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Endogenously increased n-3 PUFA levels in fat-1 transgenic mice do not protect from non-alcoholic steatohepatitis

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Hepatobiliary Surgery and Nutrition 2019年第5期8卷 447-458页

作者： Marie Liebig Dirk Dannenberger Brigitte vollmar Kerstin Abshagen Rudolf-Zenker-Institute for Experimental Surgery University Medicine Rostock18057 RostockGermany Institute of Muscle Biology and Growth Leibniz Institute for Farm Animal Biology(FBN)18196 DummerstorfGermany

Background:Non-alcoholic fatty liver disease(NAFLD)is the most common chronic liver diseaseworldwide,ranging from simple steatosis to non-alcoholic steatohepatitis(NASH)and *** for the NAFLD epidemic in industrialized countries are the high intake of pro-inflammatory n-6polyunsaturated fatty acids(n-6 PUFAs)and low consumption of healthy n-3 *** to their antiinflammatoryproperties,n-3 PUFAs may have the potential to alleviate chronic liver ***,weexamined the therapeutic effect of increased n-3 PUFA tissue levels in fat-1 transgenic mice on ***:Disease was induced in mice by streptozotocin and high fat diet(STZ/HFD)resulting in *** in 6 and 8 weeks old wild type and fat-1 transgenic STZ/HFD treated mice was *** other mammals,fat-1 transgenic mice ubiquitously express an n-3 fatty acid desaturase,which converts n-6to n-3 PUFAs,leading to increased n-3 and decreased n-6 PUFA tissue ***:Liver damage,NAFLD activity score(NAS),hepatic lipid accumulation and inflammation weresignificantly reduced in fat-1 transgenic STZ/HFD treated mice in the early(6 weeks)but not late(8 weeks)phase of ***,mRNA expression of genes involved in fatty acid uptake and storage(Cd36and Plin3,respectively)was significantly down-regulated in 6 week old but not 8 week old fat-1 transgenicSTZ/HFD treated ***:Endogenously elevated n-3 PUFA levels in fat-1 transgenic mice transiently delay the onsetof STZ/HFD induced NASH but failed to efficiently protect from NASH development.

关键词： Non-alcoholic fatty liver disease(NAFLD) non-alcoholic steatohepatitis(NASH) n-6/n-3 fat-1 steatosis

Limited potential of resolvin D1 in treatment of cholestatic liver fibrosis

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Hepatobiliary Surgery and Nutrition 2020年第5期9卷 587-596页

作者： Kerstin Abshagen Alexander Hartmann Laura Grüner Marie Liebig Brigitte vollmar Institute for Experimental Surgery University Medicine RostockRostockGermany

Background:Several studies suggest a role for EPA-and DHA-derived pro-resolving mediators like resolvins in reversing metabolic and inflammatory disturbances seen in various chronic ***,we investigated the effects of resolvin D1(RvD1)on bile duct ligation(BDL)-induced cholestatic liver ***:Mice were treated daily with RvD1 or 0.1%ethanol(control)from the day of BDL until the final observation time *** and liver tissue were collected 2,5 and 14 days after BDL for different ***:RvD1 treatment of mice had no impact on the extent of cholestatic liver injury upon BDL,neither in the acute phase nor in the progressive state of liver *** RvD1 treatment resulted in a significantly reduced activity of hepatic stellate cells as well as reduced deposition of extracellular matrix 2 days after BDL,mice were not protected from inflammation and further fibrosis ***:These data indicate that RvD1 has a limited therapeutic potential to treat cholestatic liver diseases,as it has no significant impact on regression of hepatic necroinflammation and fibrotic changes in bile duct-ligated mice.

关键词： Lipid mediator n-3 polyunsaturated fatty acids bile duct ligation(BDL) mouse model

Impact of hyperglycemia on autoimmune pancreatitis and regulatory T-cells

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World Journal of Gastroenterology 2018年第28期24卷 3120-3129页

作者： Franz-Tassilo Müller-Graff Brit Fitzner Robert Jaster Brigitte vollmar Dietmar Zechner Institute for Experimental Surgery Rostock University Medical Center Division of Gastroenterology Department of Medicine Ⅱ Rostock University Medical Center

