Life sciences

Publisher: Elsevier

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Current impact factor: 2.56

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5-year impact 2.67
Cited half-life 8.20
Immediacy index 0.37
Eigenfactor 0.04
Article influence 0.69
ISSN 1879-0631

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Publications in this journal

  • Life sciences 02/2015;
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    ABSTRACT: AIMS: The alteration of ROS level is frequently observed in the course of morphine addiction, and ROS is proverbially involved in this process. This study aims to explore the relationship among morphine addiction, reactive oxygen species (ROS) and expression of μ-opioid receptor (MOR) in differentiated SH-SY5Y cells. MAIN METHODS: SH-SY5Y cells were induced to differentiation by treatment with retinoic acid (RA); the activity of lactate dehydrogenase (LDH) and the nitro blue tetrazolium (NBT) reduction were assessed by spectrophotometry. Intracellular reactive oxygen species (ROS) was measured with the 2,7-dichlorofluorescin diacetate (DCFH-DA) assay. Cellular cAMP was determined by using a competitive protein binding kit. The mRNA expression of μ-opioid receptor (MOR) was evaluated by qRT-PCR. KEY FINDINGS: Morphine-induced ROS are generated in a concentration- and time-dependent manner and inhibited by naloxone. Exogenous oxidants increase the level of ROS and aggravate morphine addiction, while the exogenous antioxidants efficiently reverse these effects. Morphine decreases the mRNA level of MOR in a concentration-dependent manner. And the mRNA level of MOR is remarkably reduced in the presence of exogenous oxidants and effectively promoted by antioxidants. SIGNIFICANCE: This study indicates that ROS can affect morphine addiction through involving MOR. Treatment with ROS scavenging can serve as a medical therapy for morphine addiction. Copyright © 2015. Published by Elsevier Inc. KEYWORDS: Morphine addiction; Reactive oxygen species (ROS); μ-Opioid receptor (MOR)
    Life sciences 01/2015; DOI:10.1016/j.lfs.2015.01.003
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    ABSTRACT: Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of nitric oxide (NO) synthase, an enzyme responsible for the generation of NO. Plasma concentrations of ADMA increase in the elderly and in postmenopausal women. In fact, an elevated ADMA level is a risk factor of cardiovascular disease. Aerobic exercise has a beneficial effect on cardiovascular disease. However, the relationship between ADMA and aerobic fitness is unknown. The aim of this study was to determine whether plasma ADMA concentrations correlate with aerobic fitness levels in postmenopausal women. Thirty healthy postmenopausal women aged 50-76 years participated in this study. We measured plasma concentrations of ADMA and oxygen consumption at the ventilatory threshold (VO2VT) as an index of aerobic fitness. Subjects were divided into the low aerobic fitness (Low fitness) and high aerobic fitness (High fitness) groups, and the dividing line was set at the median VO2VT value. VO2VT was significantly higher in the High fitness group than in the Low fitness group (P<0.01). The plasma ADMA concentrations in the High fitness group were significantly lower than those in the Low fitness group (P<0.05). There was a negative correlation between plasma ADMA concentrations and VO2VT (r=-0.532, P<0.01). We found that plasma ADMA concentrations were associated with aerobic fitness in postmenopausal women. The results of this study suggest that habitual aerobic exercise may decrease plasma ADMA concentrations.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.05.003
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    ABSTRACT: Inflammation and cancer are the two major disorders in the gastrointestinal tract. They are causally related in their pathogenesis. Animal models are important to study their causal relationship and in particular to discover new therapeutic agents for these diseases. There are several criteria for these models in order to make them useful to better understand the etiology and treatment of these diseases in man. In this regard, animal models should be similar as possible to human diseases and also be easy to produce and reproducible and also economic to allow a continuous replication in different laboratories. In this review, we summarize the various animal models for inflammatory and cancerous disorders in the upper and lower gastrointestinal tract. Experimental approaches are as simple as by giving a single oral dose of alcohol or other noxious agents or by injections of multiple dosages of ulcer inducing agents or by parenteral administration or in drinking water of carcinogens or by modifying the genetic makeups of animals to produce relatively long-term pathological changes in particular organs. With these methods they could induce consistent inflammatory responses or tumorigenesis in the gastrointestinal mucosa. These animal models are widely used in laboratories in understanding the pathogenesis as well as the mechanisms of action for therapeutic agents in the treatment of gastrointestinal inflammation and cancer.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.04.036
