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[PMID]: 29524881
[Au] Autor:Liu Z; Yu D; Xu J; Li X; Wang X; He Z; Zhao T
[Ad] Address:Department of Plastic, The Second Affiliated Hospital of Soochow University, Suzhou, China; Department of the Burns and Plastic, The Affiliated Hospital of Guizhou Medical University, Guiyang, China.
[Ti] Title:Human umbilical cord mesenchymal stem cells improve irradiation-induced skin ulcers healing of rat models.
[So] Source:Biomed Pharmacother;101:729-736, 2018 Mar 07.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Irradiation-induced skin ulcers can be resultant from nuclear accident or reaction to radiation therapy of tumor and is intractable for healing. Human umbilical cord mesenchymal stem cells (hUC-MSCs) have been considered to be the potential therapeutic tools for tissue regeneration. However, the underlying mechanisms are still not well understood. This study aims to investigate the effects of hUC-MSCs on irradiation-induced skin ulcers healing and the related mechanisms. The ulcers were induced by irradiating the skin of adult SD rats. The ulcers of SD rats were treated with vehicle or hUC-MSCs donated from mother giving birth. The ulcer healing was measured by imaging the healing rate and the H&E staining. CD31 and VEGF expression was measured with immunohistochemistry assay. iTRAQ proteomics analysis was used to analyze the signaling pathway. The results showed that hUC-MSCs improved healing of irradiation-induced skin ulcers in vivo using a rat model of skin ulcer. Transplantation of hUC-MSCs promoted keratin generation and keratinocytes proliferation of ulcer areas. Furthermore, the results demonstrated that hUC-MSCs increased expression of CD31 and VEGF in ulcers and promoted neovascularization. iTRAQ proteomics analysis results indicated that PI3K/Akt signaling pathway involved in hUC-MSCs-mediated repairing of irradiation-induced skin ulcer. In conclusion, human umbilical cord mesenchymal stem cells promoted neovascularization and re-epithelization, and improved healing of irradiation-induced skin ulcers. This healing improvement may be conducted through activating the PI3K/Akt signaling pathway, however, which needs to be proven by the further investigations.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 1555135 MEDLINE  
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[PMID]: 29524879
[Au] Autor:Abass SA; El-Hamid NMA; Abouzed TK; El-Shishtawy MM
[Ad] Address:Biochemistry Department, Faculty of Pharmacy, Kafrelsheikh University, Kafrelsheikh, 33516, Egypt.
[Ti] Title:Chemosensitizing effect of Alpinia officinarum rhizome extract in cisplatin-treated rats with hepatocellular carcinoma.
[So] Source:Biomed Pharmacother;101:710-718, 2018 Mar 07.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:This study was conducted to estimate the preventing and sensitizing efficiency of Alpinia officinarum rhizome extract (AORE) in an experimental model of hepatocellular carcinoma (HCC) +/- cisplatin. HCC was induced by a single intraperitoneal (i.p) dose of diethylnitrosamine (DENA, 200mg/kg). After 14 days, phenobarbitone (PB, 0.05%) was added to drinking water for 14 weeks to promote hepatocarcinogenesis. Cisplatin (CP) was given in a dose of 1.5 mg/kg (i.p), twice a week, alone or with AORE (400 mg/kg daily, orally) for 21 days. AORE was tried as a protective before the induction of HCC for three weeks as well. Results revealed that DENA/PB elevated hepatic indices as ALT and AST and total bilirubin with declining serum total protein. It increased oxidative stress, as hepatic malondialdehyde (MDA) with depressed hepatic reduced glutathione (GSH) contents, superoxide dismutase (SOD) and catalase activities. This was accompanied by an increase in hepatic expression of antioxidant genes (thioredoxin and glutaredoxin). Hepatocarcinogenesis was detected by histopathological changes in liver sections and the elevation of serum alpha-fetoprotein (AFP) level. Treatment with CP partially restored altered hepatic functions and oxidative stress markers. It also showed a partial decrease in the expression of antioxidant genes, improving histopathological changes in the liver and AFP level in serum. The treatment with AORE alone or AORE+CP enhanced hepatic function and oxidative stress markers. It also caused a decrease in the expression of antioxidant genes and improved histopathological changes in liver and serum AFP level. This effect is more potent than the treatment with CP alone. Our study suggested that AORE can be used as a promising natural chemoprevention or a chemosensitizing agent against hepatocarcinogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 1555135 MEDLINE  
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[PMID]: 29524841
[Au] Autor:Zhao L; Tao X; Qi Y; Xu L; Yin L; Peng J
[Ad] Address:College of Pharmacy, Dalian Medical University, Western 9 Lvshunnan Road, Dalian 116044, China.
[Ti] Title:Protective effect of dioscin against doxorubicin-induced cardiotoxicity via adjusting microRNA-140-5p-mediated myocardial oxidative stress.
