Clinical and Experimental Pharmacology and Physiology最新文献_第10页

Interactive effects of morphine and dopamine receptor agonists on spatial recognition memory in mice. 吗啡和多巴胺受体激动剂对小鼠空间识别记忆的交互作用。

4区医学

Clinical and Experimental Pharmacology and Physiology Pub Date : 2018-04-01 Epub Date: 2017-12-19 DOI: 10.1111/1440-1681.12889

Yanmei Chen, Yu Fu, Yingjie An, Jun Cao, Jianhong Wang, Jichuan Zhang

{"title":"Interactive effects of morphine and dopamine receptor agonists on spatial recognition memory in mice.","authors":"Yanmei Chen, Yu Fu, Yingjie An, Jun Cao, Jianhong Wang, Jichuan Zhang","doi":"10.1111/1440-1681.12889","DOIUrl":"https://doi.org/10.1111/1440-1681.12889","url":null,"abstract":"Both opiates and dopamine play important roles in learning and memory. Although synergistic action between these two neurotransmitters has been found, their functional roles remain unclear. Here, low dose morphine (2.5 mg/kg) and low dose dopamine receptor agonists (apomorphine 0.05 mg/kg; SKF38393 0.01 mg/kg; bromocriptine 0.05 mg/kg), which have no effects on spatial recognition memory, were injected intraperitoneally into mice 30 minutes before a memory test in a two-trial recognition Y-maze. The Y-maze is based on the innate tendency of rodents to explore novel environments and is therefore suitable for exploring the effects of morphine on learning and memory. Our results showed that both D1-like and D2-like dopamine receptor agonists dose-dependently impaired the retrieval of spatial recognition memory in the Y-maze, and co-administration of memory ineffective doses of apomorphine (0.05 mg/kg), SKF38393 (0.01 mg/kg), or bromocriptine (0.05 mg/kg) and of morphine (2.5 mg/kg) resulted in impaired spatial recognition memory retrieval in mice. These findings suggest the existence of interactions between morphine and dopamine receptor agonists in memory processing and that activation of the dopamine system might contribute to morphine-induced impairment of memory, which could provide insight into human addiction.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"45 4","pages":"335-343"},"PeriodicalIF":0.0,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/1440-1681.12889","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35233386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Diastolic dysfunction in pulmonary artery hypertension: Creatine kinase and the potential therapeutic benefit of beta-blockers. 肺动脉高压的舒张功能障碍：肌酸激酶和β受体阻滞剂的潜在治疗益处。

IF 2.4 4区医学

Clinical and Experimental Pharmacology and Physiology Pub Date : 2018-04-01 Epub Date: 2018-01-10 DOI: 10.1111/1440-1681.12898

Ewan D Fowler, Mark J Drinkhill, Rachel Stones, Ed White

{"title":"Diastolic dysfunction in pulmonary artery hypertension: Creatine kinase and the potential therapeutic benefit of beta-blockers.","authors":"Ewan D Fowler, Mark J Drinkhill, Rachel Stones, Ed White","doi":"10.1111/1440-1681.12898","DOIUrl":"10.1111/1440-1681.12898","url":null,"abstract":"Passive properties of the myocardium influence diastolic filling and cardiac output. In heart failure, changes in contributors to the passive properties of the ventricle, such as titin and collagen, and loss of the metabolic enzyme creatine kinase, increase resistance to filling resulting in diastolic dysfunction. Pulmonary artery hypertension (PAH) arises from interactions between the pulmonary vasculature and the right ventricle (RV) which ultimately leads to RV failure. Beta1-adrenergic receptor blockers (BB) act on the myocardium and are beneficial in left heart failure but are not used in PAH. We investigated whether BB improved survival and RV function in a rat model of PAH. Rats were injected with monocrotaline (60 mg/kg) to induce PAH and RV failure, or saline as controls (CON). When PAH was established, rats were treated with metoprolol (10 mg/kg per day) (MCT+BB) or vehicle (sucrose) (MCT); CON were treated with vehicle. In vivo measurement of RV compliance using pressure-volume catheter, indicated diastolic dysfunction in the RV of MCT rats was improved with BB treatment. Expression of creatine kinase protein and mRNA was lower in MCT rats compared to CON, with a trend for reversion by BB treatment. Isolated CON RV myocytes had a positive contraction response to faster pacing, whereas it was negative in MCT. MCT+BB cells had an intermediate response, indicating improved ability to respond to increased demand. BB improved diastolic function, partially restored metabolic enzymes and augmented contractility in PAH. These data support the hypothesis that BB may be beneficial in PAH by supporting RV function.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"45 4","pages":"384-389"},"PeriodicalIF":2.4,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5887930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35300688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The neuronal and endocrine roles of RCAN1 in health and disease. RCAN1在健康和疾病中的神经元和内分泌作用。

