Potential Role of Dipeptidyl Peptidase-4 in Regulating Mitochondria and Oxidative Stress in Cardiomyocytes.

Oxidative stress causes mitochondrial damage and bioenergetic dysfunction and inhibits adenosine triphosphate production, contributing to the pathogenesis of cardiac diseases. Dipeptidyl peptidase 4 (DPP4) is primarily a membrane-bound extracellular peptidase that cleaves Xaa-Pro or Xaa-Ala dipeptides from the N terminus of polypeptides. DPP4 inhibitors have been used in patients with diabetes and heart failure; however, they have led to inconsistent results. Although the enzymatic properties of DPP4 have been well studied, the substrate-independent functions of DPP4 have not. In the present study, we knocked down DPP4 in cultured cardiomyocytes to exclude the effects of differential alteration in the substrates and metabolites of DPP4 then compared the response between the knocked-down and wild-type cardiomyocytes during exposure to oxidative stress. H2O2 exposure induced DPP4 expression in both types of cardiomyocytes. However, knocking down DPP4 substantially reduced the loss of cell viability by preserving mitochondrial bioenergy, reducing intracellular reactive oxygen species production, and reducing apoptosis-associated protein expression. These findings demonstrate that inhibiting DPP4 improves the body's defense against oxidative stress by enhancing Nrf2 and PGC-1α signaling and increasing superoxide dismutase and catalase activity. Our results indicate that DPP4 mediates the body's response to oxidative stress in individuals with heart disease.

Caffeic acid ethanolamide induces antifibrosis, anti-inflammatory, and antioxidant effects protects against bleomycin-induced pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive interstitial lung disease; its cause is unknown, and it leads to notable health problems. Currently, only two drugs are recommended for IPF treatment. Although these drugs can mitigate lung function decline, neither can improve nor stabilize IPF or the symptoms perceived by patients. Therefore, the development of novel treatment options for pulmonary fibrosis is required. The present study investigated the effects of a novel compound, caffeic acid ethanolamide (CAEA), on human pulmonary fibroblasts and evaluated its potential to mitigate bleomycin-induced pulmonary fibrosis in mice. CAEA inhibited TGF-ß-induced α-SMA and collagen expression in human pulmonary fibroblasts, indicating that CAEA prevents fibroblasts from differentiating into myofibroblasts following TGF-ß exposure. In animal studies, CAEA treatment efficiently suppressed immune cell infiltration and the elevation of TNF-α and IL-6 in bronchoalveolar lavage fluid in mice with bleomycin-induced pulmonary fibrosis. Additionally, CAEA exerted antioxidant effects by recovering the enzymatic activities of oxidant scavengers. CAEA directly inhibited activation of TGF-ß receptors and protected against bleomycin-induced pulmonary fibrosis through inhibition of the TGF-ß/SMAD/CTGF signaling pathway. The protective effect of CAEA was comparable to that of pirfenidone, a clinically available drug. Our findings support the potential of CAEA as a viable method for preventing the progression of pulmonary fibrosis.

Technical Refinement of a Bilateral Renal Ischemia-Reperfusion Mouse Model for Acute Kidney Injury Research.

Cardiac arrest poses a large public health burden. Acute kidney injury (AKI) is an adverse marker in survivors of cardiac arrest following the return of spontaneous circulation (ROSC) after successful cardiopulmonary resuscitation. Conversely, recovery of kidney function from AKI is a predictor of favorable neurological outcomes and hospital discharge. However, an effective intervention to prevent kidney damage caused by cardiac arrest after ROSC is lacking, suggesting that additional therapeutic strategies are required. Renal hypoperfusion and reperfusion are two pathophysiological mechanisms that cause AKI after cardiac arrest. Animal models of ischemia-reperfusion-induced AKI (IR-AKI) of both kidneys are comparable with patients with AKI following ROSC in a clinical setting. However, IR-AKI of both kidneys is technically challenging to analyze because the model is associated with high mortality and wide variation in kidney damage, which may affect the analysis. Lightweight mice were chosen, placed under general anesthesia with isoflurane, subjected to surgery with a dorsolateral approach, and their body temperature maintained during operation, thereby reducing tissue damage and establishing a reproducible acute renal IR-AKI research protocol.

Soluble dipeptidyl peptidase-4 induces epithelial-mesenchymal transition through tumor growth factor-ß receptor.