[So] Source:Redox Biol;16:189-198, 2018 Mar 06.
[Is] ISSN:2213-2317
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Clinical application of doxorubicin (DOX) is limited because of its cardiotoxicity. Thus, exploration of effective lead compounds against DOX-induced cardiotoxicity is necessary. The aim of the present study was to investigate the effects and possible mechanisms of dioscin against DOX-induced cardiotoxicity. The in vitro model of DOX- treated H9C2 cells and the in vivo models of DOX-treated rats and mice were used in this study. The results showed that discoin markedly increased H9C2 cell viability, decreased the levels of CK, LDH, and improved histopathological and electrocardio- gram changes in rats and mice to protect DOX-induced cardiotoxicity. Furthermore, dioscin significantly inhibited myocardial oxidative insult through adjusting the levels of intracellular ROS, MDA, SOD, GSH and GSH-Px in vitro and in vivo. Our data also indicated that dioscin activated Nrf2 and Sirt2 signaling pathways, and thereby affected the expression levels of HO-1, NQO1, Gst, GCLM, Keap1 and FOXO3a through decreasing miR-140-5p expression level. In addition, the level of intracellular ROS was significantly increased in H9C2 cells treated by DOX after miR-140-5p mimic transfection, as well as the down-regulated expression levels of Nrf2 and Sirt2, which were markedly reversed by dioscin. In conclusion, our data suggested that dioscin alleviated DOX-induced cardiotoxicity through modulating miR-140-5p-mediated myocardial oxidative stress. This natural product should be developed as a new candidate to alleviate cardiotoxicity caused by DOX in the future.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524763
[Au] Autor:Atsak P; Morena M; Schoenmaker C; Tabak E; Oomen CA; Jamil S; Hill MN; Roozendaal B
[Ad] Address:Department of Cognitive Neuroscience, Radboud University Medical Center, 6500 HB Nijmegen, The Netherlands; Donders Institute for Brain, Cognition and Behaviour, Radboud University, 6525 EN Nijmegen, The Netherlands. Electronic address: PirayAtsak@gmail.com.
[Ti] Title:Glucocorticoid-endocannabinoid uncoupling mediates fear suppression deficits after early - Life stress.
[So] Source:Psychoneuroendocrinology;91:41-49, 2018 Feb 21.
[Is] ISSN:1873-3360
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Early-life stress (ELS) creates life-long vulnerability to stress-related anxiety disorders through altering stress and fear systems in the brain. The endocannabinoid system has emerged as an important regulator of the stress response through a crosstalk with the glucocorticoid system, yet whether it plays a role in the persistent effects of ELS remains unanswered. By combining, behavioral, pharmacological and biochemical approaches in adult male rats, we examined the impact of ELS on the regulation of endocannabinoid function by stress and glucocorticoids. We employed a postnatal limited-nesting/bedding induced ELS between postnatal days 2-9 in rats. Exposure to postnatal ELS compromised the ability of both acute stress and glucocorticoid administration to mobilize the endocannabinoid ligand 2-arachidonoyl glycerol (2-AG) in the hippocampus of adult male rats. These findings suggest that ELS compromises the coupling of the glucocorticoid and endocannabinoid systems in the hippocampus. Since 2-AG signaling is essential in mediating glucocorticoid-induced suppression of fear recall, we further examined the impact of ELS on the ability of glucocorticoids to suppress fear memory recall. While ELS did not affect normative fear recall, it impaired the ability of glucocorticoids to dampen fear recall. Notably, bypassing glucocorticoids and directly amplifying hippocampal 2-AG signaling with a monoacyl glycerol lipase inhibitor produced a suppression of fear memory recall in animals exposed to ELS. These findings suggest that ELS results in an uncoupling of glucocorticoid-endocannabinoid signaling in the hippocampus, which, in turn, relates to alterations in stress regulation of memory recall. These data provide compelling evidence that ELS-induced deficits in the glucocorticoid-endocannabinoid coupling following stress could predispose susceptibility to stress-related psychopathology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 1555135 MEDLINE  
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[PMID]: 29524702
[Au] Autor:Wu J; Lu Y; Hua X; Ma S; Xu J
[Ad] Address:School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
[Ti] Title:A Longitudinal Mapping study on Cortical Plasticity of Peripheral Nerve Injury Treated by direct Anastomosis Electroacupuncture in Rats.
[So] Source:World Neurosurg;, 2018 Mar 07.
