Life sciences Journal Impact Factor & Information

Publisher: Elsevier

Journal description

Current impact factor: 2.70

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.702
2013 Impact Factor 2.296
2012 Impact Factor 2.555
2011 Impact Factor 2.527
2010 Impact Factor 2.451
2009 Impact Factor 2.56
2008 Impact Factor 2.583
2007 Impact Factor 2.257
2006 Impact Factor 2.389
2005 Impact Factor 2.512
2004 Impact Factor 2.158
2003 Impact Factor 1.944
2002 Impact Factor 1.824
2001 Impact Factor 1.758
2000 Impact Factor 1.808
1999 Impact Factor 1.774
1998 Impact Factor 1.937
1997 Impact Factor 2.275
1996 Impact Factor 2.352
1995 Impact Factor 2.345
1994 Impact Factor 2.5
1993 Impact Factor 2.381
1992 Impact Factor 2.053

Impact factor over time

Impact factor

Additional details

5-year impact 2.67
Cited half-life >10.0
Immediacy index 0.69
Eigenfactor 0.02
Article influence 0.69
ISSN 1879-0631

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Aim: Formulation and evaluation of anastrozole, an anti-cancer drug loaded in different biodegradable polymeric nanoparticles. Materials and methods: Different carrier systems such as poly(lactide-co-glycolide) (PLGA 50:50), poly(lactic-acid) (PLA) and poly(ε-caprolactone) (PCL) are used to prepare nanoparticles by simple emulsion technique. The surfactants polyvinyl alcohol and sodium deoxycholate were studied for their use as stabilizing agents at varying concentrations. The formulations were studied for their particle size, zeta potential, entrapment efficiency and solid state characteristics, and also were tested for their in vitro cytotoxicity and in vivo behavior in rats. Key findings: The entrapment ranged from 35 to 85%, depending on the drug-polymer ratio used. Particle size ranged from 100 to 350nm with optimal zeta potential. Accordingly, discrete spherical nanoparticles with smooth surface were obtained as evidence from Field Emission Scanning Electron Microscopy (FESEM) study. The solid state characteristics revealed dispersion of drug at the molecular level in the polymeric matrix of nanoparticles. A non-Fickian transport with initial burst release followed by slow release was observed with nanoparticles. The remarkable decrease in cell viability at various time points was observed for PLGA nanoparticles compared to other polymer matrices. The AUC(0→∞) of PLGA, PLA and PCL nanoparticles were found to be 4.77, 19.31 and 19.81 fold higher than (p<0.05) anastrozole in solution, respectively. Also, pharmacokinetics study revealed the long time circulation of anastrozole loaded polymeric nanoparticles. Significance: The results suggest that developed nanoparticles could be used successfully for effective management of breast cancer chemotherapy.
