shows reduced expression levels of COX-2, TNF-α, IL-1β, and IL-6 following AST treatment (P < 0.05). The activity of antioxidant enzymes was evaluated using ELISA. Therefore, ELISA experiments showed a significant reduction in the level of oxidative stress in SCI rat following AST treatment (P < 0.05). Furthermore, histopathological evaluations revealed that myelinated white matter and motor neuron number were significantly preserved after treatment with AST (P < 0.05). In conclusion, our study shows that AST could improve SCI through anti-inflammatory and antioxidant effects which leads to decreased tissue damage and mechanical pain after SCI., (Copyright © 2021 Elsevier Inc. All rights reserved.)

The aim of the current study was to evaluate the probabilistic health risk and the concentration of 16 polycyclic aromatic hydrocarbons (PAHs) in commercial tea and coffee samples. For determining the mentioned contaminants in sixty-four samples, a reliable and sensitive technique was validated and developed. The technique is established on magnetic solid-phase extraction and gas chromatography-mass spectrometry analysis (MSPE/GC-MS). The maximum mean of ƩPAHs in coffee samples was 13.75 ± 2.90 μg kg -1 , while the minimum mean ƩPAHs in tea samples was 4.77 ± 1.01 μg kg -1 . The mean concentration of benzo(a)pyrene (BaP) in samples ranged from 0.64 to 2.07 μg kg -1 which was lower than that of standard levels (10 μg kg -1 ) established by the European Union (EU). The Monte Carlo simulation results showed that the actual target hazard quotient (THQ) for the adult and children was equal to 1.63E-04 and 1.67E-04, respectively; hence, non-carcinogenic health risk for consumers is negligible. The result of actual incremental lifetime cancer risk (ILCR) was lower than the limits of safe risk (1E-4), indicating no notable possibility of cancer risk due to the digestion of tea and coffee for children and adults. Therefore, it can be concluded that the amount of contamination of popular commercial coffee and tea available in the Iranian market with PAHs is often similar to that found in other countries and was lower than the standard of EU. Thus, the processing conditions of these products must be controlled to prevent the formation of PAHs due to the suspicion of carcinogenicity and mutation.

Parkinson's disease (PD) is a neurodegenerative disease accompanied by a low expression level of cerebral hypoxia-inducible factor (HIF-1α). Hence, activating the hypoxia-signaling pathway may be a favorable therapeutic approach for curing PD. This study explored the efficacy of hydralazine, a well-known antihypertensive agent, for restoring the impaired HIF-1 signaling in PD, with the aid of 6-hydroxydopamine (6-OHDA)-exposed SH-SY5Y cells. The cytotoxicity of hydralazine and 6-OHDA on the SH-SY5Y cells were evaluated by MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] and apoptosis detection assays. The activities of malondialdehyde, nitric oxide (NO), ferric reducing antioxidant power (FRAP), and superoxide dismutase (SOD) were also measured. Expression levels of HIF-1α and its downstream genes at the protein level were assessed by Western blotting. Hydralazine showed no toxic effects on SH-SY5Y cells, at the concentration of ≤50 μmol/L. Hydralazine decreased the levels of apoptosis, malondialdehyde, and NO, and increased the activities of FRAP and SOD in cells exposed to 6-OHDA. Furthermore, hydralazine up-regulated the protein expression levels of HIF-1α, vascular endothelial growth factor, tyrosine hydroxylase, and dopamine transporter in the cells also exposed to 6-OHDA, by comparison with the cells exposed to 6-OHDA alone. In summary, hydralazine priming could attenuate the deleterious effects of 6-OHDA on SH-SY5Y cells by increasing cellular antioxidant capacity, as well as the protein levels of HIF-1α and its downstream target genes.

The systemic lupus erythematosus (SLE) is an autoimmune disease, leading to inflammatory response and systemic consequences. The mammalian target of rapamycin (mTOR) is a therapeutic target for autoimmune diseases like SLE. The aim of this study was to evaluate the effects of the mTOR rs2295080 and rs2536 polymorphisms and AKT1 rs2494732 gene polymorphism on SLE development. 2 ml of peripheral blood was collected from 165 SLE patients and 170 controls in EDTA-containing tubes. The salting-out and PCR-RFLP methods were used for DNA extraction and genotype analysis, respectively. Based on the regression analysis, the frequency of TT genotype of mTOR rs2295080 polymorphism was significantly higher in the case group than that of the control group, with a 2.6-fold increased risk of SLE. There was also a significant difference between the two groups in terms of allelic distribution. No statistically significant association was found between The AKT1 rs2494732 and mTOR rs2536 polymorphisms and SLE development. Our results showed that the TT genotype and T allele of mTOR rs2295080 polymorphism were risk factors for developing SLE. However, there was no significant association between mTOR rs2536 and AKT1 rs2494732 polymorphisms and the SLE risk.

