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Do-Sung Kim Ki-Chan Ha Dae-Young Kwon Myung-Sunny Kim Hyung-Ryong Kim Soo-Wan Chae 《Immunopharmacology and immunotoxicology》2013,35(2):257-270
This study examined whether or not the ER stress and Bcl-2 proteins are linked to the protective effect of kaempferol, a phytoestrogen, on ischemia-reperfusion (I/R)-induced cardiac damage. In order to determine if kaempferol modifies the I/R-induced response in H9c2 cardiac muscle cells, the cells were exposed to kaempferol followed by ischemia 12h/reperfusion 4h. kaempferol had a protective effect on the apoptosis induced by I/R in the cardiac muscle cells. The Kaempferol treatment significantly increased the expression level of the anti-apoptotic protein, Bcl-2, but decreased the level of the pro-apoptotic protein, bax. Kaempferol down-regulated the expressions of the endoplasmic reticulum (ER) stress proteins, GRP78, ATF-6alpha, XBP-2, IRE1-alpha, phosphor-eIF-2alpha and CHOP. In ex vivo-Langendorff experiment, the kaempferol treatment regulated the expression of ER stress proteins-CHOP and GRP78. The kaempferol also improved the post-ischemic LVEDP and LVDP significantly after 20, 30, 40 and 50 min of reperfusion compared with the untreated control hearts, which shows that kaempferol offers protection against I/R-associated cardiac dysfunction. 相似文献
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天麻对大鼠肾缺血再灌注损伤中SOD、MDA作用的研究 总被引:2,自引:0,他引:2
目的 探讨天麻在大鼠肾缺血再灌注损伤中的抗氧化作用 .方法 通过建立大鼠急性肾缺血再灌注损伤模型 ,测定天麻对肾缺血再灌注后肾组织SOD活力与MDA含量的变化 .结果 与对照组相比 ,使用天麻后 ,在再灌注 6h、12h和 2 4h后肾组织SOD活力明显升高 (p值分别 <0 .0 1,0 .0 5 ,0 .0 1) ,MDA含量明显降低 (p值分别 <0 .0 5 ,0 .0 1,0 .0 5 ) .结论 天麻在大鼠肾缺血再灌注损伤模型中 ,有抗自由基损伤和减轻脂质过氧化的作用 . 相似文献
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Ernesto Perez-Chanona Marcus Mühlbauer Christian Jobin 《The American journal of pathology》2014,184(11):2965-2975
Nucleotide-binding oligomerization domain-containing protein 2 (NOD2), an intracellular pattern recognition receptor, induces autophagy on detection of muramyl dipeptide (MDP), a component of microbial cell walls. The role of bacteria and NOD2 signaling toward ischemia/reperfusion (I/R)–induced intestinal injury response is unknown. Herein, we report that I/R-induced intestinal injury in germ-free (GF) C57BL/6 wild-type (WT) mice is worse than in conventionally derived mice. More important, microbiota-mediated protection against I/R-induced intestinal injury is abrogated in conventionally derived Nod2−/− mice and GF Nod2−/− mice. Also, WT mice raised in specific pathogen-free (SPF) conditions fared better against I/R-induced injury than SPF Nod2−/− mice. Moreover, SPF WT mice i.p. administered 10 mg/kg MDP were protected against injury compared with mice administered the inactive enantiomer, l-MDP, an effect lost in Nod2−/− mice. However, MDP administration failed to protect GF mice from I/R-induced intestinal injury compared with control, a phenomenon correlating with undetectable Nod2 mRNA level in the epithelium of GF mice. More important, the autophagy-inducer rapamycin protected Nod2−/− mice against I/R-induced injury and increased the levels of LC3+ puncta in injured tissue of Nod2−/− mice. These findings demonstrate that NOD2 protects against I/R and promotes wound healing, likely through the induction of the autophagy response.The epithelium lining the intestinal track is composed of a single layer sheet of epithelial cells that provides nutrient absorption, hormone secretion, and innate immune sampling of luminal contents.1,2 In addition, the epithelium provides a physical barrier between the host and gut microbes, where intestinal epithelial cells (IECs) are stitched together by tight junctions that maintain the architecture of the epithelial sheet and prevent uncontrolled access of luminal content (eg, microbes and dietary toxins) to subepithelial tissues.3 The epithelium is preserved by the homeostatic migration and proliferation of IECs from the base of the intestinal crypts to tips of the villi. Events that disrupt this equilibrium could have deleterious consequences for the host, as seen in patients experiencing