    Life sciences 10/2015; DOI:10.1016/j.lfs.2015.09.021
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    ABSTRACT: Aims: Sepsis is a life threatening condition that is characterized by the loss of vascular reactivity. The factor(s) responsible for the diminished vascular function seen in sepsis are not well understood. The purpose of this study was to characterize the vascular dysfunction from the rat cecal inoculum (CI) sepsis model using cecal ligation and puncture (CLP), and lipopolysaccharide (LPS) sepsis as reference models. Materials and methods: Experiments were performed on isolated aorta from CI, CLP and LPS treated rats using a combination of pharmacological approaches. Key findings: Phenylephrine (PE)-induced aortic contraction was significantly decreased in each model (p<0.05) and not normalized by L-NAME or indomethacin. The vascular response elicited in the CI model for acetylcholine (Ach) was more similar to that seen in the CLP than the LPS model. The removal of the endothelial layer increased sensitivity to L-NAME (p<0.05) in aortae from CI group. Inhibition of the large conductance Ca(2+)/voltage sensitive K(+) (BKCa) channel did not normalize PE hyporesponsiveness but did abolish sepsis-induced contractile oscillation. Inhibition of the voltage dependent Kv1.5 channel was not able to reverse the vascular hyporesponsiveness, however, inhibition of the ATP dependent (KATP) channel inhibition partially restored the contractile response (p<0.05). Elevation of VCAM expression and aortic structural alternation were observed in each model. Significance: These results suggest that the CI model may be an additional tool that could be used to investigate the mechanisms of vascular hyporesponsiveness in sepsis.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.020
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    ABSTRACT: Aims: In vitro expansion changes replication and differentiation capacity of mesenchymal stem cells (MSCs), increasing challenges and risks, while limiting the sufficient number of MSCs required for cytotherapy. Here, we characterized and compared proliferation, differentiation, telomere length and pluripotency marker expression in MSCs of various origins. Main methods: Immunophenotyping, proliferation and differentiation assays were performed. Pluripotency marker (Nanog, Oct-4, SOX-2, SSEA-4) expression was determined by immunofluorescence. Quantitative PCR was performed for relative telomere length (RTL) analyses, while expression of relevant genes for pluripotency markers, differentiation state (Cbfa1, human placental alkaline phosphatase, peroxisome proliferator activated receptor, Sox9 and Collagen II a1), and telomerase reverse transcriptase (hTERT) was determined by semiquantitative RT-PCR. Key findings: Peripheral blood MSCs (PB-MSCs) and umbilical cord MSCs (UC-MSCs) showed the highest, while periodontal ligament MSCs (PDL-MSCs) and adipose tissue MSCs (AT-MSCs) the lowest values of both the replication potential and RTL. Although MSCs from exfoliated deciduous teeth (SHEDs), PDL-MSCs and AT-MSCs showed higher mRNA expression of pluripotency markers, all MSCs expressed pluripotency marker proteins. SHEDs and PDL-MSCs showed prominent capacity for osteogenesis, PB-MSCs and UC-MSCs showed strengthened adipogenic differentiation potential, while AT-MSCs displayed similar differentiation into both lines. Significance: The MSCs populations derived from different sources, although displaying similar phenotype, exhibited high degree of variability regarding biological properties related to their self-renewal and differentiation capacity. These data indicate that for more accurate use in cell therapy, individualities of MSCs isolated from different tissues should be identified and taken into consideration when planning their use in clinical protocols.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.019
  • Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.014
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    ABSTRACT: Aims: Obesity and diabetes mellitus type 2 (DM2) frequently coexist and increase the propensity of cardiovascular dysfunction by numerous mechanisms. Chief among them are oxidative stress and Ca(2+) dysregulation, and both are inducers of the mitochondrial permeability transition pore (MPTP). Nevertheless, it is unknown whether MPTP formation is triggered in DM2 animals, and thereby contributing to cardiac dysfunction. We assessed MPTP sensitivity and reactive oxygen species production in cardiac mitochondria, as well as cytosolic Ca(2+) handling in ventricular myocytes from rats with DM2. Main methods: Male Zucker Fa/fa rats (Fa/fa) 32weeks old presenting DM2, concentric hypertrophy, and diastolic dysfunction were used. MPTP