Database : MEDLINE
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[PMID]: 29524517
[Au] Autor:Hong JM; Lee SM
[Ad] Address:School of Pharmacy, Sungkyunkwan University, Suwon, Gyeonggi-do 440-746, Republic of Korea.
[Ti] Title:Heme oxygenase-1 protects liver against ischemia/reperfusion injury via phosphoglycerate mutase family member 5-mediated mitochondrial quality control.
[So] Source:Life Sci;, 2018 Mar 07.
[Is] ISSN:1879-0631
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:AIMS: Heme oxygenase-1 (HO-1), an endogenous cytoprotective enzyme, is reported that can be localized in mitochondria under stress, contributing to preserve mitochondrial function. Mitochondrial quality control (QC) is essential to cellular health and recovery linked with redox homeostasis. Recent studies reported that phosphoglycerate mutase family member (PGAM) 5, a mitochondria-resident phosphatase, plays critical role in mitochondrial homeostasis. Therefore, we aim to investigate cytoprotective mechanisms of HO-1 in I/R-induced hepatic injury focusing on mitochondrial QC associated with PGAM5 signaling. MAIN METHODS: Mice were subjected to 60 min of hepatic ischemia followed by 6 h reperfusion and were pretreated twice with hemin (HO-1 inducer, 30 mg/kg) or zinc protoporphyrin (ZnPP; HO-1 inhibitor, 10 mg/kg) 16 and 3 h before ischemia. KEY FINDINGS: I/R increased hepatic and mitochondrial HO activity, which was augmented by hemin. I/R-induced hepatocellular and mitochondrial damages were attenuated by hemin and augmented by ZnPP. Meanwhile, I/R increased mitochondrial biogenesis, as evidenced by increased mitochondrial DNA contents and mitochondrial transcription factor A protein expression. Hemin augmented these results. I/R impaired mitophagy, as indicated by decreases in Parkin protein expression and the number of mitophagic vacuoles. These changes were attenuated by hemin. Hemin attenuated the I/R-induced increase in mitochondrial fission-related protein, dynamin-related protein 1, and the decrease in PGAM5 protein expression. Furthermore, PGAM5 siRNA abolished the effect of HO-1 on mitochondrial QC in HepG2 cells subjected to hypoxia/reoxygenation. SIGNIFICANCE: Our findings suggest that HO-1 protects against I/R-induced hepatic injury via regulation of mitochondrial QC by PGAM5 signaling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 253585 MEDLINE  
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[PMID]: 29516010
[Au] Autor:Liu J; Zhang KS; Hu B; Li SG; Li Q; Luo YP; Wang Y; Deng ZF
[Ad] Address:Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
[Ti] Title:Systematic Analysis of RNA Regulatory Network in Rat Brain after Ischemic Stroke.
[So] Source:Biomed Res Int;2018:8354350, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Although extensive studies have identified large number of microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) in ischemic stroke, the RNA regulation network response to focal ischemia remains poorly understood. In this study, we simultaneously interrogate the expression profiles of lncRNAs, miRNAs, and mRNAs changes during focal ischemia induced by transient middle cerebral artery occlusion. A set of 1924 novel lncRNAs were identified and may involve brain injury and DNA repair as revealed by coexpression network analysis. Furthermore, many short interspersed elements (SINE) mediated lncRNA:mRNA duplexes were identified, implying that lncRNAs mediate Staufen1-mediated mRNA decay (SMD) which may play a role during focal ischemia. Moreover, based on the competitive endogenous RNA (ceRNA) hypothesis, a stroke regulatory ceRNA network which reveals functional lncRNA:miRNA:mRNA interactions was revealed in ischemic stroke. In brief, this work reports a large number of novel lncRNAs responding to focal ischemia and constructs a systematic RNA regulation network which highlighted the role of ncRNAs in ischemic stroke.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/8354350

  3 / 253585 MEDLINE  
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[PMID]: 29511691
[Au] Autor:Guaricci AI; De Santis D; Carbone M; Muscogiuri G; Guglielmo M; Baggiano A; Serviddio G; Pontone G
[Ad] Address:Institute of Cardiovascular Disease, Department of Emergency and Organ Transplantation, University Hospital Policlinico of Bari, Bari, Italy.