intestinal ischemia.4Ischemia occurs when blood supply to the small bowel is occluded, which is followed by reperfusion, the return of blood flood flow, and simultaneous re-oxygenation of the tissue. During ischemia, an imbalance of metabolic demand and supply results in hypoxic response with activation of hypoxia-inducible factor-1 as well as cell death programs,5 autophagy,6–8 and necrosis (organelle swelling and plasma membrane rupturing).4,9 Paradoxically, the restoration of blood flow causes the release of inflammatory mediators, such as IL-6, tumor necrosis factor-α, and IL-1β, which exacerbate the injury.4 As a result, extra-intestinal organs, such as liver and the lung, may experience inflammatory activation and fatal multiorgan dysfunction syndrome. In the clinic, causes of intestinal ischemia/reperfusion (I/R)–induced injury include atherosclerosis, hypotension, blood clots, hernias, cardiac and mesenteric surgery, venous thrombosis, and necrotizing enterocolitis.Nucleotide-binding oligomerization domain-containing protein 2 (NOD2) is a pattern-recognition receptor whose function is the intracellular reconnaissance of pathogen-associated molecular patterns. NOD2 is important for the recognition of muramyl dipeptide, MDP, a component of peptidoglycan that is present in the cell walls of Gram-positive and Gram-negative bacteria. Loss-of-function mutations of NOD2 have been associated with Crohn''s disease and, recently, NOD2-associated autoinflammatory disease.10 The mechanism by which NOD2 maintains intestinal homeostasis has yet to be clearly defined, although a current paradigm suggests an involvement of this innate sensor in controlling microbial composition,11,12 likely through expression of antimicrobial peptides from Paneth cells.13 In addition, NOD2 is implicated in other important biological responses, such as inflammasome activation14 and autophagy.6 More important, in a preclinical model of necrotizing enterocolitis, NOD2 signaling was shown to protect against hypoxic stress through down-regulation of the Toll-like receptor (TLR) 4 pathway.15 However, the role of commensal bacteria and NOD2 signaling in intestinal I/R injury response has not been elucidated.A balance between innate inflammatory responses and cytoprotective mechanisms dictates the extent of end-organ damage during I/R injury. During injury-induced hypoxic stress, cells undergo a prosurvival process called autophagy.16 This autophagic response occurs on inhibition of mammalian target of rapamycin, thereby inducing the encapsulation of cytoplasmic components in a double membrane (autophagosome), which is delivered to the lysosome for degradation.16 In hepatic ischemia, autophagy has been shown to be a protective mechanism that favors cell survival and proliferation,8 two key processes in epithelial injury response. Interestingly, NOD2 recruits ATG16L1 to the plasma membrane to initiate autophagosome formation in response to MDP and at the site of Shigella flexneri entry.17 However, the role of commensal bacteria–induced autophagy in the context of hypoxic stress and intestinal damage is currently unknown.Herein, we investigated the role of microbes and NOD2 signaling in I/R-induced intestinal injury using germ-free (GF) and conventionally derived (CONV-D) Nod2−/− mice. We demonstrate that microbes are important for optimal intestinal response to injury, an effect mediated by NOD2 signaling. 相似文献
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E. A. Antipenko A. V. Gustov K. S. Davydova E. V. Krylova 《Bulletin of experimental biology and medicine》2009,147(1):24-25
We studied the effect of antioxidant therapy on the state of glutathione system in erythrocytes in patients with stage 1,
2, and 3 circulatory encephalopathy treated with antioxidant cytoflavin against the background of basic therapy (kavinton
and pyracetam). It was demonstrated that the response of the erythrocyte glutathione system to antioxidant therapy was quantitatively
and qualitatively different at different stages of cerebrovascular failure, which was related to changes in the glutathione
