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Remote ischemic preconditioning protects liver ischemia-reperfusion injury by regulating eNOS-NO pathway and liver microRNA expressions in fatty liver rats

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Hepatobiliary & Pancreatic Diseases International 2017年第4期16卷 387-394页

作者： Yun-Fei Duan Yong An Feng Zhu Yong Jiang Department of Hepatobiliary Surgery The Third Affiliated Hospital of Soochow UniversityChangzhou 213003China

BACKGROUND: Ischemic preconditioning (IPC) is a strategy to reduce ischemia-reperfusion (I/R) injury. The protective effect of remote ischemic preconditioning (RIPC) on liver I/R injury is not clear. This study aimed to investigate the roles of RIPC in liver I/R in fatty liver rats and the involvement of endothelial nitric oxide synthase-nitric oxide (eNOS-NO) pathway and microRNA expressions in this process. METHODS: A total of 32 fatty rats were randomly divided into the sham group, I/R group, RIPC group and RIPC+I/R group. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and nitric oxide (NO) were measured. Hematoxylin-eosin staining was used to observe histological changes of liver tissues, TUNEL to detect hepatocyte apoptosis, and immunohistochemistry assay to detect heat shock protein 70 (HSP70) expression. Western blotting was used to detect liver inducible NOS (iNOS) and eNOS protein levels and realtime quantitative polymerase chain reaction to detect miR-34a, miR-122 and miR-27b expressions. RESULTS: Compared with the sham and RIPC groups, serum ALT, AST and iNOS in liver tissue were significantly higher in other two groups, while serum NO and eNOS in liver tissue were lower, and varying degrees of edema, degeneration and inflammatory cell infiltration were found. Cell apoptosis number was slightly lower in the RIPC+I/R group than that in I/R group. Compared with the sham group, HSP70 expressions were significantly increased in other three groups (all P<0.05). Compared with the sham and RIPC groups, elevated miR-34a expressions were found in I/R and RIPC+I/R groups (P<0.05). MiR-122 and miR-27b were found significantly decreased in I/R and RIPC+I/R groups compared with the sham and RIPC groups (all P<0.05). CONCLUSION: RIPC can reduce fatty liver I/R injury by affecting the eNOS-NO pathway and liver microRNA expressions.

关键词： fatty liver ischemia-reperfusion remote ischemic preconditioning nitric oxide heat shock protein 70 endothelial nitric oxide synthase inducible nitric oxide synthase liver microRNA

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Acacetin protects against cerebral ischemia-reperfusion injury via the NLRP3 signaling pathway

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Neural Regeneration Research 2019年第4期14卷 605-612页

作者： Juan Bu Shen Shi Hui-Qin Wang Xiao-Shan Niu Zong-Feng Zhao Wei-Dong Wu Xiao-Ling Zhang Zhi Ma Yan-Jun Zhang Hui Zhang Yi Zhu Clinical Research Center People's Hospital of Xinjiang Uygur Autonomous Region Laboratory Animal Research Center Center for Disease Control and Prevention Xinjiang Uygur Autonomous Region Department of Neurology People's Hospital of Xinjiang Uygur Autonomous Region