4区医学

Clinical and Experimental Pharmacology and Physiology Pub Date : 2018-04-01 Epub Date: 2017-11-29 DOI: 10.1111/1440-1681.12884

Heshan Peiris, Damien J Keating

{"title":"The neuronal and endocrine roles of RCAN1 in health and disease.","authors":"Heshan Peiris, Damien J Keating","doi":"10.1111/1440-1681.12884","DOIUrl":"https://doi.org/10.1111/1440-1681.12884","url":null,"abstract":"The regulator of calcineurin 1 (RCAN1) was first discovered as a gene located on human chromosome 21, expressed in neurons and overexpressed in the brains of Down syndrome individuals. Increased expression of RCAN1 has been linked with not only Down syndrome-associated pathology but also an associated neurological disorder, Alzheimer's Disease, in which neuronal RCAN1 expression is also increased. RCAN1 has additionally been demonstrated to affect other cell types including endocrine cells, with links to the pathogenesis of β-cell dysfunction in type 2 diabetes. The primary functions of RCAN1 relate to the inhibition of the phosphatase calcineurin, and to the regulation of mitochondrial function. Various forms of cellular stress such as reactive oxygen species and hyperglycaemia cause transient increases in RCAN1 expression. The short term (hours to days) induction of RCAN1 expression is generally thought to have a protective effect by regulating the expression of pro-survival genes in multiple cell types, many of which are mediated via the calcineurin/NFAT transcriptional pathway. However, strong evidence also supports the notion that chronic (weeks-years) overexpression of RCAN1 has a detrimental effect on cells and that this may drive pathophysiological changes in neurons and endocrine cells linked to Down syndrome, Alzheimer's Disease and type 2 diabetes. Here we review the evidence related to these roles of RCAN1 in neurons and endocrine cells and their relationship to these human health disorders.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"45 4","pages":"377-383"},"PeriodicalIF":0.0,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/1440-1681.12884","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35214298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 24

Regulation of thyroid sodium-iodide symporter in different stages of goiter: Possible involvement of reactive oxygen species. 甲状腺碘化钠同转运体在甲状腺肿不同阶段的调节:活性氧的可能参与。

4区医学

Clinical and Experimental Pharmacology and Physiology Pub Date : 2018-04-01 Epub Date: 2017-12-19 DOI: 10.1111/1440-1681.12887

Lívia P L Matos, Ricardo Cortez Cardoso Penha, Luciene C Cardoso-Weide, Mariana L Freitas, Diorney L S G Silva, Andrea C F Ferreira