BACKGROUND: Kidney fibrosis is the final manifestation of chronic kidney disease, a condition mainly caused by diabetic nephropathy. Persistent tissue damage leads to chronic inflammation and excessive deposition of extracellular matrix (ECM) proteins. Epithelial-mesenchymal transition (EMT) is involved in a variety of tissue fibrosis and is a process during which epithelial cells transform into mesenchymal-like cells and lose their epithelial functionality and characteristics Dipeptidyl peptidase-4 (DPP4) is widely expressed in tissues, especially those of the kidney and small intestine. DPP4 exists in two forms: a plasma membrane-bound and a soluble form. Serum-soluble DPP4 (sDPP4) levels are altered in many pathophysiological conditions. Elevated circulating sDPP4 is correlated with metabolic syndrome. Because the role of sDPP4 in EMT remains unclear, we examined the effect of sDPP4 on renal epithelial cells. METHODS: The influences of sDPP4 on renal epithelial cells were demonstrated by measuring the expression of EMT markers and ECM proteins. RESULTS: sDPP4 upregulated the EMT markers ACTA2 and COL1A1 and increased total collagen content. sDPP4 activated SMAD signaling in renal epithelial cells. Using genetic and pharmacological methods to target TGFBR, we observed that sDPP4 activated SMAD signaling through TGFBR in epithelial cells, whereas genetic ablation and treatment with TGFBR antagonist prevented SMAD signaling and EMT. Linagliptin, a clinically available DPP4 inhibitor, abrogated sDPP4-induced EMT. CONCLUSIONS: This study indicated that sDPP4/TGFBR/SMAD axis leads to EMT in renal epithelial cells. Elevated circulating sDPP4 levels may contribute to mediators that induce renal fibrosis.

A novel caffeic acid derivative prevents angiotensin II-induced cardiac remodeling.

Differentiation of cardiac fibroblasts into myofibroblasts is a critical event in the progression of cardiac fibrosis that causes pathological cardiac remodeling. Cardiac fibrosis is a hallmark of heart disease and is associated with a stiff myocardium and heart failure. This study investigated the effect of caffeic acid ethanolamide (CAEA), a novel caffeic acid derivative, on cardiac remodeling. Angiotensin (Ang) II was used to induce cardiac remodeling both in cell and animal studies. Treating cardiac fibroblast with CAEA in Ang II-exposed cell cultures reduced the expression of fibrotic marker α-smooth muscle actin (α-SMA) and collagen and the production of superoxide, indicating that CAEA inhibited the differentiation of fibroblast into myofibroblast after Ang II exposure. CAEA protects against Ang II-induced cardiac fibrosis and dysfunction in vivo, characterized by the alleviation of collagen accumulation and the recovery of ejection fraction. In addition, CAEA decreased Ang II-induced transforming growth factor-ß (TGF-ß) expression and reduced NOX4 expression and oxidative stress in a SMAD-dependent pathway. CAEA participated in the regulation of Ang II-induced TGF-ß/SMAD/NOX4 signaling to prevent the differentiation of fibroblast into myofibroblast and thus exerted a cardioprotective effect. Our data support the administration of CAEA as a viable method for preventing the progression of Ang II-induced cardiac remodeling.

A pilot study of digital bedside cards in the emergency room of a medical centre in Taiwan.

The emergency room (ER) digital bedside card is a simple and important invention. It can be directly connected to the hospital information system to display important patient information in real time, reduce the workload of ER staff, improve their satisfaction, and provide useful information for patients and their families. We conducted a prospective study of ER staff using questionnaires and conducted Wilcoxon signed-rank test to compare before and after ER digital bedside card implementation in the Tamsui MacKay Memorial Hospital. Sixty participants of the ER staff joined the study before and after digital card implementation. After the ER digital bedside card was set up, the number of round trips from the nursing station to the ER bedside and the number of common questions asked by patients and their family members were significantly reduced. The cards reduced the response time for frequently asked questions by patients and their family members and significantly improved the satisfaction of ER staff. Our study showed that ER digital bedside cards reduced the workload of ER staff, provided patients and their families with useful information, and greatly improved ER staff satisfaction. This marks an important milestone in the future development of smart ER.

The impact of antimicrobial stewardship program designed to shorten antibiotics use on the incidence of resistant bacterial infections and mortality.