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    ABSTRACT: Preventive and/or therapeutic interventions using natural products for ischemic heart disease have gained considerable attention worldwide. This study investigated the cardioprotective effect and possible mechanism of embelin, a major constituent of Embelia ribes Burm, using isoproterenol (ISO)-induced myocardial infarction model in rats. Rats were pretreated for three days with embelin (50mg/kg, p.o) before inducing myocardial injury by administration of ISO (85mg/kg) subcutaneously at an interval of 24h for 2 consecutive days. Serum was analyzed for cardiac specific injury biomarkers, lipids and lipoproteins content. Heart tissues were isolated and were used for histopathology, antioxidant and mitochondrial respiratory enzyme activity assays and western blot analysis. Results showed that pretreatment with embelin significantly decreased the elevated levels of serum specific cardiac injury biomarkers (CK-MB, LDH and AST), serum levels of lipids and lipoproteins and histopathological changes when compared to ISO-induced controls. Exploration of the underlying mechanisms of embelin action revealed that embelin pretreatment restored the myocardial mitochondrial respiratory enzyme activities (NADH dehydrogenase, succinate dehydrogenase, cytochrome c oxidase and mitochondrial redox activity), strengthened antioxidant status and attenuated ISO-induced myocardial lipid peroxidation. Immunoblot analysis revealed that embelin interrupted mitochondria dependent apoptotic damage by increasing the myocardial expression of Bcl-2 and down regulating the expression of Bax, cytochrome c, cleaved-caspase-3 & 9 and PARP. Histopathology findings further strengthened the cardioprotective findings of embelin. Result suggested that embelin may have a potential benefit in preventing ischemic heart disease like myocardial infarction.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.04.035
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    ABSTRACT: Occupational exposure to organophosphate pesticides is becoming a common and increasingly alarming world-wide phenomenon. The present study is designed to investigate the preventive effect of N-acetylcysteine on malathion-induced hepatic injury and inflammation in rats. Adult male Wistar rats of body weight 200-230g were used for the study. Malathion (200mg/kg b.w./day) was administered to rats by oral intubation and N-acetylcysteine (2g/l) in drinking water for 28days. Rats were sacrificed on the 28th day, 2hours after the last administration. Markers of liver injury (aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate desyhdogenase), inflammation (leukocyte counts, myeloperoxidase, immunophenotyping of CD4+ and CD8+, interleukin-1β, interleukin-6 and interferon-γ expression) and oxidative stress (lipid peroxidation, reduced glutathione and antioxidant status) were assessed. Malathion induced an increase in activities of hepatocellular enzymes in plasma, lipid peroxidation index, CD3+/CD4+ and CD3+/CD4+ percent and pro-inflammatory cytokines, when decreased antioxidant status in liver was noted. When malathion-treated rats were compared to NAC supplemented rats, leukocytosis, T cell count and IL-1β, IL-6, INF-γ expression were reduced. Furthermore, NAC restored liver enzyme activities and oxidative stress markers. Malathion induces hepatotoxicity, oxidative stress and liver inflammation. N-acetylcysteine showed therapeutic effects against malathion toxicity.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.04.033
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    ABSTRACT: We previously reported anti-dyslipidemic effects of a farnesoid X receptor antagonist in monkeys. In this study, we compared the cholesterol-lowering effects of single and combined administration of a farnesoid X receptor antagonist, compound-T8, and the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor atorvastatin in guinea pig model. Plasma levels of 7α-hydroxy-4-cholesten-3-one, a marker of hepatic cholesterol 7α-hydroxylase activity, were measured after a single administration of compound-T8. The effects of compound-T8 or atorvastatin on plasma cholesterol levels and low-density lipoprotein (LDL) clearance were investigated after 14 or 16days of repeated dosing, respectively. Fractional catabolic rate of plasma LDL was estimated by intravenous injection of DiI-labeled human LDL. The cholesterol-lowering effects of combination therapy were investigated after 7days of repeated treatment. Compound-T8 (10 and 30mg/kg) increased plasma 7α-hydroxy-4-cholesten-3-one levels in a dose-dependent manner. Single administration of compound-T8 (30mg/kg) and atorvastatin (30mg/kg) reduced plasma non-high-density lipoprotein (non-HDL) cholesterol levels by 48% and 46%, respectively, and increased clearance of plasma DiI-labeled LDL by 29% and 35%, respectively. Compound-T8 (10mg/kg) or atorvastatin (10mg/kg) reduced non-HDL cholesterol levels by 19% and 25%, respectively, and combination therapy showed an additive effect and lowered cholesterol levels by 48%. Similar to atorvastatin, compound-T8 reduced plasma non-HDL cholesterol levels accompanied with accelerated LDL clearance in guinea pigs. Combination therapy additively decreased plasma non-HDL cholesterol levels. Therefore, monotherapy with a farnesoid X receptor antagonist and combination therapy of a farnesoid X receptor antagonist with atorvastatin would be attractive dyslipidemia treatment options.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.04.029