AIM To evaluate the influence of hyperglycemia on the progression of autoimmune *** We induced hyperglycemia by repetitive intraperitoneal(ip) injection of 50 mg/kg streptozotocin in MRL/Mp J mice, which develop autoimmune pancreatitis due to a genetic predisposition. We compared the extent of inflammation(histological score, CD3^+ lymphocytes, CD8^+ T-cells, CD4^+ T-cells, Foxp3^+ T-helper cells) in the pancreas of hyperglycemic and normoglycemic mice. We also analyzed the number of leukocytes, lymphocytes, granulocytes and monocytes in the blood. In addition, we determined the percentage of CD3^+ lymphocytes, CD8^+ T-cells, CD4^+ T-cells, Foxp3^+ T-helper cells, Foxp3^+ CD25^+ T-helper and Foxp3^+T-helper cells in the spleen by flow *** Treatment with streptozotocin caused a strong induction of hyperglycemia and a reduction in body weight(P < 0.001). Severe hyperglycemia did not, however, lead to an aggravation, but rather to a slight attenuation of autoimmune pancreatitis. In the pancreas, both the histological score of the pancreas as well as the number of CD3+ lymphocytes(P < 0.053) were decreased by hyperglycemia. No major changes in the percentage of CD8^+ T-cells, CD4^+ T-cells, Foxp3^+ T-helper cells were observed between hyperglycemic and normoglycemic mice. Hyperglycemia increased the numbers of leukocytes(P < 0.001), lymphocytes(P = 0.016), granulocytes and monocytes(P = 0.001) in the blood. Hyperglycemia also moderately reduced the percentage of CD3^+ lymphocytes(P = 0.057), significantly increased the percentage of Foxp3^+ T-helper cells(P = 0.018) and Foxp3^+ CD25^+ T-helper cells(P = 0.021) and reduced the percentage of Foxp3^+T-helper cells(P = 0.034) in the spleen. CONCLUSION Hyperglycemia does not aggravate but moderately attenuates autoimmune pancreatitis, possibly by increasing the percentage of regulatory T-cells in the spleen.

关键词： Autoimmune disease Diabetes Treg FoxP3 Autoimmune pancreatitis MRL/MpJ mice

Stimulation of p38 MAPK by hormal preconditioning with atrial natriuretic peptide

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World Journal of Gastroenterology 2002年第4期8卷 707-711页

作者： Alexandra K. Kiemer Stefanie Kulhanek-Heinze Tobias Gerwig Alexander L. Gerbes Angelika M. vollmar Department of Pharmacy Center of Drug ResearchUniversity of MunichGermany Department of Medicine ⅡKlinikum GrosshadernUniversity of MunichGermany Department of Medicine Ⅱ Klinikum GrosshadernUniversity of MunichGermany Department of Pharmacy Center of Drug ResearchUniversity of MunichGermany

AIM：Stress-activated signaling pathways responsible for hepatic ischemia reperfusion injury and their modulation by protective interventions are widely *** of rat livers with Atrial Natriuretic Peptide(ANP)attenuates ischemia reperfusion injury(Gerbes et ***1998,18:1309-1317),SinANP has recently been shown to be a regulator of the p38MAPKpathway in endothelial cells(Kiemer et ***2002,90:874-881).aim of this thudy was to investigate activities of MAPK during ischemia and reperfusion and effects of ANP on ***:Rat livers were perfused with KH-buffer in the presence or absence of ANP for 20min,kept in cold UWsloution for 24h,and reperfused forupto120min,Activities of p38MAPKand JNKwas determined by in vitro phosphorylation assays using MBP and c-jun as *** SDS/PAGE electrophoresis,gels were quantified by ***:Activity of p38MAPKin control organs decreased in the course of ischemia and reperfusion by85%,whereas ANPincreased p38 activity by up to *** of control livers increased in the course of ischemia and reperfusion by up to *** increase in JNK activrity was slightly elevated in ANP preconditioned ***:This work represents a systematic investigation of MAPK activation during liver ischemia and *** ANP,for the first time a pharmacological approach to modulate these central signal transduction molecules is presented.

关键词：血浆心纳素 p38MAPK 缺血预处理肝脏缺血

Hepatocyte cytoskeleton during ischemia and reperfusion -influence of ANP-mediated p38 MAPK activation

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World Journal of Gastroenterology 2005年第47期11卷 7418-7429页

作者： Melanie Keller Alexander L Gerbes Stefanie Kulhanek-Heinze Tobias Gerwig Uwe Grützner Nico van Rooijen Angelika M vollmar Alexandra K Kiemer Department of Pharmacy Centre of Drug ResearchUniversity of MunichButenandtstr. 5-1381377 MunichGermany Department of Medicine Ⅱ Klinikum GroβhadernUniversity of MunichMarchionistr. 1781377 MunichGermany Angelika M vollmar Alexandra K KiemerDepartment of PharmacyCentre of Drug ResearchUniversity of MunichButenandtstr. 5-1381377 MunichGermany Department of Pharmacy Centre of Drug ResearchUniversity of MunichButenandtstr. 5-1381377 MunichGermany Department of Medicine ⅡKlinikum GroβhadernUniversity of MunichMarchionistr. 1781377 MunichGermany Institute for Surgical Research Klinikum GroβhadernUniversity of MunichMarchionistr. 1781377 MunichGermany Vrije Universiteit VUMCDepartment of Molecular Cell BiologyFaculty of Medicine1081 BT AmsterdamThe Netherlands