Reassessing the continuing need for and choice of antibiotics by using an antibiotic "time out'' program may reduce unnecessary treatment. This study aimed to explore the effect of an antibiotic stewardship program (ASP) on the antibiotics consumption, incidence of resistant bacterial infections and overall hospital mortality in a tertiary medical center during the study period 2012-2014. An ASP composed of multidisciplinary strategies including pre-prescription approval and post-approval feedback and audit, and a major "time out'' intervention (shorten the default antibiotic prescription duration) usage was introduced in year 2013. Consumption of antibiotics was quantified by calculating defined daily doses (DDDs). Interrupted time series (ITS) analysis was used to explore the changes of antibiotics consumption before and after intervention, accounting for temporal trends that may be unrelated to intervention. Our results showed that following the intervention, DDDs showed a decreased trend in overall (in particular the major consumed penicillins and cephalosporins), in both intensive care unit (ICU) and non-ICU, and in non-restrictive versus restrictive antibiotics. Importantly, ITS analysis showed a significantly slope change since intervention (slope change p value 0.007), whereas the incidence of carbapenem-resistant and vancomycin-resistant pathogens did not change significantly. Moreover, annual overall mortality rates were 3.0%, 3.1% and 3.1% from 2012 to 2014, respectively. This study indicates that implementing a multi-disciplinary strategy to shorten the default duration of antibiotic prescription can be an effective manner to reduce antibiotic consumption while not compromising resistant infection incidence or mortality rates.

Left Anterior Descending Coronary Artery Ligation for Ischemia-reperfusion Research: Model Improvement via Technical Modifications and Quality Control.

Coronary heart disease is the leading cause of death globally. Complete cessation of blood flow in coronary arteries causes ST-segment elevation myocardial infarction (STEMI), resulting in cardiogenic shock and fatal arrhythmia, which are associated with high mortality. Primary coronary intervention (PCI) for recanalizing the coronary artery significantly improves the outcomes of STEMI, but advancements made in shortening the door-to-balloon time have failed to reduce in-hospital mortality, suggesting that additional therapeutic strategies are required. Left anterior descending coronary artery (LAD) ligation in rats is an animal model for acute myocardial IR research that is comparable to the clinical scenario in which rapid coronary recanalization through PCI is used for STEMI; however, PCI-induced STEMI is a technically challenging and complicated operation associated with high mortality and great variation in infarction size. We identified the ideal position for LAD ligation, created a gadget to control a snare loop, and supported a modified surgical maneuver, thereby reducing tissue damage, to establish a reliable and reproducible acute myocardial ischemia-reperfusion (IR) research protocol for rats. We also propose a method for validating the quality of study results, which is a critical step for determining the accuracy of subsequent biochemical analyses.

A survey of PM2.5 preventive behavioral intention and related factors among community elderly in Northern Taiwan.

ABSTRACT: Population aging and air pollution are global concerns. The purpose of this study is to explore the relationship among particulate matter with a diameter of 2.5 µm or less (PM2.5) knowledge, PM2.5 preventive attitude, and PM2.5 preventive behavioral intention in the elderly.A cross-sectional survey design was applied in this study, including usage intention and snowball sampling. A total of 617 elderly people aged over 65 participated, and the collected data were quantitatively analyzed.The results showed that the mean score of PM2.5 knowledge of the elderly was 10.34 (79.53%) with the standard deviation (SD) of 3.42, the mean score of PM2.5 preventive attitude was 4.58 (91.60%) with SD of 0.49, and the mean score of PM2.5 preventive behavioral intention was 4.72 (94.40%) with SD of 0.40. Elderly people's characteristics regarding PM2.5 knowledge and PM2.5 preventive attitude explained 22% (adjusted R2 = 0.22, F = 30.44, P < .001) of the variance in PM2.5 preventive behavioral intention.It is concluded that we found no difference in PM2.5 knowledge, PM2.5 preventive attitude, or PM2.5 preventive behavioral intention among the elderly with or without chronic diseases. In our opinion, health education regarding the threat of PM2.5 to the health of the elderly should be strengthened, to enhance their knowledge, preventive attitude, and preventive behavioral intention of PM2.5.

A novel caffeic acid derivative prevents renal remodeling after ischemia/reperfusion injury.