{"title":"Regulation of thyroid sodium-iodide symporter in different stages of goiter: Possible involvement of reactive oxygen species.","authors":"Lívia P L Matos, Ricardo Cortez Cardoso Penha, Luciene C Cardoso-Weide, Mariana L Freitas, Diorney L S G Silva, Andrea C F Ferreira","doi":"10.1111/1440-1681.12887","DOIUrl":"https://doi.org/10.1111/1440-1681.12887","url":null,"abstract":"Na+ /I- symporter (NIS) transports iodide into thyrocytes, a fundamental step for thyroid hormone biosynthesis. Our aim was to evaluate NIS regulation in different status of goitrogenesis and its underlying mechanisms. Wistar rats were treated with methimazole (MMI) for 5 and 21 days, to achieve different status of goiter. We then evaluated the effect of MMI removal for 1 day (R1d), after 5 (R1d-5d) or 21 (R1d-21d) days of MMI treatment. MMI increased thyroid weight, iodide uptake and in vitro TPO activity in a time-dependent way. Although MMI removal evoked a rapid normalization of TPO activity in R1d-5d, it was still high in R1d-21d. On the other hand, iodide uptake was rapidly down-regulated in R1d-21d, but not in R1d-5d, suggesting that the increased TPO activity in R1d-21d led to increased intraglandular organified iodine (I-X), which is known to inhibit iodide uptake. Since TGFβ has been shown to mediate some effects of I-X, we evaluated TGFβ and TGFβ receptor mRNA levels, which were increased in R1d-21d. Moreover, it has been demonstrated that TGFβ stimulates NOX4. Accordingly, our data revealed increased NOX4 expression and H2 O2 generation in R1d-21d. Finally, we evaluated the effect of H2 O2 on NIS function and mRNA levels in PCCL3 thyroid cell line, which were reduced. Thus, the present study suggests that there is a relationship between the size of the goiter and NIS regulation and that the mechanism might involve I-X, TGFβ, NOX4 and increased ROS production.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"45 4","pages":"326-334"},"PeriodicalIF":0.0,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/1440-1681.12887","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35233391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Inhibitory effect of naringenin via IL-13 level regulation on thymic stromal lymphopoietin-induced inflammatory reactions. 柚皮素通过调节IL-13水平抑制胸腺基质淋巴生成素诱导的炎症反应。

4区医学

Clinical and Experimental Pharmacology and Physiology Pub Date : 2018-04-01 Epub Date: 2017-11-29 DOI: 10.1111/1440-1681.12880

Na-Ra Han, Phil-Dong Moon, Ka-Jung Ryu, Na-Rae Kim, Hyung-Min Kim, Hyun-Ja Jeong

{"title":"Inhibitory effect of naringenin via IL-13 level regulation on thymic stromal lymphopoietin-induced inflammatory reactions.","authors":"Na-Ra Han, Phil-Dong Moon, Ka-Jung Ryu, Na-Rae Kim, Hyung-Min Kim, Hyun-Ja Jeong","doi":"10.1111/1440-1681.12880","DOIUrl":"https://doi.org/10.1111/1440-1681.12880","url":null,"abstract":"Naringenin (NG) has various beneficial properties, such as anti-cancer and anti-inflammatory effects. Thymic stromal lymphopoietin (TSLP) induces mast cell proliferation and inflammatory reactions. The aim of this study was to investigate the regulatory effect of NG on TSLP-induced mast cell proliferation and inflammatory reactions using human mast cell line (HMC-1) cells. HMC-1 cells were pre-treated with NG and then treated with TSLP. HMC-1 cells proliferation was determined by quantifying bromodeoxyuridine incorporation. Levels of anti-apoptotic and pro-apoptotic factors were analyzed by western blot analysis. The productions and mRNA expressions of interleukin (IL)-13 and tumour necrosis factor-α (TNF-α) were analyzed by ELISA and quantitative real-time PCR. We found that NG significantly attenuated HMC-1 cells proliferation and Ki-67 mRNA expression promoted by TSLP. NG significantly suppressed mRNA expression of TSLP receptor and IL-7 receptor α in TSLP-treated HMC-1 cells. NG significantly down-regulated levels of phosphorylated-signal transducer and activation of transcription 6 and murine double-minute 2 in TSLP-treated HMC-1 cells, up-regulated levels of cleaved poly ADP-ribose polymerase and p53 in TSLP-treated HMC-1 cells. Furthermore, NG significantly decreased the productions and mRNA expressions of IL-13 and TNF-α in TSLP-treated HMC-1 cells. These results suggest NG has an inhibitory effect on mast cell-mediated allergic inflammatory reactions.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"45 4","pages":"362-369"},"PeriodicalIF":0.0,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/1440-1681.12880","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35299539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Involvement of NF-κB in the upregulation of cystathionine-γ-lyase, a hydrogen sulfide-forming enzyme, and bladder pain accompanying cystitis in mice. NF-κB参与半胱硫氨酸-γ-裂解酶(一种硫化氢形成酶)的上调和小鼠膀胱炎伴膀胱疼痛。

4区医学

Clinical and Experimental Pharmacology and Physiology Pub Date : 2018-04-01 Epub Date: 2017-12-11 DOI: 10.1111/1440-1681.12875