[Is] ISSN:1878-8769
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: We utilized fMRI to provide a longitudinal description of cortical plasticity caused by electroacupuncture(EA) of sciatic nerve transection and direct anastomosis rats. METHODS: Sixteen rats of sciatic nerve transection and direct anastomosis model were randomly divided into intervention and control group. EA intervention in the position of ST-36, GB-30 was conducted continuously for 4 months in the intervention group. Functional MRI and gait assessment was performed every one month after intervention. RESULTS: The somatosensory area was more activated in the first 2 months and then deactivated in the rest 2 months when EA was applied. And the pain-related areas have the same activation pattern as the somatosensory area. The limbic/paralimbic areas acted in a more fluctuated way during the EA intervention, which was not constantly activated or deactivated as previous studies reported. We attributed such changes in somatosensory and pain-related areas to the gradual reduction of sensory afferentation. The alterations in limbic/paralimbic system might be associated with the confrontation between the up-regulating effect of paresthesia or pain and down-regulating effect of EA intervention through autonomic nerve system. And the gait analysis showed significantly higher maximum contact mean intensity (MCMI) of intervention group. CONCLUSIONS: The alterations of brain brought by long term therapeutic effect of EA could be described as a synchronized activation pattern of somatosensory area & pain-related areas and fluctuated pattern of limbic/paralimbic system.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 1555135 MEDLINE  
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[PMID]: 29524682
[Au] Autor:Ghosh K; N I
[Ad] Address:Unit of Toxicology, Department of Zoology, School of Life Sciences, Bharathiar University, Coimbatore, 641046, Tamil Nadu, India; Department of Zoology, Annamalai University, Annamalainagar, Chidambaram, 608002, Tamil Nadu, India. Electronic address: kavisa9@gmail.com.
[Ti] Title:Cadmium treatment induces echinocytosis, DNA damage, inflammation, and apoptosis in cardiac tissue of albino Wistar rats.
[So] Source:Environ Toxicol Pharmacol;59:43-52, 2018 Feb 27.
[Is] ISSN:1872-7077
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Cadmium (Cd), a potent carcinogen present in almost all foods, poses a major health risk to humans. Major routes of exposure to Cd for humans are occupation, diet, and tobacco use. Cd elicits various deleterious effects on cellular molecules mainly by causing oxidant-antioxidant imbalance. Cd has been implicated in the pathogenesis of many cancers, Itai-itai disease, diabetic nephropathy, hypertension, peripheral artery disease, and myocardial infarction. This study was designed to investigate the effects of Cd intake on erythrocytes and cardiac tissue in male albino Wistar rats. We treated male albino Wistar rats with cadmium chloride (CdCl ) by intra-gastric administration for 30 days and examined Cd burden and changes in blood constituents and antioxidant status of blood and cardiac tissue. We also studied the structural alterations in the erthrocytes, elemental changes and Cd burden in cardiac tissue using scanning electron microscope (SEM/EDX). Inflammation and apoptosis were analysed in the cardiac tissue by polymerase chain reaction (PCR), western blotting, and DNA fragmentation assay. Cd treatment resulted in echinocytosis of erythrocytes and distorted myofibrils arrangement, vacuolization and congestion in the vessels. Cd administration has also induced inflammation and apoptosis in the cardiac tissue. At molecular level, Cd administration caused oxidative damage to DNA, lipids, and proteins and diminished the activities of various antioxidants. The present study provides a compelling evidence of Cd-induced imbalance in oxidant-antioxidant system with damage to erythrocytes and cardiac tissue that may contribute to various cardiac diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 1555135 MEDLINE  
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[PMID]: 29524647
[Au] Autor:Zhao M; Wu J; Li X; Gao Y
[Ad] Address:Department of Laboratory Medicine, Beijing Hospital, National Center of Gerontology, Beijing, China; Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
[Ti] Title:Urinary candidate biomarkers in an experimental autoimmune myocarditis rat model.
[So] Source:J Proteomics;, 2018 Mar 07.
[Is] ISSN:1876-7737
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Urine is a better source than plasma for biomarker studies, as it can accumulate all changes in the body. Various candidate urinary biomarkers of physiological condition, kidney disease and even brain dysfunction, have been detected in urine; however, urine has rarely been used to reflect cardiac diseases. In this study, urine at day 0, 14, 21 and 28 were collected from the myosin-induced autoimmune myocarditis rat models. The candidate urinary biomarkers were then characterized using the isobaric tandem mass tag labeling approach coupled with offline two-dimensional reverse-phase liquid chromatography and high-resolution mass spectrometry. Compared with controls, forty-six urinary proteins were significantly changed in the myocarditis rats; among them, ten had previously been associated with myocarditis, twelve corresponding gene products had annotated as mainly cardiovascular network genes by the Ingenuity Pathway Analysis, four urinary proteins were validated by western blot, thirteen were reported in previous urine proteome studies of other diseases and twenty-six were reported the first time to be related to myocarditis. SIGNIFICANCE: This is the first study to use isobaric tandem mass tag labeling approach in the urine proteome analysis of experimental autoimmune myocarditis. These findings may provide clues for the pathogenesis of myocarditis. And the study showed that urine can be a good source of myocarditis biomarkers.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 1555135 MEDLINE  
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[PMID]: 29524643
[Au] Autor:Onishi O; Ikoma K; Oda R; Yamazaki T; Fujiwara H; Yamada S; Tanaka M; Kubo T
[Ad] Address:Department of Orthopaedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 602-8566 465, Kajiicho, Kamigyo-ku Kyoto-shi, Kyoto, Japan. Electronic address: pni_oki@yahoo.co.jp.