Acute kidney disease due to renal ischemia/reperfusion (I/R) is a major clinical problem without effective therapies. The injured tubular epithelial cells may undergo epithelial-mesenchymal transition (EMT). It will loss epithelial phenotypes and express the mesenchymal characteristics. The formation of scar tissue in the interstitial space during renal remodeling is caused by the excessive accumulation of extracellular matrix components and induced fibrosis. This study investigated the effect of caffeic acid ethanolamide (CAEA), a novel caffeic acid derivative, on renal remodeling after injury. The inhibitory role of CAEA on EMT was determined by western blotting, real-time PCR, and immunohistochemistry staining. Treating renal epithelial cells with CAEA in TGF-ß exposed cell culture successfully maintained the content of E-cadherin and inhibited the expression of mesenchymal marker, indicating that CAEA prevented renal epithelial cells undergo EMT after TGF-ß exposure. Unilateral renal I/R were performed in mice to induce renal remodeling models. CAEA can protect against I/R-induced renal remodeling by inhibiting inflammatory reactions and consecutively inhibiting TGF-ß-induced EMT, characterized by the preserved E-cadherin expression and alleviated α-SMA and collagen expression, as well as the alleviated of renal fibrosis. We also revealed that CAEA may exhibits biological activity by targeting TGFBRI. CAEA may antagonize TGF-ß signaling by interacting with TGFBR1, thereby blocking binding between TGF-ß and TGFBR1 and reducing downstream signaling, such as Smad3 phosphorylation. Our data support the administration of CAEA after I/R as a viable method for preventing the progression of acute renal injury to renal fibrosis.

Soluble Dipeptidyl Peptidase-4 Induces Fibroblast Activation Through Proteinase-Activated Receptor-2.

Fibroblasts are the chief secretory cells of the extracellular matrix (ECM) responsible for basal deposition and degradation of the ECM under normal conditions. During stress, fibroblasts undergo continuous activation, which is defined as the differentiation of fibroblasts into myofibroblasts, a cell type with an elevated capacity for secreting ECM proteins. Dipeptidyl peptidase-4 (DPP4) is a ubiquitously expressed transmembrane glycoprotein and exerts effects that are both dependent and independent of its enzymatic activity. DPP4 has been demonstrated to define fibroblast populations in human skin biopsies of systemic sclerosis. Shedding of DPP4 from different tissues into the circulation appears to be involved in the pathogenesis of the diseases. The mechanism underlying soluble DPP4-induced dermal fibrosis has not been clearly determined. The effects of DPP4 on murine 3T3 fibroblasts and human dermal fibroblasts were evaluated by measuring the expression of fibrotic proteins, such as α-SMA and collagen. Soluble DPP4 stimulated the activation of fibroblasts in a dose-dependent manner by activating nuclear factor-kappa B (NF-κB) and suppressor of mothers against decapentaplegic (SMAD) signaling. Blocking proteinase-activated receptor-2 (PAR2) abrogated the DPP4-induced activation of NF-κB and SMAD and expression of fibrosis-associated proteins in fibroblasts. Linagliptin, a clinically available DPP4 inhibitor, was observed to abrogate the soluble DPP4-induced expression of fibrotic proteins. This study demonstrated the mechanism underlying soluble DPP4, which activated NF-κB and SMAD signaling through PAR2, leading to fibroblast activation. Our data extend the current view of soluble DPP4. Elevated levels of circulating soluble DPP4 may contribute to one of the mediators that induce dermal fibrosis in patients.

Ultrasonic-assisted preparation and characterization of magnetic ZnFe2O4/g-C3N4 nanomaterial and their applications towards electrocatalytic reduction of 4-nitrophenol.

Nanoball-structured ferromagnetic zinc ferrite nanocrystals (ZnFe2O4 NPs) entrapped with graphitic-carbon nitride (g-C3N4) was produced via straightforward and facile sonochemical synthetical technique (titanium probe; 100 W/cm2 and 50 KHz). The morphological (SEM), elemental (EDS), diffraction (XRD), XPS, and electrochemical studies (CV) have been carry out to verify the nanostructure and shape of the materials. The ZnFe2O4 NPs/g-C3N4 electrode (GCE) was constructed which displayed outstanding electrochemical ability towards toxic 4-nitrophenol (NTP). A sensitive, selective, reproducible, and durable electrochemical NTP sensor was developed by ZnFe2O4 NPs/g-C3N4 modified electrode. The modified sensor exhibited a high sensitivity and 4.17 nanomolars of LOD. It's greater than the LOD of previously reported NTP modified sensors. The real-time experiments of the modified electrochemical (ZnFe2O4 NPs/g-C3N4 electrode) sensor were successfully explained in various water (river and drinking) samples and its showed high standard recoveries. Therefore, sonochemical synthetical method and fabrication of modified electrode were developed this work based on environmental analysis of NTP sensor.

Sonochemical approach to the synthesis of metal tungstate/nafion composite with electrocatalytic properties and its electrochemical sensing performance.