[Ti] Title:Coronary Atherosclerosis Assessment by Coronary CT Angiography in Asymptomatic Diabetic Population: A Critical Systematic Review of the Literature and Future Perspectives.
[So] Source:Biomed Res Int;2018:8927281, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The prognostic impact of diabetes mellitus (DM) on cardiovascular outcomes is well known. As a consequence of previous studies showing the high incidence of coronary artery disease (CAD) in diabetic patients and the relatively poor outcome compared to nondiabetic populations, DM is considered as CAD equivalent which means that diabetic patients are labeled as asymptomatic individuals at high cardiovascular risk. Lessons learned from the analysis of prognostic studies over the past decade have challenged this dogma and now support the idea that diabetic population is not uniformly distributed in the highest risk box. Detecting CAD in asymptomatic high risk individuals is controversial and, what is more, in patients with diabetes is challenging, and that is why the reliability of traditional cardiac stress tests for detecting myocardial ischemia is limited. Cardiac computed tomography angiography (CCTA) represents an emerging noninvasive technique able to explore the atherosclerotic involvement of the coronary arteries and, thus, to distinguish different risk categories tailoring this evaluation on each patient. The aim of the review is to provide a wide overview on the clinical meaning of CCTA in this field and to integrate the anatomical information with a reliable therapeutic approach.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/8927281

  4 / 253585 MEDLINE  
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[PMID]: 29511679
[Au] Autor:Xu F; Liu X; Wang C; Dai C
[Ad] Address:Department of Hepatobiliary and Spleen Surgery, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning 110004, China.
[Ti] Title:Prostaglandin E1 Preconditioning Attenuates Liver Ischemia Reperfusion Injury in a Rat Model of Extrahepatic Cholestasis.
[So] Source:Biomed Res Int;2018:3812424, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The aim of this study is to explore the hepatoprotective effect of intraportal prostaglandin E1 (PGE1) on liver ischemia reperfusion (IR) injury using an extrahepatic cholestatic model, observing oxidative stress markers, proinflammatory factors, apoptotic marker proteins, and an adhesion molecule. The extrahepatic cholestatic model was induced by common bile duct ligation. After seven days, rats were subjected to ischemia by Pringle maneuver for 15 min, followed by 1, 6, or 24 h of reperfusion. Prostaglandin E1 (PGE group) or normal saline (NS group) was continuously infused from 15 min before liver ischemia to 1 h after reperfusion. After reperfusion, histopathological evaluation of the liver was performed, as were measurements of bilirubin, biochemical enzymes, oxidative stress markers (GSH and MDA), proinflammatory factors (MPO, TNF- , and IL-1 ), apoptotic marker proteins (Bcl-2 and Bax), and the adhesion molecule (ICAM-1). PGE1 pretreatment attenuated IR injury in extrahepatic cholestatic liver probably by suppressing MDA, MPO, TNF- , IL-1 , ICAM-1, and Bax levels and improving GSH and Bcl-2 levels. In conclusion, PGE1 protects extrahepatic cholestatic liver from IR injury by improving hepatic microcirculation and reducing oxidative stress damage, intrahepatic neutrophil infiltration, and hepatocyte apoptosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/3812424

  5 / 253585 MEDLINE  
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[PMID]: 29511370
[Au] Autor:Seo EH; Song GY; Namgung JH; Oh CS; Lee SH; Kim SH
[Ad] Address:BK21 Plus, Department of Cellular and Molecular Medicine, Konkuk University School of Medicine, Seoul, Korea.
[Ti] Title:Receptor for activated C kinase 1 in rats with ischemia-reperfusion injury: intravenous versus inhalation anaesthetic agents.
[So] Source:Int J Med Sci;15(4):352-358, 2018.