system during the development of chronic cerebral ischemia. Endogenous reserve of the antioxidant defense system should be
taken into account when prescribing antioxidant therapy; the glutathione system can be a marker of this reserve.
Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 147, No. 1, pp. 25–26, January, 2009 相似文献
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Zhou Ling Yang Xinlu Shu Shuhua Wang Sheng Guo Fenglin Yin Ying Zhou Weide Han Han Chai Xiaoqing 《Inflammation》2021,44(3):1160-1174
Inflammation - Liver ischemia-reperfusion (I/R) injury is a pathological process that often occurs during liver and trauma surgery. This study aimed to investigate the protective effect and... 相似文献
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Podkolzin AA Dontsov VI Chernilevskii VE Megreladze AG Mrakaeva OS Zhukova EA 《Bulletin of experimental biology and medicine》2001,131(1):53-55
Electrochemically activated systems normalized activity of antioxidant enzymes catalase, peroxidase, and superoxide dismutase. The baseline activity of antioxidant enzymes considerably varies in humans and animals. This effect of electrochemically activated systems having negative oxidation-reduction potential was probably related to a training effect of excess electrons. 相似文献
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Zharikova G. V. Zharikov A. Yu. Mazko O. N. Makarova O. G. Bobrov I. P. Kalnitsky A. S. 《Bulletin of experimental biology and medicine》2022,173(2):210-214
Bulletin of Experimental Biology and Medicine - We studied the effect of tripeptide Leu-Ile-Lys on kidney function in rats with experimental diabetes mellitus modeled by single intraperitoneal... 相似文献
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Activation of Lysosomal Enzymes in Rabies-Infected Tissue Culture Cells Without Accompanying Cytopathic Effect 下载免费PDF全文
Lactic dehydrogenase and beta-glucuronidase were assayed in tissue culture fluids and cellular lysates, respectively, from BHK-21/13S and Iota cell cultures infected with rabies virus. Activation of lysosomal enzymes was shown from the day 4 of infection on, without any indication of cytopathic effect. 相似文献
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丹参对左肾静脉狭窄大鼠肾脏氧化应激及组织纤维化的影响 总被引:1,自引:1,他引:1
目的:探讨丹参治疗左肾静脉狭窄大鼠肾脏过氧化损伤和纤维化的效果,为临床药物治疗左肾静脉受压综合征提供实验依据。方法:将大鼠分为3组,假手术组、模型组和丹参治疗组。采用左肾静脉不全结扎的方法建立大鼠左肾静脉狭窄模型,用丹参进行干预,于治疗6周后处死动物,取肾组织制备匀浆查超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,免疫组化法检测转化生长因子-β1(TGF-β1)和I型纤溶酶原激活物抑制因子(PAI-1)的表达。结果:模型组大鼠较假手术组左肾组织MDA含量显著增高,SOD活性显著降低,TGF-β1和PAI-1表达增加。丹参治疗可降低MDA含量,提高SOD的活性,减少TGF-β1和PAI-1的表达。结论:左肾静脉狭窄大鼠肾脏氧自由基生成增多,抗氧化能力下降,肾组织纤维化增多,丹参可通过消除氧自由基,提高抗氧化能力,减少组织纤维化来保护肾脏。 相似文献
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目的:研究肝缺血/再灌注损伤(I/R)对肺组织结构和leptin蛋白表达的影响,探讨leptln与肝I/R后肺损伤的联系。方法:建立大鼠70%肝I/R模型,设立假手术、缺血60min/再灌注60min(I60’R60’)、I60’R150’、I60’R240’、I60’R360’等实验组,每组9只大鼠。于相应时间点采集肺组织,分别用石蜡切片H.E.染色和免疫组化法观察肺组织结构和leptin蛋白表达的变化。结果:肝I/R对肺组织造成损害,随着再灌注时间的延长发生不同程度的改变。与假手术组肺leptin蛋白表达水平相比,四个损伤组均显著降低。四个损伤组之间leptin蛋白表达两两相比均有显著差异,以I60’R150’组最高,I60’R60’、I60’R360’、I60’R240’组依次递减。结论:肝I/R造成肺组织结构不同程度的损害,并直接抑制了肺leptin蛋白的表达,提示leptin与肝I/R后的肺损伤存在密切的联系。 相似文献
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应用显微外科技术建立大鼠肾冷缺血/移植再灌注模型。移植再灌注1小时组,肾皮质微粒体丙二醛含量明显高于对照组,而肾组织匀浆还原型谷胱甘肽水平降低。提示氧自由基引起的脂质过氧化作用在肾缺血时是重要的,更重要的损伤发生在1小时的再灌注期。 相似文献
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山莨菪碱对过度训练大鼠急性肾损伤的保护作用 总被引:24,自引:0,他引:24
目的 研究过度训练致急性肾损伤的特点及山莨菪碱的保护作用。方法 采用大鼠游泳至力竭建立过度训练致急性肾损伤模型。将大鼠随机分为7组,即安静对照组、力竭即刻组、力竭6h组、力竭12h组、力竭24h组、山莨菪碱6h组、山莨菪碱24h组,用全自动生化仪检测各组大鼠血Cr、Ur、CK及尿γ-GT的改变;光镜观察各组肾组织结构的改变:用TUNEL法检测各组大鼠肾组织细胞凋亡,采用图像分析仪计算肾组织细胞凋亡率。结果 力竭后大鼠站立不稳,对声光刺激反应淡漠。力竭后即刻组大鼠血Ur、CK明显升高(P〈0.05),力竭6h后血Ur、CK继续升高(P〈0.01),力竭12h后血ur、Cr、CK均有所下降,尿γ-GT明显升高(P〈0.01),力竭24h后血Ur、Cr、CK均恢复到正常,尿γ-GT继续升高(P〈0.01)。光镜下力竭后即刻组大鼠肾组织结构仅见部分肾小球囊及肾小管扩张.在皮髓质交界处及髓质小血管内可见大量红细胞堆积,力竭12h大鼠可见肾小管上皮细胞刷状缘不规整,部分脱落,肾小管管腔内可见颗粒管型和透明管型,在皮髓质交界处及髓质可见大量细胞核深染,有固缩现象;力竭后即刻、6、12、24h组大鼠肾组织凋亡细胞数逐渐增多,多位于皮髓质交界处及髓质的肾小管和集合管,各组大鼠尿γ-GT与肾组织细胞凋亡率有明显相关性(P〈0.01)。应用山莨菪碱后,力竭大鼠精神状态较好,游泳时间明显延长(P〈0.01);力竭后6h及24h血Ur、Cr、CK及尿γ-GT均明显降低(P〈0.05),肾组织结构改善,肾组织凋亡细胞数明显减少。结论 过度训练可引起急性肾损伤,肾组织细胞捌亡是其损伤的主要表现形式:山莨菪碱可提高运动能力,同时可减少肾组织细胞凋亡,进而对肾损伤起到明显的保护作用。 相似文献