formation was evaluated in isolated mitochondria and Ca(2+) handling in ventricular myocytes, by spectrophotometric and confocal microscope techniques, respectively. Key findings: We found that the systolic Ca(2+) transient relaxation was ~40% slower, while mitochondrial H2O2 production increased by ~6-fold. MPTP opening in isolated mitochondria from Fa/fa (mFa/fa) was more sensitive to Ca(2+) than in mitochondria from lean rats (mLean), and correlated with increased thiol groups exposure. The mFa/fa showed decreased oxidative phosphorylation capacity. The ATP content decreased in myocytes, while the PCr/ATP ratio remained unchanged and caspase 9 activity largely increased in myocytes from Fa/fa animals. Significance: Our results showed that oxidative stress and diastolic Ca(2+) dysregulation increased MPTP sensitivity leading to mitochondrial dysfunction and apoptosis. Mitochondrial dysfunction could compromise ATP synthesis, and lower ATP could be linked to decreased SERCA2 activity, which might underlie diastolic dysfunction. Prolonged Ca(2+) transients might further exacerbate mitochondrial dysfunction.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.018
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    ABSTRACT: Aim: Neuroinflammatory response triggered by the stimulation of matrix metalloproteinases plays a pivotal role in the development of autistic phenotype. MMPs stimulate inflammatory cytokines release along with mitochondrial deficits that ultimately lead to neuronal dysfunction and precipitate autistic symptoms. The aim of the present study was to explore the neuropsychopharmacotherapeutic efficacy of curcumin in the experimental paradigm of autism spectrum disorders. Materials and methods: 1M propanoic acid (4μl) was infused over 10min into the anterior portion of the caudoputamen to induce autistic behavior in rats. Curcumin (50, 100 and 200mg/kg) was administered per orally starting from 2nd day of surgery and continued up to 28th day. Rats were tested for various neurobehavioural paradigms like social interaction, stereotypy, locomotor activity, anxiety, novelty, depression, spatial learning and memory as well as for repetitive and pervasive behavior. In addition, biochemical tests for oxidative stress, mitochondrial complexes, TNF-α and MMP-9 were also carried out. Key findings: Intracerebroventricular injection of propanoic acid produced neurological, sensory, behavioral, biochemical and molecular deficits which were assessed as endophenotype of autism spectrum disorders. Regular treatment with curcumin for four weeks significantly and dose dependently restored neurological, behavioral, biochemical and molecular changes associated with autistic phenotype in rats. Significance: The major finding of the study is that curcumin restored the core and associated symptoms of autistic phenotype by suppressing oxidative-nitrosative stress, mitochondrial dysfunction, TNF-α and MMP-9 in PPA-induced autism in rats. Therefore, curcumin can be developed as a potential neuropsychopharmacotherapeutic adjunct for autism spectrum disorders (ASD).
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.012
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    ABSTRACT: Aims: The purpose of this study is to explore whether antioxidant DJ-1 protein affects the atrophy of skeletal muscle cell induced by undernutrition. Main methods: To determine cell atrophic responses, L6 cell line and skeletal primary cells from mouse hind limbs were cultivated under condition of FBS-free and low glucose. Changes of protein expression were analyzed using Western blot. Overexpression and knockdown of DJ-1 was performed in cells to assess its influence on cell atrophic responses. Key findings: Undernutrition decreased cell size and increased the abundance of oxidized form and total form of DJ-1 protein in L6 myoblasts. The undernourished cells revealed an elevation in the expression of muscle-specific RING finger-1 (MuRF-1) and atrogin-1, and in the phosphorylations of p38 mitogen-activated protein kinase (MAPK) and stress-activated protein kinase/c-Jun. N-terminal kinase compared with control groups. Moreover, DJ-1-knockout mice showed a decrease in cell size and an enhancement in the expression of MuRF-1 and atrogin-1, as well as in the phosphorylation of MAPKs in gastrocnemius muscles; these changes were also observed in L6 cells transfected with siRNA of DJ-1. On the other hand, L6 cells overexpressing full-length DJ-1 did not exhibit the alterations in cell size and ubiquitin ligases seen after undernourished states of control cells. Myotubes differentiated from L6 cells also showed elevated expression of MuRF-1 and atrogin-1 in response to undernutrition. Significance: These results suggest that DJ-1 protein may contribute to undernutrition-induced atrophy via MAPKs/ubiquitin ligase pathway in skeletal muscle cells.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.016