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    ABSTRACT: Obesity and insulin resistance are associated with increased oxidant stress. However, treatments of obese subjects with different types of antioxidants often give mixed outcomes. In this work, we sought to determine if long-term supplementation of a thiol antioxidant, β-mercaptoethanol, to diet-induced obese mice may improve their health conditions. Middle-age mice with pre-existing diet-induced obesity were provided with low concentration β-mercaptoethanol (BME) in drinking water for six months. Animals were assessed for body composition, gripping strength, spontaneous physical and metabolic activities, as well as insulin and pyruvate tolerance tests. Markers of inflammation were assessed in plasma, fat tissue, and liver. BME-treated mice gained less fat mass and more lean mass than the control animals. They also showed increased nocturnal locomotion and respiration, as well as greater gripping strength. BME reduced plasma lipid peroxidation, decreased abdominal fat tissue inflammation, reduced fat infiltration into muscle and liver, and reduced liver and plasma C-reactive protein. However, BME was found to desensitize insulin signaling in vivo, an effect also confirmed by in vitro experiments. Long-term supplementation of low dose thiol antioxidant BME improved functional outcomes in animals with pre-existing obesity. Additional studies are needed to address the treatment impact on insulin sensitivity if a therapeutic value is to be explored.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.04.031
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    ABSTRACT: Compound K (CK) is known to possess anti-diabetic activities but the mechanism for this action is unknown. The present study observed the protective effect of CK on islet cell apoptosis through the AMP-activated protein kinase (AMPK) mediated C-Jun N-terminal kinase (JNK) pathway. Treatment effect of CK on type 2 diabetic (T2D) mice and palmitate-induced MIN6 β-cells injury were observed. Fasting plasma glucose, triacylglycerol, total cholesterol, insulin levels and glucose tolerance test were evaluated. The expression of AMPK and JNK was detected in islet and MIN6 cells. CK treatment (30mg/kg) decreased fasting plasma glucose, triacylglycerol, total cholesterol, elevated plasma insulin levels and improved glucose tolerance in T2D mice. CK treatment attenuated islet cell apoptosis, caspase-3 activity accompanied by a decrease in AMPK and JNK activation. Meanwhile, CK treatment attenuated the palmitate-induced reduction in MIN6 β-cells viability, apoptosis and caspase-3 activity and activation of AMPK and JNK. The AMPK activator AICAR attenuated the CK-mediated inhibition of palmitate-induced apoptosis. These data suggest that CK treatment provides a beneficial anti-diabetic effect in mice with T2D and this protective effect may be mediated through prevention of β-cell apoptosis via inhibition of the AMPK-JNK pathway.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.04.034
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    ABSTRACT: Cardiac fibrosis is a final outcome of many clinical conditions that lead to cardiac failure and is characterized by a progressive substitution of cellular elements by extracellular-matrix proteins, such as collagen type I, collagen type II, connective tissue growth factor (CTGF), etc. AIM: : The aim of this study was to identify the mechanisms responsible for angiotensin II (Ang II)-stimulated cardiac fibrosis using rat neonatal cardiac fibroblasts. Neonatal fibroblasts were transfected with IκBα mutant, constitutively active (ca) integrin-linked kinase (ILK), dominant negative of ILK and small interfering RNA (siRNA) of ILK in the presence and absence of Ang-II stimulation. The pro-fibrotic gene expression and protein levels were determined by quantitative real time PCR and western blotting using their specific probes and antibodies. NF-κB translocation was determined by immunocytochemistry and confocal microscopy images were analyzed. Our results indicate that overexpression of ILK promotes a pro-fibrotic process by upregulating collagen type I and CTGF genes via activation of nuclear factor-κB (NF-κB) in cardiac fibroblasts. Inactivation of either NF-κB by the super-repressor IκBα or ILK by siRNA significantly attenuates the pro-fibrotic process. Moreover, ILK overexpression triggers NF-κB-p65 translocation to the nucleus, and ILK inhibition prevents the translocation in cardiac fibroblasts stimulated with Ang II. Our data suggest that the Ang II-stimulated pro-fibrotic process is regulated by a complex mechanism involving crosstalk between ILK and NF-κB activation. This dual mechanism may play a critical role in the progression of cardiac fibrosis.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.04.030
