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| 1 | Role of mitochondria in cell apoptosis during hepatic ischemia-reperfusion injury and protective effect of ischemic postconditioning显示文摘AIM: To investigate the role of mitochondria in cell apoptosis during hepatic ischemia-reperfusion injury and protective effect of ischemic postconditioning (IPC).METHODS: A rat model of acute hepatic ischemia-reperfusion was established, 24 healthy male Wistar rats were randomly divided into sham-operated group, ischemia-reperfusion group (IR) and IPC group. IPC was achieved by several brief pre-reperfusions followed by a persistent reperfusion.Concentration of malondialdehyde (MDA) and activity of several antioxidant enzymes in hepatic tissue were measured respectively. Apoptotic cells were detected by TdT-mediated dUTP-biotin nick end labeling (TUNEL) and expression of Bcl-2 protein was measured by immunohistochemical techniques. Moreover, mitochondrial ultrastructure and parameters of morphology of the above groups were observed by electron microscope.RESULTS: Compared with IR group, the concentration of MDA and the hepatocellular apoptotic index in IPC group was significantly reduced (P<0.05), while the activity of antioxidant enzymes and OD value of Bcl-2 protein were markedly enhanced (P<0.05). Moreover, the injury of mitochondrial ultrastructure in IPC group was also obviously relieved.CONCLUSION: IPC can depress the synthesis of oxygen free radicals to protect the mitochondrial ultrastructure and increase the expression of Bcl-2 protein that lies across the mitochondrial membrane. Consequently, IPC can reduce hepatocellular apoptosis after reperfusion and has a protective effect on hepatic ischemia-reperfusion injury. | KaiSun Zhi-SuLiu QuanSun | 2004 | World Journal of Gastroenterology2004，10，13： | 86 |
| 2 | Protective effect of doxorubicin induced heat shock protein 72 on cold preservation injury of rat livers显示文摘AIM: To observe the protective effect of heat shock protein 72 (HSP 72) induced by pretreatment of doxorubicin (DXR) on long-term cold preservation injury of rat livers.METHODS: Sprague-Dawley rats were administered intravenously DXR at a dose of 1 mg/kg body mass in DXR group and saline in control group. After 48 h, the rat liver was perfused with cold Linger's and University of Wisconsin (UW) solutions and then was preserved in UW solution at 4℃ for 24, 36 and 48 h. AST, ALT, LDH and hyaluronic acid in preservative solution were determined. Routine HE,immunohistochemical staining for HSP 72 and electron microscopic examination of hepatic tissues were performed.RESULTS: After 24, 36 and 48 h, the levels of AST, ALT and hyaluronic acid in preservative solution were significantly higher in control group than in DXR group (P<0.05), while LDH level was not significantly different between the 2 groups (P>0.05). Hepatic tissues in DXR group were morphologically normal and significantly injured in control group. HSP 72 was expressed in hepatocytes and sinusoidal endothelial cells in DXR group but not in control group.CONCLUSION: Pretreatment of DXR may extend the time of rat liver cold preservation and keep liver alive. The expression of HSP 72 in liver can prevent hepatocytes and sinusoidal endothelial cells from long-term cold preservation injury. | HaoChen Ying-YanYu Ming-JunZhang Xia-XingDeng Wei-PingYang JunJi Cheng-HongPeng Hong-WeiLi | 2004 | World Journal of Gastroenterology2004，10，9： | 5 |