Background: An adaptive neuro-fuzzy inference system (ANFIS) was employed to predict the oxidative stability of virgin olive oil (VOO) during storage as a function of time, storage temperature, total polyphenol, α-tocopherol, fatty acid profile, ultraviolet (UV) extinction coefficient (K 268 ), and diacylglycerols (DAGs)., Results: The mean total quantities of polyphenols and DAGs were 1.1 and 1.9 times lower in VOOs stored at 25 °C than in the initial samples, and the mean total quantities of polyphenols and DAGs were 1.3 and 2.26 times lower in VOOs stored at 37 °C than in the initial samples, respectively. In a single sample, α-tocopherol was reduced by between 0.52 and 0.91 times during storage, regardless of the storage temperature. The mean specific UV extinction coefficients (K 268 ) for VOO stored at 25 and 37 °C were reported as 0.15 (ranging between 0.06-0.39) and 0.13 (ranging between 0.06-0.35), respectively. The ANFIS model created a multi-dimensional correlation function, which used compositional variables and environmental conditions to assess the quality of VOO. The ANFIS model, with a generalized bell-shaped membership function and a hybrid learning algorithm (R 2  = 0.98; MSE = 0.0001), provided more precise predictions than other algorithms., Conclusion: Minor constituents were found to be the most important factors influencing the preservation status and freshness of VOO during storage. Relative changes (increases and reductions) in DAGs were good indicators of oil oxidative stability. The observed effectiveness of ANFIS for modeling oxidative stability parameters confirmed its potential use as a supplemental tool in the predictive quality assessment of VOO. © 2019 Society of Chemical Industry., (© 2019 Society of Chemical Industry.)

Background: A high expression of prostaglandin E2 (PGE2) is found in colorectal cancer. Therefore, blocking of PGE2 generation has been identified as a promising approach for anticancer therapy. Sulforaphane (SFN), an isothiocyanate derived from glucosinolate, is used as the antioxidant and anticancer agents., Methods: HT-29 cells were treated with various concentrations of SFN and compared to untreated cells for the expression of microsomal prostaglandin E synthase-1 (mPGES-1), cyclooxygenase 2 (COX-2), hypoxia-inducible factor-1 (HIF-1), C-X-C chemokine receptor type 4 (CXCR4), vascular endothelial growth factor (VEGF), and matrix metalloproteinase (MMP)-2 and MMP-9 at the mRNA level. The PGE2 level was measured by ELISA assay. Apoptosis was evaluated by the proportion of sub-G1 cells. The activity of caspase-3 was determined using an enzymatic assay. HT-29 cell migration was assessed using a scratch test., Results: SFN preconditioning decreased the expression of COX-2, mPGES-1, HIF-1, VEGF, CXCR4, MMP-2, and MMP-9. An apoptotic effect of SFN was preceded by the activation of caspase-3 as well as accumulation of cells in the sub-G1 phase of the cell cycle. SFN decreased PGE2 generation and inhibited the in vitro motility/wound-healing activity of HT-29 cells., Conclusions: SFN anticancer effects are associated with antiproliferative, antiangiogenic, and antimetastatic activities arising from the downregulation of the COX-2/ mPGES-1 axis., (© 2018 S. Karger AG, Basel.)

Background: Environmental factors that are involved in the development of autoimmune diseases include bacteria, viruses, and xenobiotics such as chemicals, drugs, and metals. Regarding the metals, a number of studies have demonstrated that oxidative stress is one of the well-directed pathways of arsenic-induced tissue damages. This study was designed to explore the serum concentrations of arsenic and its correlation with markers associated with oxidative stress in relapsing-remitting MS (RRMS) patients., Methods: This case-controlled study comprised 50 patients with RRMS and 50 healthy subjects. Serum arsenic levels, total antioxidant potential, malondialdehyde (MDA), and lactate levels were measured., Results: The arsenic value, MDA, and lactate levels were elevated meaningfully while FRAP level significantly was decreased in RRMS patients with respect to healthy subjects (P <0.05). Furthermore, arsenic serum levels were positively correlated with serum concentrations of MDA and lactate. In contrast, serum levels were negatively correlated to FRAP values in RRMS patients., Conclusion: Taken together, the association between arsenic level and oxidative stress parameters supports the hypothesis that high serum arsenic levels may play a critical role in the pathogenesis of MS progression., (Copyright © 2017 Elsevier B.V. All rights reserved.)