AIM： To determine functional consequences of this activation, whereby we focused on a potential regulation of the hepatocyte cytoskeleton during ischernia and reperfusion. METHODS： For in vivo experiments, animals received ANP （5 μg/kg） intravenously. In a different experimental setting, isolated rat livers were perfused with KH-buffer ＋ANP （200 nmol/L）＋SB203580 （2 μmol/L）. Livers were then kept under ischernic conditions for 24 h, and either transplanted or reperfused. Actin, Hsp27, and phosphorylated Hsp27 were determined by Western blotting, p38 MAPK activity by in vitro phosphorylation assay. F-actin distribution was determined by confocal microscopy. RESULTS： We first confirmed that ANP preconditioning leads to an activation of p38 MAPK and observed alterations of the cytoskeleton in hepatocytes of ANP- preconditioned organs. ANP induced an increase of hepatic F-actin after ischemia, which could be prevented by the p38 MAPK inhibitor SB203580 but had no effect on bile flow. After ischemia untreated livers showed a translocation of Hsp27 towards the cytoskeleton and an increase in total Hsp27, whereas ANP preconditioning prohibited translocation but caused an augmentation of Hsp27 phosphorylation. This effect is also mediated via p38 MAPK, since it was abrogated by the p38 MAPK inhibitor SB203580. CONCLUSION： This study reveals that ANP-mediated p38 MAPK activation leads to changes in hepatocyte cytoskeleton involving an elevation of phosphorylated Hsp27 and thereby for the first time shows functional consequences of ANP-induced hepatic p38 MAPK activation.

关键词： Hormonal preconditioning Atrial natriuretic peptide Hsp 27 Actin Polymerization

PI 3-kinase pathway is responsible for antiapoptotic effects of atrial natriuretic peptide in rat liver transplantation

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World Journal of Gastroenterology 2006年第7期12卷 1049-1055页

作者： Uwe Grutzner Melanie Keller Michael Bach Alexandra K Kiemer Herbert Meissner Manfred Bilzer Stefan Zahler Alexander L Gerbes Angelika M vollmar Institute for Surgical Research Klinikum GroBhadernUniversity of MunichD-81377 MunichGermany Department of Pharmacy University of MunichD-81377 MunichGermany Department Institute of Pathology University of MunichD-81377 MunichGermany

AIM： To investigate the in vivo effect of atrial natriuretic peptide （ANP） and its signaling pathway during orthotopic rat liver transplantation.METHODS： Rats were infused with NaCI, ANP （5 μg/ kg）, wortmannin （WH, 16μg/kg）, or a combination of both for 20 min. Livers were stored in UW solution （4℃） for 24 h, transplanted and reperfused. Apoptosis was examined by caspase-3 activity and TUNEL staining. Phosphorylation of Akt and Bad was visualized by Western blotting and phospho-Akt-localization by confocal microscopy.RESULTS： ANP-pretreatment decreased caspase-3 activity and TUNELopositive cells after cold ischemia, indicating antiapoptotic effects of ANP in vivo. The an- tiapoptotic signaling of ANP was most likely caused by phosphorylation of Akt and Bad, since pretreatment with PI 3-kinase inhibitor WM abrogated the ANP-induced reduction of caspase-3 activity. Interestingly, analysis of liver tissue by confocal microscopy showed translocation of phosphorylated Akt to the plasma membrane of hepa- tocytes evoked by ANP.CONCLUSION： ANP activates the PI-3-kinase pathway in the liver in vivo leading to phosphorylation of Bad an event triggering antiapoptotic signaling cascade in ischemic liver.

关键词： Bad Apoptosis Hormonal preconditioning Ischemia reperfusion injury

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使用三维立体成像定义大脑负性运动皮质区

中山大学学报（医学科学版） 2008年第S2期29卷 12-14页

作者：林晶霞 vollmar C 广东医学院东莞松山湖校区心理学教研室广东东莞523000 慕尼黑大学附属医院神经外科

【目的】通过大脑硬膜下的电极刺激,精确地定义负性运动皮质区,进一步研究这些区域的临床意义。【方法】85名癫痫病人接受了大脑皮层的电刺激实验,其中12名病人出现了负性运动。我们用三维立体成像技术定义5名病人的负性运动功能区域,... 详细信息