Acacetin(5,7-dihydroxy-4′-methoxyflavone), a potential neuroprotective agent, has an inhibitory effect on lipopolysaccharide-induced neuroinflammatory reactions. However, whether acacetin has an effect on inflammatory corpuscle 3(NLRP3) after cerebral ischemia-reperfusion injury has not been fully determined. This study used an improved suture method to establish a cerebral ischemia-reperfusion injury model in C57BL/6 mice. After ischemia with middle cerebral artery occlusion for 1 hour, reperfusion with intraperitoneal injection of 25 mg/kg of acacetin(acacetin group) or an equal volume of saline(0.1 mL/10 g, middle cerebral artery occlusion group) was used to investigate the effect of acacetin on cerebral ischemia-reperfusion injury. Infarct volume and neurological function scores were determined by 2,3,5-triphenyltetrazolium chloride staining and the Zea-Longa scoring method. Compared with the middle cerebral artery occlusion group, neurological function scores and cerebral infarction volumes were significantly reduced in the acacetin group. To understand the effect of acacetin on microglia-mediated inflammatory response after cerebral ischemia-reperfusion injury, immunohistochemistry for the microglia marker calcium adapter protein ionized calcium-binding adaptor molecule 1(Iba1) was examined in the hippocampus of ischemic brain tissue. In addition, tumor necrosis factor-α, interleukin-1β, and interleukin-6 expression in ischemic brain tissue of mice was quantified by enzyme-linked immunosorbent assay. Expression of Iba1, tumor necrosis factor-α, interleukin-1β and interleukin-6 was significantly lower in the acacetin group compared with the middle cerebral artery occlusion group. Western blot assay results showed that expression of Toll-like receptor 4, nuclear factor kappa B, NLRP3, procaspase-1, caspase-1, pro-interleukin-1β, and interleukin-1β were significantly lower in the acacetin group compared with the middle cerebral artery occlusion group. Our finding

关键词： nerve regeneration acacetin cerebral ischemia-reperfusion injury microglia NLRP3 inflammasome inflammatory factor infarct volume signaling pathway nuclear factor-κB neuroprotection neural regeneration

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Hydrogen-rich saline protects against hepatic injury induced by ischemia-reperfusion and laparoscopic hepatectomy in swine

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Hepatobiliary & Pancreatic Diseases International 2019年第1期18卷 48-61页

作者： Yan-Song Ge Qian-Zhen Zhang Hui Li Ge Bai Zhi-Hui Jiao Hong-Bin Wang College of Veterinary Medicine Northeast Agricultural University

Background: Hydrogen-rich saline(HRS) has antioxidative, anti-inflammatory and anti-apoptotic properties. We investigated the effects of hydrogen on hepatic ischemia-reperfusion(I/R) and laparoscopic hepatectomy in swine. Methods: Twenty-one healthy Bama miniature pigs were randomly divided into the sham group, ischemia-reperfusion injury(IRI) group, HRS-5(5 m L/kg) group, and HRS-10(10 m L/kg) group. HRS was injected through the portal vein 10 min before reperfusion and at postoperative day 1, 2 and 3. The roles of HRS on oxidative stress, inflammatory response and liver regeneration were studied. Results: Compared with the IRI group, HRS treatment attenuated oxidative stress by increasing catalase activity and reducing myeloperoxidase. White blood cells in the HRS-10 group were reduced compared with the IRI group( P < 0.01). In the HRS-10 group, interleukin-1 beta, interleukin-6 and tumor necrosis factor alpha, C-reactive protein and cortisol were downregulated, whereas interleukin-10 was upregulated. In addition, HRS attenuated endothelial cell injury and promoted the secretion of angiogenic cytokines, including vascular endothelial growth factor, angiopoietin-1 and angiopoietin-2. HRS elevated the levels of hepatocyte growth factor, Cyclin D1, proliferating cell nuclear antigen, Ki-67 and reduced the secretion of transforming growth factor-beta. Conclusions: HRS treatment may exert a protective effect against I/R and hepatectomy-induced hepatic damage by reducing oxidative stress, suppressing the inflammatory response and promoting liver regeneration.