[Is] ISSN:1449-1907
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:: The study examined the difference in the expression of the receptor for activated C kinase 1 (RACK1) between anaesthesia with propofol and isoflurane in rats with myocardial ischemia-reperfusion injury (IRI). : Male Sprague-Dawley rats were studied. Anaesthesia was induced with xylazine 20 g/g by intraperitoneal injection and maintained with propofol or isoflurane. Myocardial IRI was induced by ligating the left anterior descending artery for 1 hour. Reactive oxygen species (ROS), cardiomyocyte apoptosis, the expression of RACK1 and toll-like receptor 4 (TLR4), and the heart injury score were compared between the two groups. : Cardiomyocyte apoptosis with ROS was significantly lower in the propofol group than in the isoflurane group. The propofol group had significantly higher RACK1 expression and lower TLR4 expression, compared with the isoflurane group (RACK1, 1970.50 120.50 . 1350.20 250.30, <0.05; TLR4, 980.50 110.75 . 1275.50 75.35, <0.05). However, the heart injury scores in the two groups did not differ significantly (3.56 0.29 . 4.33 0.23 in the propofol and isoflurane groups, respectively, =0.33). : There were significant differences in inflammation and apoptosis, including the expression of RACK1 and TLR4, after myocardial IRI between the propofol and isoflurane groups. However, both groups had similar heart injury scores.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.7150/ijms.22591

  6 / 253585 MEDLINE  
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[PMID]: 29501622
[Au] Autor:Yan YT; Li SD; Li C; Xiong YX; Lu XH; Zhou XF; Yang LQ; Pu LJ; Luo HY
[Ad] Address:Department of Pharmacology, College of Basic Medicine, Kunming Medical University, Kunming, Yunnan, PR China.
[Ti] Title:Panax notoginsenoside saponins Rb1 regulates the expressions of Akt/ mTOR/PTEN signals in the hippocampus after focal cerebral ischemia in rats.
[So] Source:Behav Brain Res;345:83-92, 2018 Mar 05.
[Is] ISSN:1872-7549
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Panax notoginsenoside saponins Rb1 (PNS-Rb1) is an important active ingredient of panax notoginseng for effective treatment of cerebrovascular diseases. However, the mechanism underlying its actions in the state of cerebral ischemia is still unclear. We asked whether the potential neuroprotection of PNS-Rb1 on the brain is due to, at least partially, its modulation of AkT/mTOR/PTEN signalling pathway along with down-regulation of caspase-3 in rats subjected to phototrombic stroke. To test this hypothesis, rats with induced photothrombotic stroke were treated with PNS-Rb1 (applied in three different doses, 25 mg/kg, 50 mg/kg,100 mg/kg, respectively) or saline, while sham operated rats injected with saline were used as the control. Our results indicate that PNS-Rb1 significantly alleviated the morphological lesion concomitant with improvement of cognitive and sensorimotor deficits induced by ischemic stroke. Moreover, immunohistochemistry and Western blot analyses showed that PNS Rb1 in a dose dependent manner increased the expressions of P-Akt, P-mTOR and reduced P-PTEN and caspase-3. The present study suggests that the improvement of cognitive and sensorimotor deficits by PNS-Rb1 is made, at least partially, by the modulation of the Akt/mTOR/PTEN signalling pathway.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 253585 MEDLINE  
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[PMID]: 29493564
[Au] Autor:He Q; Zhao X; Bi S; Cao Y
[Ad] Address:Department of Emergency Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China (mainland).
[Ti] Title:Pretreatment with Erythropoietin Attenuates Lung Ischemia/Reperfusion Injury via Toll-Like Receptor-4/Nuclear Factor-κB (TLR4/NF-κB) Pathway.
[So] Source:Med Sci Monit;24:1251-1257, 2018 Mar 01.