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    ABSTRACT: Aims: Allopregnanolone has shown potent anticonvulsant activity in the adult brain. However, none of the studies have shown its effect in neonatal animal models of seizures. The current study explored the effect of allopregnanolone in animal models of neonatal status epilepticus. Main methods: Allopregnanolone was administered 10min before administration of kainic acid or 4-aminopyridine in postnatal 9 (PN9) day old rats. Various phases of convulsions such as latency to myoclonic jerks, continuous clonic movements with loss of righting reflex (status epilepticus) and mortality were measured; the effect was compared with its effect in pentylenetetrazol (PTZ) -induced generalized tonic-clonic convulsions. Key findings: Exogenous administration of kainic acid (2mg/kg., i.p.) or 4-aminopyridine (5mg/kg., i.p.) in rat pups (PN9) resulted in continuous clonic movements with loss of righting reflex (status epilepticus). Pre-treatment with allopregnanolone at doses of 5 and 10mg/kg., i.p. dose-dependently delayed the onset of status epilepticus, but not myoclonic jerks. Allopregnanolone did not prevent kainic acid-induced mortality at theses doses. In the kainic acid model, pretreatment of bumetanide before allopregnanolone delayed various phases of convulsions; the effect was significantly higher compared to per se groups. Allopregnanolone only at the higher dose extended the latency of 4-aminopyridine-induced seizures. In contrast, allopregnanolone at a low dose markedly shielded neonatal rats against PTZ convulsions. Significance: Allopregnanolone is protective in animal models of neonatal status epilepticus and generalized tonic-clonic convulsions and further clinical studies are required to establish its use in therapeutics.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.008
  • Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.011
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    ABSTRACT: Aims: Spontaneous hypertensive rats provide a genetic model for exploring the pathogenesis of urine storage dysfunction related to hypertension (HT). In humans, however, HT develops by both genetic and environmental factors including lifestyle factors such as a high-calorie diet, excessive salt intake and stress. We investigated the influence of salt-loading on bladder function and the underlying mechanisms of storage dysfunction related to HT. Main methods: Six-week-old male Dahl salt-sensitive (DS) and Dahl salt-resistant (DR) rats were fed with a normal or high-salt diet for 12weeks. Micturition parameters were obtained from a metabolic cage. Whole bladders were excised from 18-week-old rats and distended in an organ bath. The releases of adenosine triphosphoric acid (ATP) and prostaglandin E2 (PGE2) from the distended bladder epithelia were measured. Changes in bladder blood flow (BBF) were determined with a laser-speckle-blood-flow imaging system. Key findings: An increase in mean blood pressure (BP) was noted only in DS rats after salt-loading. During the inactive (sleeping) period, voided volume per micturition gradually increased in DR rats fed a normal or high-salt diet and normal-diet DS rats, while it did not change in the DS rats fed a high-salt diet. Bladder distension significantly increased ATP and PGE2 release from the urothelium in DS rats fed a high-salt diet. BBF was significantly decreased in high-salt-diet DS rats. Significance: One mechanism behind the relationship between salt-sensitive HT and urine storage dysfunction may be an increase in ATP and PGE2 release from the urothelium via suppression of BBF.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.010
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    ABSTRACT: Aims: The study was to examine the effect of Hylan G-F 20 on the progression of posttraumatic osteoarthritis (PTOA) and the expression of the circadian genes neuronal PAS domain protein 2 (NPAS2) and period 2 (Per2). Main methods: We used the anterior cruciate ligament transaction and medial menisectomy (ACLT + MMx) model in Wistar rats. The rats were divided into three groups, the sham-operated group, the Hylan G-F 20-treated group, and the saline-treated group. Rats which underwent ACLT + MMx surgery were injected intraarticulary with, respectively, Hylan G-F 20 or saline once a week for 3 consecutive weeks, starting 7days after surgery. The gross morphology and histopathology of the experimental knee joints were evaluated at the end of week 6. Expression of the NPAS2 and Per2 genes was measured by real-time