关键词： Hydrogen-rich saline Laparoscopic hepatectomy ischemia-reperfusion Oxidative stress Inflammation Regeneration

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Heme oxygenase system in hepatic ischemia-reperfusion injury

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World Journal of Gastroenterology 2010年第48期16卷 6068-6078页

作者： James A Richards Stephen J Wigmore Luke R Devey Centre for Inflammation Research The University of EdinburghThe Queen's Medical Research Institute

Hepatic ischemia-reperfusion injury (IRI) limits access to transplantation. Heme oxygenase-1 (HO-1) is a powerful antioxidant enzyme which degrades free heme into biliverdin,free iron and carbon monoxide. HO-1 and its metabolites have the ability to modulate a wide variety of inflammatory disorders including hepatic IRI. Mechanisms of this protective effect include reduction of oxygen free radicals,alteration of macrophage and T cell phenotype. Further work is required to understand the physiological importance of the many actions of HO-1 identified experimentally,and to harness the protective effect of HO-1 for therapeutic potential.

关键词： ischemia-reperfusion injury Heme oxygenase Transplantation Ischemic pre-conditioning

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MicroRNA regulatory pattern in spinal cord ischemia-reperfusion injury

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Neural Regeneration Research 2020年第11期15卷 2123-2130页

作者： Zhi-Gang Liu Yin Li Jian-Hang Jiao Hao Long Zhuo-Yuan Xin Xiao-Yu Yang Department of Orthopedics The Second Hospital of Jilin UniversityChangchunJilin ProvinceChina School of Public Health Jilin UniversityChangchunJilin ProvinceChina Pain Clinic The Sixth Affiliated Hospital of Xinjiang Medical UniversityUrumqiXinjiang Uygur Autonomous RegionChina The Key Laboratory of Zoonosis Search Chinese Ministry of EducationCollege of Basic MedicineJilin UniversityChangchunJilin ProvinceChina

After spinal cord injury, dysregulated miRNAs appear and can participate in inflammatory responses, as well as the inhibition of apoptosis and axon regeneration through multiple pathways. However, the functions of miRNAs in spinal cord ischemia-reperfusion injury progression remain unclear. miRCURY LNATM Arrays were used to analyze miRNA expression profiles of rats after 90 minutes of ischemia followed by reperfusion for 24 and 48 hours. Furthermore, subsequent construction of aberrantly expressed miRNA regulatory patterns involved cell survival, proliferation, and apoptosis. Remarkably, the mitogen-activated protein kinase(MAPK) signaling pathway was the most significantly enriched pathway among 24-and 48-hour groups. Bioinformatics analysis and quantitative reverse transcription polymerase chain reaction confirmed the persistent overexpression of miR-22-3 p in both groups. These results suggest that the aberrant miRNA regulatory network is possibly regulated MAPK signaling and continuously affects the physiological and biochemical status of cells, thus participating in the regulation of spinal cord ischemia-reperfusion injury. As such, miR-22-3 p may play sustained regulatory roles in spinal cord ischemia-reperfusion injury. All experimental procedures were approved by the Animal Ethics Committee of Jilin University, China [approval No. 2020(Research) 01].

关键词： gene regulatory networks microarray analysis microRNA miR-22-3p mitogen-activated protein kinase signaling pathway nerve regeneration neural regeneration spinal cord ischemia-reperfusion injury transcriptome

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Role of nitric oxide in hepatic ischemia-reperfusion injury

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World Journal of Gastroenterology 2010年第48期16卷 6079-6086页

作者： Arunotai Siriussawakul Ahmed Zaky John D Lang Department of Anesthesiology and Pain Medicine and the VA Puget Sound Healthcare System the University of Washington School of Medicine

Hepatic ischemia-reperfusion injury (IRI) occurs upon restoration of hepatic blood flow after a period of ischemia. Decreased endogenous nitric oxide (NO) production resulting in capillary luminal narrowing is central in the pathogenesis of IRI. Exogenous NO has emerged as a potential therapy for IRI based on its role in decreasing oxidative stress,cytokine release,leukocyte endothelial-adhesion and hepatic apoptosis. This review will highlight the influence of endogenous NO on hepatic IRI,role of inhaled NO in ameliorating IRI,modes of delivery,donor drugs and potential side effects of exogenous NO.