[Is] ISSN:1643-3750
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND Lung ischemia/reperfusion injury (LIRI) is a medical problem featuring pulmonary dysfunction and damage. The present study aimed to investigate the protective effects of erythropoietin (EPO), which has been reported to be an anti-inflammatory agent, on LIRI through inhibiting the TLR-4/NF-κB signaling pathway. MATERIAL AND METHODS All rats were randomly divided into 3 groups (n=8): a control group, a vehicle+LIRI group, and an EPO+LIRI group. LIRI included 90-min ischemia and 120-min reperfusion, while RhEpo was administered (3 kU/kg) intraperitoneally 2 h before the operation. Levels of pulmonary inflammatory responses were examined by analyzing pulmonary permeability index (PPI), oxygenation index, histology, and expressions of inflammatory cytokines. RESULTS Pretreatment with EPO significantly decreased lung W/D ratio, BALF leukocytes count and percentage, and PPI but increased oxygenation index compared with the LIRI group (P<0.05). More importantly, with EPO pretreatment there was less pathological damage compared with the vehicle group. Expressions of inflammatory cytokines (TNF-α, IL-6, and IL-1) in the serum were significantly lower in the EPO group than in the LIRI group (P<0.05). In addition, gene expression and protein expression of TLR-4 and NF-κB were significantly inhibited with EPO pretreatment compared with the LIRI group (P<0.05). CONCLUSIONS Our study id the first to report that EPO protects lung injuries after LIRI through inhibiting the TLR4-NF-κB signaling pathway, which provides solid evidence for the use of EPO as a therapeutic agent for treating LIRI in the future.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process

  8 / 253585 MEDLINE  
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[PMID]: 29480936
[Au] Autor:Tecuatl C; Herrrera-Lpez G; Martn-vila A; Yin B; Weber S; Barrionuevo G; Galvn EJ
[Ad] Address:Departamento de Farmacobiologa Centro de Investigacin y de Estudios Avanzados del, Instituto Politcnico Nacional Calzada de los Tenorios No. 235, Mxico City, 14330, Mxico.
[Ti] Title:TrkB-mediated activation of the phosphatidylinositol-3-kinase/Akt cascade reduces the damage inflicted by oxygen-glucose deprivation in area CA3 of the rat hippocampus.
[So] Source:Eur J Neurosci;, 2018 Feb 26.
[Is] ISSN:1460-9568
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:The selective vulnerability of hippocampal area CA1 to ischemia-induced injury is a well-known phenomenon. However, the cellular mechanisms that confer resistance to area CA3 against ischemic damage remain elusive. Here, we show that oxygen-glucose deprivation-reperfusion (OGD-RP), an in vitro model that mimic the pathological conditions of the ischemic stroke, increases the phosphorylation level of Tropomyosin-receptor-kinase B (TrkB) in area CA3. Slices preincubated with Brain-derived neurotrophic factor (BDNF) or 7,8-Dihydroxyflavone (7,8-DHF) exhibited reduced depression of the electrical activity triggered by OGD-RP. Consistently, blockade of TrkB suppressed the resistance of area CA3 to OGD-RP. The protective effect of TrkB activation was limited to area CA3, as OGD-RP caused permanent suppression of CA1 responses. At the cellular level, TrkB activation leads to phosphorylation of the accessory proteins SHC and Gab as well as the serine/threonine kinase Akt, members of the phosphoinositide 3-kinase/Akt (PI-3-K/Akt) pathway, a cascade involved in cell survival. Hence, acute slices pretreated with the Akt antagonist MK2206 in combination with BDNF lost the capability to resist the damage inflicted with OGD-RP. Consistently with these results, CA3 pyramidal cells exhibited reduced propidium iodide uptake and caspase-3 activity in slices pre-treated with BDNF and exposed to OGD-RP. We propose that PI-3-K/Akt downstream activation mediated by TrkB represents an endogenous mechanism responsible for the resistance of area CA3 to ischemic damage. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1111/ejn.13880

  9 / 253585 MEDLINE  
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[PMID]: 29477597
[Au] Autor:Masuko T; Takao K; Samejima K; Shirahata A; Igarashi K; Casero RA; Kizawa Y; Sugita Y
[Ad] Address:Laboratory of Physiology and Anatomy, School of Pharmacy, Nihon University, 7-7-1 Narashinodai, Funabashi, Chiba 274-8555, Japan.
[Ti] Title:N -Nonyl-1,4-diaminobutane ameliorates brain infarction size in photochemically induced thrombosis model mice.