Tomoka Ozaki, Maho Tsubota, Fumiko Sekiguchi, Atsufumi Kawabata

{"title":"Involvement of NF-κB in the upregulation of cystathionine-γ-lyase, a hydrogen sulfide-forming enzyme, and bladder pain accompanying cystitis in mice.","authors":"Tomoka Ozaki, Maho Tsubota, Fumiko Sekiguchi, Atsufumi Kawabata","doi":"10.1111/1440-1681.12875","DOIUrl":"https://doi.org/10.1111/1440-1681.12875","url":null,"abstract":"Hydrogen sulfide (H2 S) is generated from l-cysteine by multiple enzymes including cystathionine-γ-lyase (CSE), and promotes nociception by targeting multiple molecules such as Cav 3.2 T-type Ca2+ channels. Bladder pain accompanying cyclophosphamide (CPA)-induced cystitis in mice has been shown to involve the functional upregulation of the CSE/H2 S/Cav 3.2 pathway. Therefore, we investigated whether NF-κB, as an upstream signal of the CSE/H2 S system, contributes to bladder pain in mice with CPA-induced cystitis. Bladder pain-like nociceptive behaviour was observed in CPA-treated mice, and referred hyperalgesia was evaluated by the von Frey test. Isolated bladder weights were assessed to estimate bladder swelling, and protein levels were measured by Western blotting. CPA, administered intraperitoneally, induced nociceptive behaviour, referred hyperalgesia and increased bladder weights in mice. β-Cyano-l-alanine, a reversible selective CSE inhibitor, prevented CPA-induced nociceptive behaviour, referred hyperalgesia, and, in part, increases in bladder weight. CPA markedly increased phosphorylated NF-κB p65 levels in the bladder, an effect that was prevented by pyrrolidine dithiocarbamate (PDTC), an NF-κB inhibitor. PDTC and curcumin, which inhibits NF-κB signals, abolished CPA-induced nociceptive behaviour, referred hyperalgesia and, in part, increases in bladder weight. CPA caused the overexpression of CSE in the bladder, and this was prevented by PDTC or curcumin. The CPA-induced activation of NF-κB signals appeared to cause CSE overexpression in the bladder, contributing to bladder pain and in part swelling, possibly through H2 S/Cav 3.2 signaling. Therefore, NF-κB-inhibiting compounds including curcumin may be useful for the treatment of cystitis-related bladder pain.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"45 4","pages":"355-361"},"PeriodicalIF":0.0,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/1440-1681.12875","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35461978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

Anti-angiogenesis effect of β-D-mannuronic acid (M2000) as a novel NSAID with immunosuppressive properties under experimental model. 具有免疫抑制作用的新型非甾体抗炎药β- d -甘露醛酸(M2000)的抗血管生成实验研究

4区医学

Clinical and Experimental Pharmacology and Physiology Pub Date : 2018-04-01 Epub Date: 2018-02-04 DOI: 10.1111/1440-1681.12907

Mohsen Rastegari-Pouyani, Ali Mostafaie, Kamran Mansouri, Seyed Shahabeddin Mortazavi-Jahromi, Hamid-Reza Mohammadi-Motlagh, Abbas Mirshafiey

{"title":"Anti-angiogenesis effect of β-D-mannuronic acid (M2000) as a novel NSAID with immunosuppressive properties under experimental model.","authors":"Mohsen Rastegari-Pouyani, Ali Mostafaie, Kamran Mansouri, Seyed Shahabeddin Mortazavi-Jahromi, Hamid-Reza Mohammadi-Motlagh, Abbas Mirshafiey","doi":"10.1111/1440-1681.12907","DOIUrl":"https://doi.org/10.1111/1440-1681.12907","url":null,"abstract":"Angiogenesis is a process through which new capillaries are formed from pre-existing ones, which contributes significantly to the pathogenesis of numerous diseases, such as cancer and chronic inflammatory disorders. The β-D-mannuronic acid (M2000) is a novel non-steroidal anti-inflammatory drug (NSAID) with immunosuppressive effects and is a matrix metalloproteinase (MMP) inhibitor. This research aimed to study the anti-angiogenesis effects of M2000 under in vitro and in vivo models. The cytotoxic and anti-proliferative effects of M2000 were examined using the trypan blue method and the MTT assay, respectively. The 3D collagen-cytodex model and the chick chorioallantoic membrane (CAM) assay were then used to evaluate the anti-angiogenesis property of M2000. Cytotoxicity assay revealed that M2000 (at concentrations of less than 100 μg/mL) had no cytotoxic effect on human umbilical vein endothelial cells (HUVECs). It was also illustrated that M2000 had little or no anti-proliferative effect on HUVECs. In addition, the anti-angiogenesis effects of M2000 were shown to be marginal in the in vitro model and both significant and dose-dependent in the in vivo status. This study showed that M2000 could be considered as an anti-angiogenic molecule which more likely exerts its activity mainly via indirect effects on endothelial cells and its anti-inflammatory effects may partly be attributable to its anti-angiogenic activity. Therefore, it could be recommended as a candidate for prevention and treatment of cancer, chronic inflammatory diseases, and other angiogenesis-related disorders.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"45 4","pages":"370-376"},"PeriodicalIF":0.0,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/1440-1681.12907","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35678555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12