关键词： Nitric oxide Liver ischemia-reperfusion injury Drug delivery

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Life and death at the mucosal-luminal interface: New perspectives on human intestinal ischemia-reperfusion

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World Journal of Gastroenterology 2016年第9期22卷 2760-2770页

作者： Joep Grootjans Kaatje Lenaerts Wim A Buurman Cornelis HC Dejong Joep PM Derikx Department of Surgery NUTRIM School of Nutrition and Translational Research in Metabolism Maastricht University Medical Center Brigham and Women’s Hospital Harvard Medical School NUTRIM School of Nutrition and Translational Research in Metabolism Maastricht University Medical Center

Intestinal ischemia is a frequently observed phenomenon. Morbidity and mortality rates are extraordinarily high and did not improve over the past decades. This is in part attributable to limited knowledge on the pathophysiology of intestinal ischemia-reperfusion(IR) in man, the paucity in preventive and/or therapeutic options and the lack of early diagnostic markers for intestinal ischemia. To improve our knowledge and solve clinically important questions regarding intestinal IR, we developed a human experimental intestinal IR model. With this model, we were able to gain insight into the mechanisms that allow the human gut to withstand short periods of IR without the development of severe inflammatory responses. The purpose of this review is to overview the most relevant recent advances in our understanding of the pathophysiology of human intestinal IR, as well as the(potential) future clinical implications.

关键词： Small intestinal ischemia Colon ischemia Epithelial lining ischemia-reperfusion Human models

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Fucoidan Ameliorates Ferroptosis in ischemia-reperfusion-induced Liver Injury through Nrf2/HO-1/GPX4 Activation

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Journal of Clinical and Translational Hepatology 2023年第6期11卷 1341-1354页

作者： Jing-Jing Li Wei-Qi Dai Wen-Hui Mo Wen-Qiang Xu Yue-Yue Li Chuan-Yong Guo Xuan-Fu Xu Department of Gastroenterology Shidong Hospital of ShanghaiShanghaiChina Department of Gastroenterology Shanghai Tenth People’s HospitalTongji University School of MedicineShanghaiChina

Background and Aims:Liver ischemia-reperfusion(IR)injury is a common pathological process in liver ***,which is closely related to lipid peroxidation,has recently been confirmed to be involved in the pathogenesis of IR ***,the development of drugs that regulate ferroptosis has been slow,and a complete understanding of the mechanisms underlying ferroptosis has not yet been ***(Fu)is a sulfated polysaccharide that has attracted research interest due to its advantages of easy access and wide biological ***:In this study,we established models of IR injury using erastin as an activator of ferroptosis,with the ferroptosis inhibitor ferrostatin-1(Fer-1)as the *** clarified the molecular mechanism of fucoidan in IR-induced ferroptosis by determining lipid peroxidation levels,mitochondrial morphology,and key pathways in theta were ***:Ferroptosis was closely related to IR-induced hepatocyte *** use of fucoidan or Fer-1 inhibited ferroptosis by eliminating reactive oxygen species and inhibiting lipid peroxidation and iron accumulation,while those effects were reversed after treatment with *** accumulation,mitochondrial membrane rupture,and active oxygen generation related to ferroptosis also inhibited the entry of nuclear factor erythroid 2-related factor 2(Nrf2)into the nucleus and reduced downstream heme oxygenase-1(HO-1)and glutathione peroxidase 4(GPX4)protein ***,fucoidan pretreatment produced adaptive changes that reduced irreversible cell damage induced by IR or ***:Fucoidan inhibited ferroptosis in liver IR injury via the Nrf2/HO-1/GPX4 axis.