High-intensity ultrasound can be used to produce novel materials, offering an atypical pathway to recognized products without high bulk temperatures, high pressures, or long reaction times. A highly sensitive and selective robust modified sensor was developed using a composition of electrochemically active strontium metal (Sr) based tungstate interconnected with nafion polymer through a facile sonochemical approach. In addition, multiple parameters are important for sonochemical methods and specifically nanomaterial or electrocatalyst development during the ultrasonic irradiation. Moreover, high-intensity ultrasonic probe (Ti-horn) was used to synthesis of nanomaterial at 50 kHz and 200 W. The SrWO4/nafion was characterized via FESEM, EDX and XRD methods. 8-HD-guanosine (8-hydroxydeoxyguanosine) is one of the major byproduct of deoxyribonucleic acid (DNA) oxidation. The concentrations of 8-HD-guanosine within a cell are a measurement of oxidative stress in body and however its excess level in body causes carcinogenic threats. Therefore, the quantification of 8-HD-guanosine in biological samples with high sensitivity is of great significance. The SrWO4/nafion modified sensor displayed low detection of 14.36 nM and wide linear range (0.025-398.6 µM), compare to previous reports.

Sonochemical preparation of carbon nanosheets supporting cuprous oxide architecture for high-performance and non-enzymatic electrochemical sensor in biological samples.

Copper (Cu) based metal oxides have high electrocatalytic ability. In this work, we are synthesized stone-like cuprous oxide particles (Cu2O SNPs) covered on acid functionalized graphene oxide (GOS) sheets using ultrasonic process (50 kHz and 100 W). Besides, the chemical structural and crystalline analyses of Cu2O SNPs@GOS composites were characterized by transmission electron microscopy, X-ray crystallography and energy-dispersive X-ray spectroscopy. The Cu2O SNPs@GOS nanomaterials were tested towards detection of 8-hydroxydeoxyguanosine (8-OHdG) in biological samples. As expected Cu2O SNPs@GOS catalyst modified electrodes performed an outstanding catalytic ability on 8-hydroxydeoxyguanosine oxidation. 8-OHdG is oxidative stress biomarker. Further, it is noted that the detection performance of Cu2O SNPs@GOS coated electrodes and it's highly enhanced due to the synergistic effect of Cu2O SNPs and GOS. Besides, the modified materials provide more electro-active faces and as well as rapid electron transport pathway and shorten diffusion. Moreover, oxidation of 8-OHdG sensor is exploring a long linear or working range of 0.02-1465 µM and high sensitivity (8.75 nM). The viability of the Cu2O SNPs@GOS proposed electrochemical methods have tested, to find out 8-OHdG concentrations in biological fluids (blood serum and urine) with a satisfying recovery ranges.

One-Pot Sustainable Synthesis of Ce2S3/Gum Arabic Carbon Flower Nanocomposites for the Detection of Insecticide Imidacloprid.

Investigating ecofriendly sustainable materials with excellent electrocatalytic activity is a pivotal approach for the analysis field. The present work reports on the preparation of novel three-dimensional (3D) cerium sulfide with gum arabic carbon flowers (Ce2S3/GACFs) via the hydrothermal method by using l-cysteine as a sulfur source, binding, and reducing agents. The intensive characterization techniques were utilized to corroborate the structural moiety, morphology, and size of Ce2S3/GACFs. The obtained 3D Ce2S3/GACF construction has excellent active sites, and hence it prevents the accumulation of carbon flowers. Furthermore, the obtained Ce2S3/GACF/glassy carbon electrode (GCE) could afford a very high electrocatalytic activity, possessing an exceedingly low detection limit of 32 nM, the high sensitivity of 2.65 µA µM-1 cm-2, good repeatability, and high stability for the detection of insecticide imidacloprid (IMC). The Ce2S3/GACF/GCE also provides a wide linear range of 0.05-1266 µM toward IMC detection. The excellent recovery results (90-99.3%) are achieved by using various spiked real food samples at Ce2S3/GACF/GCE. Confidently, this work gives up novel construction of 3D metal-carbon-based bioderived material for its catalytic application in the future.

Do patients with non-ST-elevation myocardial infarction without chest pain suffer a poor prognosis?