Co-ingestion of aspirin and acetaminophen promoting fulminant liver failure: A critical review of Reye syndrome in the current perspective at the dawn of the 21st century. 阿司匹林和对乙酰氨基酚共同摄入促进暴发性肝衰竭:21世纪初当前视角下Reye综合征的重要回顾。

4区医学

Clinical and Experimental Pharmacology and Physiology Pub Date : 2018-02-01 Epub Date: 2017-12-04 DOI: 10.1111/1440-1681.12861

Deepak Dinakaran, Consolato M Sergi

{"title":"Co-ingestion of aspirin and acetaminophen promoting fulminant liver failure: A critical review of Reye syndrome in the current perspective at the dawn of the 21st century.","authors":"Deepak Dinakaran, Consolato M Sergi","doi":"10.1111/1440-1681.12861","DOIUrl":"https://doi.org/10.1111/1440-1681.12861","url":null,"abstract":"In the paediatric population, there is some evidence of possible interaction, synergism, and co‐toxicity of aspirin and acetaminophen. The toxicity of salicylates such as aspirin in this population is well known and documented, specifically in the form of Reye syndrome. The possible toxic synergism with aspirin and acetaminophen, however, is not previously described; though case reports suggest such co‐toxicities with low levels of aspirin and other compounds can exist. In vitro studies into mechanistic processes of salicylate toxicity propose that there is a bi‐directional link and potentiation with glutathione (GSH) depletion and salicylate toxicity. Data may suggest a plausible explanation for salicylate and acetaminophen toxic synergism. Further studies investigating this potential toxic synergism are warranted. Given the lack of awareness in the clinical community about potential toxic synergism between these relatively common medications, caution is advised in the co‐administration of these drugs, particularly in communities using natural or alternative therapy.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"45 2","pages":"117-121"},"PeriodicalIF":0.0,"publicationDate":"2018-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/1440-1681.12861","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35543236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 16

The effect of enoxaparin on seroma and mesh-tissue adhesion in a hernia model. 依诺肝素对疝模型血清肿及网状组织粘连的影响。

4区医学

Clinical and Experimental Pharmacology and Physiology Pub Date : 2016-07-01 DOI: 10.1111/1440-1681.12582

Ziya T Ozkececi, Yucel Gonul, Afra Karavelioglu, Mehmet F Bozkurt, Emre Kacar, Ahmet Bal, Mustafa Ozsoy, Ozan Turamanlar, Bahadir Celep