PCR. Key findings: Hylan G-F 20 suppressed the articular cartilage destruction and synovitis compared to the saline-treated group. Compared to the sham-operated group, the Hylan G-F 20-treated group showed significantly upregulated expression of NPAS2 in cartilage (2.53±0.08-fold higher; p<0.05) and a non-significant increase in Per2 expression (2.35±1.26-fold higher p=0.28), while the saline-treated group showed significant downregulation of NPAS2 expression and a non-significant decrease in Per2 expression. Significance: Our data suggested that early intraarticular injection of Hylan G-F 20 attenuates the progression of PTOA and significantly upregulates NPAS2 expression. These findings provide a new direction for studying associations between the use of a pharmacological agent, the degenerative process, and circadian gene expression.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.007
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    ABSTRACT: Aims: Investigate the effect of ascorbic acid (vitamin C) on the endothelial dysfunction induced by acute ethanol intake. Main methods: Ethanol (1 g/kg; p.o. gavage) effects were assessed within 30 min in male Wistar rats. Key findings: Ethanol intake decreased the endothelium-dependent relaxation induced by acetylcholine in the rat aorta and treatment with vitamin C (250 mg/kg; p.o. gavage, 5 days) prevented this response. Ethanol increased superoxide anion (O2(-)) generation and decreased aortic nitrate/nitrite levels and these responses were not prevented by vitamin C. Superoxide dismutase (SOD) and catalase (CAT) activities as well as hydrogen peroxide (H2O2) and reduced glutathione (GSH) levels were not affected by ethanol. RhoA translocation as well as the phosphorylation levels of protein kinase B (Akt), eNOS (Ser(1177) or Thr(495) residues), p38MAPK, SAPK/JNK and ERK1/2 was not affected by ethanol intake. Vitamin C increased SOD activity and phosphorylation of Akt, eNOS (Ser(1177) residue) and p38MAPK in aortas from both control and ethanol-treated rats. Incubation of aortas with tempol prevented ethanol-induced decrease in the relaxation induced by acetylcholine. Ethanol (50 mM/1 min) increased O2(-) generation in cultured aortic vascular smooth muscle cells (VSMC) and vitamin C did not prevent this response. In endothelial cells, vitamin C prevented the increase on ROS generation and the decrease in the cytosolic NO content induced by ethanol. Significance: Our study provides novel evidence that vitamin C prevents the endothelial dysfunction induced by acute ethanol intake by a mechanism that involves reduced ROS generation and increased NO availability in endothelial cells.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.006
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    ABSTRACT: Aims: The incidence of secondary systemic fungal infections has sharply increased in bacterial septic patients. Antimycotics exhibit immunomodulatory properties, yet these effects are incompletely understood in secondary systemic fungal infections following bacterial sepsis. We investigated a model of systemic inflammation to determine whether antimycotics (liposomal amphotericin B (L-AMB), itraconazol (ITC), and anidulafungin (ANI)) modulate the gene and protein expression as well as the phagocytic activity of lipopolysaccharide (LPS)-stimulated human monocytes. Main methods: THP-1 monocytes were incubated with L-AMB, ITC or ANI and LPS. Gene expression levels of cytokines (TNF- , IL-1 , IL-6, and IL-10) were measured after 2h, 6h, and 24h. Cytokine protein levels were evaluated after 24h and phagocytic activity was determined following co-incubation with Escherichia coli. Key findings: All antimycotics differentially modulated the gene and protein expression of cytokines in sepsis-like conditions. In the presence of LPS, we identified L-AMB as immunosuppressive, whereas ITC demonstrated pro-inflammatory properties. Both compounds induced remarkably less phagocytosis. Significance: Our study suggests that antimycotics routinely used in septic patients alter the immune response in sepsis-like conditions by modulating cytokine gene and protein expression levels and phagocytic activity. Future treatment strategies should consider the immune status of the host and apply antimycotics accordingly in bacterial septic patients with secondary fungal infections.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.004