| 3 | Effect of atrial natriuretic peptide on ischemia-reperfusion injury in a porcine total hepatic vascular exclusion model显示文摘AIM: To evaluate the effect of ANP on warm I/R injury in a porcine THVE model. METHODS: Miniature pigs (mini-pigs) weighing 16-24 kg were observed for 120 min after reperfusion following 120 min of THVE. The animals were divided into two groups. ANP (0.1 μg/kg per min) was administered to the ANP group (n = 7), and vehicle was administered to the control group (n = 7). Either vehicle or ANP was intravenously administered from 30 min before the THVE to the end of the experiment. Arterial blood was collected to measure AST, LDH, and TNF-α. Hepatic tissue blood ? ow (HTBF) was also measured. Liver specimens were harvested for p38 MAPK analysis and histological study. Those results were compared between the two groups. RESULTS: The AST and LDH levels were lower in the ANP group than in the control group; the AST levels were signifi cantly different between the two groups (60 min: 568.7 ± 113.3 vs 321.6 ± 60.1, P = 0.038 < 0.05, 120 min: 673.6 ± 148.2 vs 281.1 ± 44.8, P = 0.004 < 0.01). No signifi cant difference was observed in the TNF-α levels between the two groups. HTBF was higher in the ANP group, but the difference was not signif icant. A signifi cantly higher level of phosphorylated p38 MAPK was observed in the ANP group compared to the controlgroup (0 min: 2.92 ± 1.1 vs 6.38 ± 1.1, P = 0.011 < 0.05).Histological tissue damage was milder in the ANP group than in the control group. CONCLUSION: Our results show that ANP has a protective role in I/R injury with p38 MAPK activation in a porcine THVE model. | Katsumi Kobayashi Kiyohiro Oshima Masato Muraoka Takahiko Akao Osamu Totsuka Hisashi Shimizu Hiroaki Sato Kazumi Tanaka Kenjiro Konno Koshi Matsumoto Izumi Takeyoshi | 2007 | World Journal of Gastroenterology2007，13，25： | 4 |
| 4 | p38MAPK信号通路与肝缺血再灌注损伤的关系研究显示文摘p38MAPK通路参与诸如细胞氧化应激、细胞凋亡和炎症等多种生理和病理过程并在其中起着重要作用。肝缺血再灌注损伤(HIRI)是肝脏外科手术面临的一大难题,由于HIRI发病机制复杂,临床上尚未发现更好的应对HIRI的防治策略。本文就p38MAPK信号通路的主要功能及其在HIRI中的相关作用作一综述,以便为防治HIRI提供一个新的思路。 | 谭金锋 崔晓光 | 2014 | 胃肠病学和肝病学杂志2014，23，1： | 3 |
| 5 | 冷保存再灌注期间离体肝组织内氧自由基及[Ca^(2+)]_i 对 p38MAPK激活的影响显示文摘目的:了解离体肝脏缺血再灌注期间氧自由基及钙离子超载是否是激活 p38MAPK 的因素之一,为进一步揭示肝脏缺血再灌注损伤的信号转导机制打下基础.方法:通过自行建立的兔离体肝脏缺血再灌注模型,根据冷保存液中别嘌呤醇浓度的不同分为 A、B、C、D4组;根据冷保仔液中维拉帕米浓度的不同又分为 E、F、G、H4组;分别于离体前、冷保存末及再灌注5min、10min、60min、120min 获取离体肝组织,分别应用免疫映迹杂交(westem-blot)和免疫沉淀法测定磷酸化 p38MAPK 的表达及活性水平;并进行肝组织内氧自由基(oxygen free radicals,OFR) 含量的测定(A、B、C、D组);用 Fura-2/AM 负载法进行肝细胞内钙离子浓度测定(A、E、F、G 组).结果:于再灌注5min 各组离体肝组织的氧自由基水平升高至峰值,但各组两两之间存在显著性差异(A、D、C、D组:2.32±0.22,1.82±0.15,1.63±0.11,1.29±0.10,P<0.05,t=2.57);于再灌注10min 供肝组织 p38MAPK磷酸化水平及活性均升高至峰值,但各组两两之间存在显著性差异(A、B、C、D 组 p38MAPK 磷酸化水平:76.2±7.0,61.4±5.9,47.3±2.5,37.7±3.0,P<0.05,t=2.61;A、B、C、D 组 p38MAPK 活性水平:82.7±6.8,69.7±5.2, 54.5±5.5,41.2±3.1,P<0.05,t=2.61;A、E、F、G 组 p38MAPK 磷酸化水平:80.3±8.7,63.3±42,50.4±5.6,39.2±5.7,P<0.05,t=2.61;A、E、F、G 组p38MPK 活性水平:80.8±8.9,66.7±4.2,53.7±4.1,39.4±5.5,P<0.05,t=2.61);再灌注5min 时氧自由基及[Ca^(2+)]_i越高的离体肝,则再灌注10min 时离体肝组织p38活性峰值越高,二者之间呈显著性相关关系.(P<0.05,R_(OFR)=0.976,R_(Ca)=0.970)结论:别嘌呤醇能显著性抑制离体肝缺血再灌注期间肝组织内 OFR 水平,而维拉帕米能显著性抑制离体肝缺血再灌注期间肝细胞内钙离子浓度超载;而且 OFR 水平及钙离子与离体肝组织 p38MAPK 的激活密切相关. | 王雨 田伏洲 汤礼军 张晓琼 | 2003 | 世界华人消化杂志2003，11，11： | 1 |
| 6 | 阿片类药物预处理对肝缺血再灌注损伤保护机制的研究进展显示文摘肝缺血再灌注损伤(IRI)是一种病理过程,与肝组织坏死、细胞凋亡、肝功能下降甚至衰竭密切相关,常因肝手术中肝门阻断而发生,严重影响手术预后。因此国内外学者对如何减轻肝IRI进行了一系列研究。阿片类药物预处理是近年来新兴的减轻脏器IRI的处理方式,通过缺血前预先给予阿片类药物处理来提高器官对缺血和低氧的耐受性。 | 郑斐 杨玲 雷航燕 | 2016 | 临床医药实践2016，25，4： | 1 |
| 7 | 心钠素预处理对大鼠肝脏缺血再灌注损伤的影响显示文摘目的:探讨心钠素(ANP)预处理对肝脏缺血再灌注损伤的影响。方法:30只雄性SD大鼠随机均分为3组:假手术组(SO组)、缺血再灌注组(IR组)和ANP预处理组。IR组和ANP预处理组分别经门静脉注入生理盐水、1mg/L的ANP3mL/kg,然后阻断左、中叶肝蒂45min,造成70%肝脏缺血,SO组仅行分离而不阻断,再恢复供血40min,采集下腔静脉血测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)水平,取肝组织测定超氧化物歧化酶(SOD)与丙二醛(MDA)水平,并行肝组织病理学观察。结果:IR组和ANP预处理组缺血再灌注后血清ALT、AST、LDH水平及肝组织MDA含量均高于SO组,肝组织SOD含量低于SO组;ANP预处理组血清ALT、AST、LDH水平及肝组织MDA含量低于IR组,肝组织SOD含量则高于IR组;ANP预处理组肝细胞形态学异常改变较IR组明显减轻。结论:ANP预处理可减轻大鼠肝脏缺血再灌注损伤,其机制可能与提高肝组织SOD含量,抑制脂质过氧化,保护线粒体有关。 | 周凯亮 庞志刚 刘超 王广田 尚闯 | 2008 | 郑州大学学报(医学版)2008，43，4： | 0 |
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