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    ABSTRACT: Aim Jaundice, potentially fatal encephalopathy, is common in approximately two-thirds of all well term infants. It is largely due to low expression of constitutive androstane receptor (CAR) in newborns; however, the mechanisms for this low expression were poorly understood. Expression of miR-137 and CAR was compared between neonatal and adult mice and between healthy and a mouse model of obstructive jaundice (OJ) using real-time RT-PCR and Western blot methods. Rate of bilirubin clearance was measured. DNA methylation of miR-137 was analyzed. Inverse expressions of miR-137 and CAR were consistently observed between newborn and adult mice, with significantly higher miR-137 level and lower CAR protein and mRNA levels in neonatal liver than in adult liver. Similar reciprocal relationship was found existing between adult OJ mice and healthy control animals with higher miR-137 level and lower CAR protein and mRNA levels in OJ than in healthy mice. Forced expression of miR-137 in primary hepatocytes repressed CAR protein levels, which was prevented by the inhibitor of miR-137. Knockdown of endogenous miR-137 by its inhibitor increased the rate of bilirubin clearance in OJ mice. Finally, we found that miR-137 was epigenetically over-activated due to hypomethylation in neonatal mice and in adult OJ mice, relative to adult healthy animals. Our findings indicate that miR-137 is a repressor of CAR thus a critical determinant of bilirubin clearance and may be considered a molecular target for the treatment of neonatal hyperbilirubinaemia.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.04.024
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    ABSTRACT: Aim Recent studies have emphasized the importance of the extracellular microenvironment in modulating cell growth, motility, and signaling. In this study we have evaluated the ability of a fibroblast derived-extracellular matrix (fd-ECM) to regulate type I collagen synthesis and degradation in fibroblasts. Main Methods Fibroblasts were plated on plastic (control) or on fd-ECM and type I collagen synthesis and degradation was evaluated. MTT, western blotting, real time PCR, zymographic analysis and inhibitor assays were utilised to investigate the molecular mechanism of type I collagen regulation by the fd-ECM. Key Findings Fibroblasts plated on fd-ECM showed significant downregulation in the production of type I collagen and COL1A2 messenger ribonucleic acid (mRNA) whilst COL1A1 mRNA remained unchanged. Cells grown on fd-ECM exhibited increased matrix metalloproteases (MMPs) and their corresponding mRNA. The use of transforming growth factor β (TGF-β) and MMP inhibitors showed that the excess COL1A1 polypeptide chains were degraded by the combined action of MMP-1, MMP-2, MMP-9 and cathepsins. Significance These results show the crucial role played by proteases in regulating extracellular matrix protein levels in the feedback regulation of connective tissue gene expression.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.03.006
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    ABSTRACT: Aims Osthole, a coumarin derivative, has been used in Chinese medicine and studies have suggested a potential use in treatment of diabetes and cancers. Therefore, we investigated the effects of osthole and other coumarins on GLUT1 activity in two cell lines that exclusively express GLUT1. Main Methods We measured the magnitude and time frame of the effects of osthole and related coumarins on glucose uptake in two cells lines; L929 fibroblast cells which have low GLUT1 expression levels and low basal glucose uptake and HCLE cells which have high GLUT1 concentrations and high basal uptake. We also explored the effects of these coumarins in combination with other GLUT1 activators. Key findings Osthole activates glucose uptake in L929 cells with a modest maximum 1.7-fold activation achieved by 50 μM with both activation and recovery occurring within minutes. However, osthole blocks full acute activation of glucose uptake by other, more robust activators. This behavior mimics the effects of other thiol reactive compounds and suggests that osthole is interacting with cysteine residues, possibly within GLUT1 itself. Coumarin, 7-hydroxycoumarin, and 7-methoxycoumarin, do not affect glucose uptake, which is consistent with the notion that the isoprenoid structure in osthole may be important to gain membrane access to GLUT1. In contrast to its effects in L929 cells, osthole inhibits basal glucose uptake in the more active HCLE cells. Significance The differential effects of osthole in L929 and HCLE cells indicated that regulation of GLUT1 varies, likely depending on its membrane concentration.
    Life sciences 05/2014; DOI:10.1016/j.lfs.2014.03.017