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    ABSTRACT: Aims: The effects of preconditioning on cardioprotection have mainly been studied in vitro. No sufficient in vivo experiments have been performed to optimize ischemic preconditioning (IPC) or hypoxic preconditioning (HPC) for clinical applications. The purpose of this study was to establish a canine double-bypass model to examine the effect of IPC and HPC on cardiomyocytes and heart function. Materials and methods: A double-bypass procedure to enable independent control of systemic and coronary circulation was established in dogs. The animals were divided into control, HPC, and IPC groups (n=6 each). Indicators of cardiac function, including cardiodynamics, hemodynamics, ATP, and cardiac troponin I (cTnI) levels; myocardium morphology; and myocardiocyte apoptosis were determined. Key findings: Both IPC and HPC attenuated the reperfusion-induced decrease in left ventricular end systolic pressure seen in the control group. Both the HPC and IPC groups had lower serum cTnI levels, better myocardiocyte histology, and lower rates of apoptosis compared to the control group without preconditioning. HPC reduced the abnormal cardiomyocyte histology and apoptosis to a greater extent than IPC, and only HPC significantly restored the depletion of ATP. Significance: This study demonstrates the effectiveness of the double-bypass model for the optimized study of both HPC and IPC. The results suggest that HPC may provide better cardioprotection than IPC.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.002
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    ABSTRACT: Aims: This study aimed to test the hypothesis that different neurotransmitters and hormones are presented at exercise fatigue in hot temperatures with differing relative humidities (RH). Main methods: Eight trained male athletes performed a graded maximum oxygen consumption (VO2max) test in five different environmental conditions, namely, 21°C/20% RH (Normal), 33°C/20% RH (Hot 20%), 33°C/40% RH (Hot 40%), 33°C/60% RH (Hot 60%), and 33°C/80% RH (Hot 80%). Blood samples were taken pre- and post-exercise and analyzed for noradrenaline (NA), adrenaline (ADR), dopamine (DA), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), and prolactin (PRL). Weight and oral and skin temperatures were recorded pre- and post-exercise. Heart rate was continuously monitored throughout the exercise. Key findings: Hot 20%, Hot 40%, and Hot 80% had lower VO2max levels compared with Normal (P<0.05). The data pooled from all five conditions indicated that the NA (P<0.0001), PRL (P<0.0001), 5-HT (P=0.002), 5-HIAA (P=0.029), and DA (P=0.016) levels were affected by exercise. Accordingly, NA level was significantly associated with performance time. However, ADR did not show any significant effect between pre- and post-exercise (P=0.187). Significance: The maximal aerobic capacity was impaired in high temperature and most humidity conditions. NA was strongly associated with exercise time, which suggested that exercise duration and intensity had an important influence on NA neurotransmitter level irrespective of the environmental conditions.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.001
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    ABSTRACT: Aim: The present study aimed to investigate the role of angiotensin II in repeated immobilization stress exposure of varying duration. Methods: Mice were subjected either to short (30min) or long duration (120min) immobilization stress for 5days. The behavioral changes were assessed by actophotometer, hole board, open field and social interaction tests on day 1 and day 5. The serum corticosterone levels were measured as an index of HPA axis on day 5. Key findings: A single exposure of short or long duration stress produced behavioral deficits and increased corticosterone levels. However, repeated exposure of stressors was followed by restoration of behavioral and biochemical changes, suggesting the development of stress adaptation. A single administration of telmisartan (5mg/kg) exacerbated the short stress-induced decrease in behavioral activity and increase in corticosterone levels on the first day of stress exposure, suggesting the anti-stress role of angiotensin II. In contrast, the normalization of behavioral and biochemical response was observed in prolonged stress-subjected mice following telmisartan treatment on the 1st day of stress exposure, suggesting stress inducing action of angiotensin II. Furthermore, telmisartan treatment for 5days abolished the restoration of behavioral and biochemical response following 5 consecutive exposures of short immobilization stress, without altering stress adaptation in prolonged stress, suggesting that angiotensin II has stress adaptive role in short stress. Significance: It is concluded that angiotensin II acts as anti-stress agent and promotes adaptation during short stress, whereas it acts as stress promoting agent, without affecting stress adaptation during prolonged stress.
    Life sciences 09/2015; DOI:10.1016/j.lfs.2015.09.005