关键词： Fucoidan ischemia-reperfusion Ferroptosis Lipid peroxidation Nrf2

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Role of sirtuins in ischemia-reperfusion injury

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World Journal of Gastroenterology 2013年第43期19卷 7594-7602页

作者： Eirini Pantazi Mohamed Amine Zaouali Mohamed Bejaoui Emma Folch-Puy Hassen Ben Abdennebi Joan Roselló-Catafau Experimental Hepatic ischemia-reperfusion Unit Institut of Biomedical Research of Barcelona-Spanish National Research CouncilBarcelona08036 CataloniaSpain Molecular Biology and Anthropology applied to development and health (UR12ES11) Faculty of PharmacyMonastir 5000Tunisia Experimental Pathology Department Institute of Biomedical Research of Barcelona-Spanish National Research CouncilBarcelona08036 CataloniaSpain

ischemia-reperfusion injury(IRI)remains an unresolved and complicated situation in clinical practice,especially in the case of organ *** factors contribute to its complexity;the depletion of energy during ischemia and the induction of oxidative stress during reperfusion initiate a cascade of pathways that lead to cell death and finally to severe organ ***,the sirtuin family of nicotinamide adenine dinucleotide-dependent deacetylases has gained increasing attention from researchers,due to their involvement in the modulation of a wide variety of cellular *** are seven mammalian sirtuins and,among them,the nuclear/cytoplasmic sirtuin 1(SIRT1)and the mitochondrial sirtuin 3(SIRT3)are ubiquitously expressed in many tissue *** are known to play major roles in protecting against cellular stress and in controlling metabolic pathways,which are key processes during *** this review,we mainly focus on SIRT1 and SIRT3 and examine their role in modulating pathways against energy depletion during ischemia and their involvement in oxidative stress,apoptosis,microcirculatory stress and inflammation during *** present evidence of the beneficial effects of sirtuins against IRI and emphasize the importance of developing new strategies by enhancing their action.

关键词： Sirtuin 1 Sirtuin 3 ischemia-reperfusion injury oxidative stress Apoptosis

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Influence of Kupffer cells and platelets on ischemia-reperfusion injury in mild steatotic liver

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World Journal of Gastroenterology 2013年第9期19卷 1396-1404页

作者： Koichi Ogawa Tadashi Kondo Takafumi Tamura Hideki Matsumura Kiyoshi Fukunaga Tatsuya Oda Nobuhiro Ohkohchi Department of Surgery Graduate School of Comprehensive Human Sciences University of Tsukuba Tsukuba 305-8575 Japan

AIM: To investigate the effect of mild steatotic liver on ischemia-reperfusion injury by focusing on Kupffer cells (KCs) and platelets. METHODS: Wistar rats were divided into a normal liver group (N group) and a mild steatotic liver group (S group) induced by feeding a choline-deficient diet for 2 wk. Both groups were subjected to 20 min of warm ischemia followed by 120 min of reperfusion. The number of labeled KCs and platelets in sinusoids and the blood perfusion in sinusoids were observed by intravital microscopy (IVM), which was performed at 30, 60 and 120 min after reperfusion. To evaluate serum alanine aminotransferase as a marker of liver deterioration, blood samples were taken at the same time as ***: In the S group, the number of platelets adhering to KCs decreased significantly compared with the N group (120 after reperfusion; 2.9±1.1 cells/acinus vs 4.8±1.2 cells/acinus, Pischemia, 19.6±3.3 cells/acinus vs 28.2±4.1 cells/acinus, Preperfusion, 29.0±4.3 cells/acinus vs 40.2±3.3 cells/acinus, Preperfusion was maintained in the S group more than in the N group. Furthermore, elevation of serum alanine aminotransferase was lower in the S group than in the N group 120 min after reperfusion (99.7±19.8 IU/L vs 166.3±61.1 IU/L, P=0.041), and histological impairment of hepatocyte structure was prevented in the S group. CONCLUSION: ischemia-reperfusion injury in mild steatotic liver was attenuated compared with normal liver due to the decreased number of KCs and the reduction of the KC-platelet interaction.

关键词： Steatotic liver Mild steatotic liver Kupffer cell Platelet ischemia-reperfusion Intravital microscopy

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