【目的】通过大脑硬膜下的电极刺激,精确地定义负性运动皮质区,进一步研究这些区域的临床意义。【方法】85名癫痫病人接受了大脑皮层的电刺激实验,其中12名病人出现了负性运动。我们用三维立体成像技术定义5名病人的负性运动功能区域,这是三维立体成像技术首次使用于负性运动研究。【结果】在大脑外侧面,控制手臂和手指大部分负性运动的皮质广泛分布在大脑的初级运动皮质区,有一些分布在前运动皮质区和感觉功能皮质区。此外,我们还发现负性运动皮质区和前额部的眼动区有部分的重叠。在脑部的内侧面,负性运动皮质区主要分布在前运动皮质区的前端。【结论】负性运动皮质区与初级运动皮质区和感觉功能皮质区,以及前额部的眼动区存在着重叠分布。

关键词：三维成像负性运动癫痫

针刺治疗瑞士白种人无先兆型偏头痛的临床疗效观察

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针刺治疗瑞士白种人无先兆型偏头痛的临床疗效观察

作者： Jing vollmar（崔晶）成都中医药大学

学位级别：硕士

目的:观察并评价针刺疗法治疗瑞士白种人无先兆型偏头痛的临床疗效及安全性,进一步明确针刺疗法治疗瑞士白种人无先兆型偏头痛的临床疗效,探讨针刺疗法在治疗瑞士白种人无先兆型偏头痛中的可行性。方法:将符合纳入标准的65例患者,按随... 详细信息

目的:观察并评价针刺疗法治疗瑞士白种人无先兆型偏头痛的临床疗效及安全性,进一步明确针刺疗法治疗瑞士白种人无先兆型偏头痛的临床疗效,探讨针刺疗法在治疗瑞士白种人无先兆型偏头痛中的可行性。方法:将符合纳入标准的65例患者,按随机对照的方法,随机分成两组(针刺治疗组和等待治疗组),其中治疗组32例,等待治疗组33例。治疗组入组患者给予针刺治疗;等待治疗组患者在头痛发作时给予口服对乙酰氨基酚颗粒。于治疗结束时对两组分别进行临床疗效评价;并分别于治疗前、治疗后及治疗后第4周对两组患者的头痛发作次数、头痛程度、头痛持续时间及头痛伴随症状与视觉疼痛模拟评分量表(Visual Analogue Scale,VAS)及头痛强度分级标准进行临床疗效评价。结果:1.治疗前两组资料基线一致(P>0.05),具有可比性。2.治疗前、后两组患者的头痛发作次数、头痛程度、头痛持续时间及头痛伴随症状和VAS评分及头痛强度分级在治疗前、后间的差异均具有显著性(P0.05),在改善患者VAS)评分、头痛强度分级方面差异无显著性(P>0.05);治疗后,两组间临床疗效评价差异显著(P0.05)。5.两组安全性均较好。结论:1.针刺疗法可以有效治疗瑞士白种人无先兆型偏头痛,且优于等待治疗组的临床疗效。2.针刺疗法治疗瑞士人白种人无先兆型偏头痛在改善患者头痛发作次数与头痛持续时间方面与等待治疗组的疗效相当;在改善患者头痛程度及头痛伴随症状方面的疗效优于等待治疗组;在改善患者头痛发作次数、头痛程度及头痛伴随症状方面,针刺治疗组的近期疗效优于等待治疗组;在改善头痛持续时间方面,两组的近期疗效相当。针刺疗法治疗瑞士人白种人无先兆型偏头痛在改善患者VAS评分、头痛强度分级方面与等待治疗组的疗效、近期疗效相当。3.本试验中两组治疗方法的安全性、依从性均较好。

关键词：针刺瑞士白种人无先兆型偏头痛临床研究

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从中医美容浅析皮肤瘙痒与情志关系

亚太传统医药 2017年第1期13卷 86-87页

作者：任宏珊乔晓青 vollmar.Jing 刘宁成都中医药大学四川成都610000 瑞士Sina-Vita诊所

皮肤瘙痒症是困扰患者的重大问题,其引起的不适感和皮损严重影响美观和心态,进而影响患者的社会交往。瘙痒性皮肤病常久治不愈,易反复发作。发现临床上此类患者常伴随情绪异常,二者相互影响,加重病情。从中医美容角度阐述二者之间的关系... 详细信息

皮肤瘙痒症是困扰患者的重大问题,其引起的不适感和皮损严重影响美观和心态,进而影响患者的社会交往。瘙痒性皮肤病常久治不愈,易反复发作。发现临床上此类患者常伴随情绪异常,二者相互影响,加重病情。从中医美容角度阐述二者之间的关系,以期提供更好的治疗思路,广泛服务于临床。

关键词：皮肤瘙痒情绪中医美容