{"title":"The effect of enoxaparin on seroma and mesh-tissue adhesion in a hernia model.","authors":"Ziya T Ozkececi, Yucel Gonul, Afra Karavelioglu, Mehmet F Bozkurt, Emre Kacar, Ahmet Bal, Mustafa Ozsoy, Ozan Turamanlar, Bahadir Celep","doi":"10.1111/1440-1681.12582","DOIUrl":"https://doi.org/10.1111/1440-1681.12582","url":null,"abstract":"The aim of this study was to investigate whether enoxaparin (ENX) administration would increase seroma risk and worsen mesh tissue recovery in an experimental rat hernia repair model. Fifty-six adult male Wistar-Albino rats were included in the study. Rats were equally and randomly separated into seven groups: Group 1, Control, only subcutaneous dissection was performed; group 2, Sham, Hernia defect was primary sutured; Group 3, Prolene mesh; Group 4, Dual mesh; Group 5, ENX + Sham; Group 6, ENX + Prolene mesh; Group 7, ENX + Dual mesh. ENX was subcutaneously injected at a dose of 180 U/kg per day for 7 days. Rats were killed after the amount of subcutaneous seroma was determined by ultrasound on day 7 following the surgical procedure. Mesh-tissue healing was evaluated using histopathological and immunohistochemical (CD31) staining methods. The mean seroma amount significantly increased in Groups 5-7 compared to Groups 2-4. CD31 immunostaining showed a reduction in neovascularization in Groups 6 and 7, compared to Groups 3 and 4. Neovascularization decreased and hemorrhage, necrosis and oedema findings remarkably increased in Groups 6 and 7, when compared to Groups 3 and 4. Fibroblastic activity and inflammation were more prominent in Groups 3 and 4. It should be kept in mind that ENX interferes with inflammation, which is desired in the early period of healing and leads to an increase in overall seroma amount with anti-coagulant effects, which in turn may disrupt wound healing and mesh-tissue adhesions, as was indicated in our study.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"43 7","pages":"690-7"},"PeriodicalIF":0.0,"publicationDate":"2016-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/1440-1681.12582","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34333105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Role of tumour necrosis factor-a in the regulation of T-type calcium channel current in HL-1 cells. 肿瘤坏死因子-a在HL-1细胞t型钙通道电流调节中的作用

4区医学

Clinical and Experimental Pharmacology and Physiology Pub Date : 2016-07-01 DOI: 10.1111/1440-1681.12585

Fang Rao, Yu-Mei Xue, Wei Wei, Hui Yang, Fang-Zhou Liu, Shao-Xian Chen, Su-Juan Kuang, Jie-Ning Zhu, Shu-Lin Wu, Chun-Yu Deng

{"title":"Role of tumour necrosis factor-a in the regulation of T-type calcium channel current in HL-1 cells.","authors":"Fang Rao, Yu-Mei Xue, Wei Wei, Hui Yang, Fang-Zhou Liu, Shao-Xian Chen, Su-Juan Kuang, Jie-Ning Zhu, Shu-Lin Wu, Chun-Yu Deng","doi":"10.1111/1440-1681.12585","DOIUrl":"https://doi.org/10.1111/1440-1681.12585","url":null,"abstract":"Increasing evidence indicates that inflammation contributes to the initiation and perpetuation of atrial fibrillation (AF). Although tumour necrosis factor (TNF)-α levels are increased in patients with AF, the role of TNF-α in the pathogenesis of AF remains unclear. Besides L-type Ca(2+) currents (IC a,L ), T-type Ca(2+) currents (IC a,T ) also plays an important role in the pathogenesis of AF. This study was designed to use the whole-cell voltage-clamp technique and biochemical assays to explore if TNF-α is involved in the pathogenesis of AF through regulating IC a,T in atrial myocytes. It was found that compared with sinus rhythm (SR) controls, T-type calcium channel (TCC) subunit mRNA levels were decreased, while TNF-α expression levels were increased, in human atrial tissue from patients with AF. In murine atrial myocyte HL-1 cells, after culturing for 24 h, 12.5, 25 and 50 ng/mL TNF-α significantly reduced the protein expression levels of the TCC α1G subunit in a concentration-dependent manner. The peak current was reduced by the application of 12.5 or 25 ng/mL TNF-α in a concentration-dependent manner (from -15.08 ± 1.11 pA/pF in controls to -11.89 ± 0.83 pA/pF and -8.54 ± 1.55 pA/pF in 12.5 or 25 ng/mL TNF-α group respectively). TNF-α application also inhibited voltage-dependent inactivation of IC a,T, shifted the inactivation curve to the left. These results suggest that TNF-α is involved in the pathogenesis of AF, probably via decreasing IC a,T current density in atrium-derived myocytes through impaired channel function and down-regulation of channel protein expression. This pathway thus represents a potential pathogenic mechanism in AF.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"43 7","pages":"706-11"},"PeriodicalIF":0.0,"publicationDate":"2016-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/1440-1681.12585","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34495802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 14