[So] Source:Neurosci Lett;672:118-122, 2018 Feb 22.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Inhibitors for polyamine oxidizing enzymes, spermine oxidase (SMOX) and N -acetylpolyamine oxidase (PAOX), were designed and evaluated for their effectiveness in a photochemically induced thrombosis (PIT) mouse model. N -Nonyl-1,4-diaminobutane (C9-4) and N -tridecyl-1,4-diaminobutane (C13-4) competitively inhibited the activity of PAOX and SMOX in a manner comparable to N ,N -bis(2,3-butadienyl)-1,4-butanediamine (MDL72527), an irreversible inhibitor of both enzymes. The two compounds were then tested for their effects in the PIT model. Both intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) administration of C9-4 decreased infarct volumes significantly. By contrast, C13-4 reduced the volume of brain infarction by i.c.v. administration, but no reduction was observed after i.p. administration. C9-4 administered by i.p. injection reduced the volume of brain infarction significantly at doses of more than 3 mg/kg, and the dosage of 5 mg/kg or 10 mg/kg demonstrated the most potent effect and were more effective than equivalent doses of the other inhibitors such as MDL72527 and N-benzylhydroxylamine. I.P. injection of 5 mg/kg of C9-4 provided a therapeutic time window of longer than 12 h. This report demonstrates that C9-4 is a potent inhibitor of the polyamine oxidizing enzymes and is useful lead compound for candidate drugs with a long therapeutic time window, to be used in the treatment of ischemic stroke.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 253585 MEDLINE  
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[PMID]: 29471086
[Au] Autor:Sousa GA; Oliveira IS; Silva-Freitas FV; Viana AFSC; Neto BPS; Cunha FVM; Gonalves RLG; Lima Filho ACM; Amaral MPM; Oliveira RCM; Fernandes PD; Maciel JKS; da Silva TMS; Souza MFV; Oliveira FA
[Ad] Address:Medicinal Plants Research Center, Federal University of Piau, (unnumbered), 64049-550 Teresina, Piau, Brazil. Electronic address: glaukham@yahoo.com.
[Ti] Title:Gastroprotective effect of ethanol extracts of cladodes and roots of Pilosocereus gounellei (A. Weber ex K. Schum.) Bly. Ex Rowl (Cactaceae) on experimental ulcer models.
[So] Source:J Ethnopharmacol;218:100-108, 2018 Feb 19.
[Is] ISSN:1872-7573
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:ETHNOPHARMACOLOGICAL RELEVANCE: Pilosocereus gounellei Cactaceae), popularly known as "xique xique", is a species native from Caatinga region of Northeast Brazil, which is used by traditional communities in folk medicine for a variety of health problems, especially inflammatory processes and gastritis. AIM OF THE STUDY: The present study investigates the possible gastric antiulceractivity of ethanol extracts obtained from the cladodes and roots of Pilosocereus gounellei (EECPG and EERPG, respectively) and mechanisms of action underlying this effect. MATERIALS AND METHODS: Mice were used for the evaluation of the acute toxicity, and mice and rats to study the gastroprotective activity. The gastroprotective action of EECPG and EERPG was analyzed in the absolute ethanol in mice, ischemia-reperfusion and cold restraint stress in rats. In the investigation of the gastroprotective mechanisms of EECPG and EERPG, the participation of the NO and prostaglandins, the levels of the non-protein sulfhydril groups (NP-SH) and the catalase activity using the ethanol-induced gastric mucosa lesion model and the quantification of the gastric mucus and the antisecretory activity through pylorus ligature model in rats were analyzed. RESULTS: The animals did not present any signs of acute toxicity for the EECPG and EERPG, and it was not possible to calculate the DL50. EECPG and EERPG (200 and 400 mg/kg) exhibited a significant gastroprotective effect in absolute ethanol, ischemia-reperfusion-induced and cold restraint stress gastric lesion models. Gastroprotection of EECPG and EERPG (200 mg/kg) was significantly decreased in pre-treated mice with L-NAME. Our studies revealed that EECPG and EERPG (200 mg/kg) prevented the decrease of the non-protein sulfhydril groups (NPSH) and increased the catalase levels in ethanol-treated animals. However, the gastric secretion parameters (volume, [H+], pH) did not show any alteration. CONCLUSIONS: Our results indicate that the ethanolic extract from the cladodes and roots of Pilosocereus gounellei exhibits a significant gastroprotection, because it inhibits the formation of gastric lesions using different models. The participation of the nitric oxide, prostaglandins, the non-protein sulfhydril groups (NP-SH), catalase seem to be involved in the gastroprotection activity of the EECPG and EERPG. Nevertheless, this activity does not seem to be related to antisecretory mechanisms.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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