[Ti] Title:Sequential Variation in Brain Functional Magnetic Resonance Imaging After Peripheral Nerve Injury: A Rat Study.
[So] Source:Neurosci Lett;, 2018 Mar 07.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Although treatment protocols are available, patients experience both acute neuropathic pain and chronic neuropathic pain, hyperalgesia, and allodynia after peripheral nerve injury. The purpose of this study was to identify the brain regions activated after peripheral nerve injury using functional magnetic resonance imaging (fMRI) sequentially and assess the relevance of the imaging results using histological findings. To model peripheral nerve injury in male Sprague-Dawley rats, the right sciatic nerve was crushed using an aneurysm clip, under general anesthesia. We used a 7.04T MRI system. T weighted image, coronal slice, repetition time, 7 ms; echo time, 3.3 ms; field of view, 30 mm  30 mm; pixel matrix, 64  64 by zero-filling; slice thickness, 2 mm; numbers of slices, 9; numbers of average, 2; and flip angle, 8 degrees. fMR images were acquired during electrical stimulation to the rat's foot sole; after 90 min, c-Fos immunohistochemical staining of the brain was performed in rats with induced peripheral nerve injury for 3, 6, and 9 weeks. Data were pre-processed by realignment in the Statistical Parametric Mapping 8 software. A General Linear Model first level analysis was used to obtain T-values. One week after the injury, significant changes were detected in the cingulate cortex, insular cortex, amygdala, and basal ganglia; at 6 weeks, the brain regions with significant changes in signal density were contracted; at 9 weeks, the amygdala and hippocampus showed activation. Histological findings of the rat brain supported the fMRI findings. We detected sequential activation in the rat brain using fMRI after sciatic nerve injury. Many brain regions were activated during the acute stage of peripheral nerve injury. Conversely, during the chronic stage, activation of the amygdala and hippocampus may be related to chronic-stage hyperalgesia, allodynia, and chronic neuropathic pain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 1555135 MEDLINE  
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[PMID]: 29524607
[Au] Autor:Khodamoradi M; Ghazvini H; Esmaeili-Mahani S; Shahveisi K; Farnia V; Zhaleh H; Abdoli N; Akbarnejad Z; Saadati H; Sheibani V
[Ad] Address:Substance Abuse Prevention Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.
[Ti] Title:Genistein attenuates seizure-induced hippocampal brain-derived neurotrophic factor overexpression in ovariectomized rats.
[So] Source:J Chem Neuroanat;, 2018 Mar 07.
[Is] ISSN:1873-6300
[Cp] Country of publication:Netherlands
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 1555135 MEDLINE  
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[PMID]: 29524570
[Au] Autor:Su B; Guan Q; Wang M; Liu N; Wei X; Wang S; Yang X; Jiang W; Xu M; Yu S
[Ad] Address:School of Public Health, Shandong University, Jinan 250012, PR China.
[Ti] Title:Calpeptin is neuroprotective against acrylamide-induced neuropathy in rats.
[So] Source:Toxicology;, 2018 Mar 07.
[Is] ISSN:1879-3185
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:The aim of this study is to explore the potent neuroprotective effect of calpeptin (CP) on neuron damage induced by acrylamide (ACR) and its mechanism. Behavioural indicators such as hind limb splay, rota-rod performance, and gait analysis were assessed weekly to evaluate neurobehavioural changes after ACR and/or CP administration. The histopathological alterations and the changes of -calpain, m-calpain, microtubule-associated protein 2 (MAP2), and α-tubulin and -tubulin protein levels in spinal cord were determined. Results showed that after administration of 30 mg/kg ACR, decreased body weight, attenuated neurobehavioural function, injury of motor neuron, increased protein levels of m-calpain and -tubulin, suppressed MAP2 protein level, and no significant changes of -calpain and α-tubulin protein levels were observed compared with the control group rats. After administration of 200 g/kg CP, partially restored body weight and neurobehavioural function, improvement of motor neuron injury, decreased protein levels of m- calpain and -tubulin, and reversed effects of MAP2 protein level were observed compared with the ACR group rats. Our results suggested that CP alleviates neuropathy induced by ACR in rats. The calpain's overactivation causes the degrading of MAP2 and eventually leads to the destruction of microtubules (MTs), which may be one of the mechanisms of cytoskeletal damage induced by ACR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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