There is a strong link between cognitive impairment and depression, but up to date it is not clear whether cognitive impairment is 'cause' or 'consequence' of depression. Therefore, we here examined the effect of cognitive impairment induced by permanent occlusion of common carotid arteries, a model known as two-vessel occlusion (2VO), on chronic unpredictable stress (CUS)-induced depression-related markers in rats. Male Sprague-Dawley rats underwent 2VO or sham surgery. Sixty days after the surgery, the cognitive function of the rats was tested using the radial arm maze task measuring working and reference memory. Subsequently, the animals were randomly assigned to undergo 21 days of CUS or to stay non-stressed. One week after the last stressor, psychomotor retardation, a feature of depression-like behavior, was assessed using the forced swim test (FST) by measuring time spent on immobility. Plasma amino acid (glutamine, glutamate and glycine) and serum pro-inflammatory cytokine (interleukin 6) levels, and hippocampus CA1 neuronal damage were measured 24h after FST exposure. Results show that 2VO increased immobility in the FST only when rats had been exposed to CUS. In addition, 2VO surgery intensified the effect of CUS on IL-6, glutamate and glycine levels and increased CA1 hippocampal damage. In conclusion, our findings show that cognitive impairment may predispose to depression by intensifying the effect of stress on depression-related behavioral, biochemical, immunological and neuronal markers., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Background Aims: Mesenchymal stromal cells (MSCs) have shown great promise for cell therapy of a wide range of diseases such as diabetes. However, insufficient viability of transplanted cells reaching to damaged tissues has limited their potential therapeutic effects. Expression of estrogen receptors on stem cells may suggest a role for 17β-estradiol (E2) in regulating some functions in these cells. There is evidence that E2 enhances homing of stem cells. Induction of hypoxia-inducible factor-1α (HIF-1α) by E2 and the profound effect of HIF-1α on migration of cells have previously been demonstrated. We investigated the effect of E2 on major mediators involved in trafficking and subsequent homing of MSCs both in vitro and in vivo in diabetic rats., Methods: E2 has been selected to improve the poor migration capacity of MSCs toward sites of injury. MSCs were incubated with different concentrations of E2 for varying periods of time to investigate whether estradiol treatment could be effective to enhance the efficiency of MSC transplantation., Results: E2 significantly enhanced the viability of the cells that were blocked by ICI 182,780 (estrogen receptor antagonist). E2 also increased HIF-1α, CXC chemokine receptor 4 and C-C chemokine receptor 2 protein and messenger RNA levels measured by Western blot and reverse transcription-polymerase chain reaction. The enzymatic activity of matrix metalloproteinase 2 and metalloproteinase 9 was elevated in E2-treated cells through the use of gelatin zymography. Finally, the improved migration capacity of E2-treated MSCs was evaluated with the use of a Boyden chamber and in vivo migration assays., Conclusions: Our data support that conditioning of MSCs with E2 promotes migration of cells in cultured MSCs in vitro and in a diabetic rat model in vivo through regulation of major mediators of cell trafficking., (Copyright © 2015 International Society for Cellular Therapy. Published by Elsevier Inc. All rights reserved.)

Background: Many studies suggested mesenchymal stem cells (MSCs) transplantation as a new approach to control hyperglycemia in type 1 diabetes mellitus through differentiation mechanism. In contrary others believed that therapeutic properties of MSCs is depends on paracrine mechanisms even if they were not engrafted. This study aimed to compare these two approaches in control of hyperglycemia in STZ-induced diabetic rats., Methods: Animals were divided into five groups: normal; diabetic control; diabetic received MSCs; diabetic received supernatant of MSCs; diabetic received co-administration of MSCs with supernatant. Blood glucose, insulin levels and body weight of animals were monitored during experiment. Immunohistochemical and immunofluorescence analysis were performed to monitor functionality and migration of labeled-MSCs to pancreas., Results: First administration of MSCs within the first 3 weeks could not reduce blood glucose, but second administration significantly reduced blood glucose after week four compared to diabetic controls. Daily injection of supernatant could not reduce blood glucose as efficient as MSCs. Interestingly; Co-administration of MSCs with supernatant significantly reduced blood glucose more than other treated groups. Insulin levels and body weight were significantly increased in MSCs + supernatant-treated animals compared to other groups. Immunohistological analysis showed an increase in number and size of islets per section respectively in supernatant, MSCs and MSCs + supernatant-treated groups., Conclusion: Present study exhibited that repeated-injection of MSCs reduced blood glucose and increased serum insulin levels in recipient rats. Injection of supernatant could not reverse hyperglycemia as efficient as MSCs. Interestingly; co-administration of MSCs with supernatant could reverse hyperglycemia more than either group alone.