OBJECTIVE: Previous studies have discussed acute myocardial infarction (AMI) patients without chest pain, but have not focused on non-ST-elevation myocardial infarction (NSTEMI). MATERIALS AND METHODS: This 1-year study investigated whether chest pain presence relates to demographics, risk factors, and outcomes in NSTEMI patients. We retrospectively reviewed 194 patients, 73 without chest pain vs. 121 with chest pain, and compared the differences between clinical presentations, risk factors, medical management, and outcomes of these two groups. RESULTS: Compared to patients with chest pain, patients without chest pain were significantly older, had lower SBP, higher HR, more cerebrovascular disease, less ischemic heart disease, higher delay to ED (emergency department) visit, lower ED medication prescriptions, lower percutaneous cardiac intervention, and higher in-hospital and one-year mortality rate. In a multivariate logistic regression, the adjusted odds ratios (OR) of patients without chest pain were 4.38 for the elderly, 0.99 for every 1 mmHg increase in SBP, 1.02 for every beat/min HR increase, 0.37 for those with ischemic heart disease, and 5.09 for those with cerebrovascular disease. The adjusted OR of in-hospital mortality were 3.09 for patients without chest pain, 0.32 for those with hypertension, 0.32 for smokers, 3.98 for those with shock, and 0.16 for those with percutaneous cardiac intervention. Finally, the only significantly adjusted OR of one-year mortality was 5.37 for patients without chest pain. CONCLUSION: NSTEMI patients without chest pain were significantly older, had lower SBP, more tachycardia, more cerebrovascular disease, but less ischemic heart disease. They also experienced higher in-hospital and one-year mortality rates.

A novel isoquinoline derivative exhibits anti-inflammatory properties and improves the outcomes of endotoxemia.

BACKGROUND: Sepsis initiates an inflammatory response that causes widespread injury, and candidates for related myocardial depressant factors include cytokines and nitric oxide (NO). Nuclear factor kappa-B (NF-κB) stimulated by toll-like receptor 4 activation in sepsis mediates the transcription of multiple proinflammatory genes. These inflammatory mediators can cause myocardial dysfunction, which may deteriorate sepsis outcomes. To address this risk, we investigated the potential beneficial effects of a novel isoquinolines derivative, CYY054c, in LPS-induced inflammatory response leading to endotoxemia. METHODS: The effects of CYY054c on cytokine and inflammatory-related protein production were evaluated in lipopolysaccharide (LPS)-stimulated macrophages. To determine whether CYY054c alleviates inflammatory storm-induced myocardial dysfunction in vivo, LPS was injected in rats, and cardiac function was measured by a pressure-volume loop. RESULTS: CYY054c inhibited LPS-induced NF-κB expression in macrophages and reduced the release of tumor necrosis factor-alpha (TNF-α), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6), as well as the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). In the animal studies, CYY054c alleviated LPS-upregulated plasma TNF-α, IL-1ß, IL-6, and NO concentrations, as well as cardiac monocyte chemotactic protein-1, iNOS, and COX-2 expression in rats, contributing to the improvement of cardiac function during endotoxemia. CONCLUSIONS: The reduction of NF-κB-mediated inflammatory mediators and the maintenance of hemodynamic performance by CYY054c improved the outcomes during endotoxemia. CYY054c may be a potential therapeutic agent for sepsis.

A sensitive electrochemical determination of chemotherapy agent using graphitic carbon nitride covered vanadium oxide nanocomposite; sonochemical approach.

We have developed a graphitic carbon nitride covered vanadium oxide nanocomposite (V2O5@g-C3N4) by a simple sonochemical approach (50 kHz and 150 W/cm2). Furthermore, the morphology and chemical composition of the V2O5@g-C3N4 nanocomposite was carried out by X-rays diffractometry (XRD), transmission electron microscopy (TEM) and electrochemical impedance spectroscopy (EIS). Furthermore, the V2O5@g-C3N4 nanocomposite modified electrode was investigate electrochemical behavior of the anticancer drug. Compared with bare SPCE, V2O5/SPCE and g-C3N4/SPCE, V2O5@g-C3N4 modified SPCE showed highest current response towards anti-cancer drug (methotrexate). Furthermore, the modified sensor exhibits with a sharp peaks and wide linear range (0.025-273.15 µM) by using DPV with the sensitivity of 7.122 µA µM-1 cm-2. Notably, we have achieved a nanomolar detection limit (13.26 nM) for the DPV detection of methotrexate. Further, the practicability of the V2O5@g-C3N4 nanocomposite modified sensor can be used for real time sensing of methotrexate in drug and blood serum samples with good recover ranges. It has potential applications in routine analysis with high specificity, excellent reproducibility and good stability.