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| 1 | Hyaluronic acid fragments evoke Kupffer cells via TLR4 signaling pathway显示文摘Kupffer cells, expressing toll-like receptor 4 (TLR4), play a central role in hepatic ischemia/reperfusion (I/R) injury. Hyaluronic acid (HA) fragments, degradative products of high-molecular-weight HA (HMW-HA), acquire the ability to activate immune cells under inflammatory conditions. Here we inves- tigated whether HA fragments could activate Kupffer cells and analyzed the underlying mechanism. Kupffer cells were isolated from wild-type mice (WT, C3H/HeN) and TLR4 mutant mice (C3H/HeJ) and HA fragments were produced by the methods of enzyme digestion and chromatography. Then Kupffer cells were stimulated by HA fragments or other control stimuli. The activation of Kupffer cells was estimated as the release of pro-inflammatory cytokines. The activation of p38 MAPK pathway of Kupffer cells was checked and blocking experiments were done as well. The results indicated that HA fragments acquired the ability to activate Kupffer cells in vitro, which was TLR4 dependent and not due to contamination of lipopolysaccharide. Experiments of p38 MAPK kinase inhibition by SB-203580 verified p38 MAPK was required in HA fragments induced Kupffer cells activation. This suggests that HA fragments, degradative products of one of the major glycosaminoglycans of the extracellular matrix, play critical roles in Kupffer cell activation mediated by TLR4 signaling pathway, which is, at least partially, de- pendent on p38 MAPK activation. | ZHANG JinXiang1, WANG Hui2, XIAO Qing3, LIANG HuiFang4, LI ZhuoYa4, JIANG ChunFang1, WU HeShui5 & ZHENG QiChang5 1 Department of Emergency Surgery, Union Hospital Affiliated to Huazhong University of Science and Technology, Wuhan 430022, China 2 Department of Medical Genetics, Tongji Medical College Affiliated to Huazhong University of Science and Technology, Wuhan 430030, China 3 Department of Ophthalmology, Union Hospital Affiliated to Huazhong University of Science and Technology, Wuhan 430022, China 4 Department of Medical Immunology, Tongji Medical College Affiliated to Huazhong University of Science and Technology, Wuhan 430030, China 5 Department of General Surgery, Union Hospital Affiliated to Huazhong University of Science and Technology, Wuhan 430022, China | 2009 | Science China(Life Sciences)2009，52，2： | 33 |
| 2 | Effects of intracoronary injection of nicorandil and tirofiban on myocardial perfusion and short-term prognosis in elderly patients with acute ST-segment elevation myocardial infarction after emergency PCI显示文摘BACKGROUND:This study investigated the effects of the intracoronary injection of nicorandil and tirofiban on myocardial perfusion and short-term prognosis in elderly patients with acute ST-segment elevation myocardial infarction(STEMI)after emergency percutaneous coronary intervention(PCI).METHODS:Seventy-eight STEMI patients with age>65 years who underwent emergency PCI were consecutively enrolled.These patients received conventional PCI and were randomly divided into a control group and a treatment group(n=39 per group).The control group received an intracoronary injection of tirofiban followed by a maintenance infusion for 36 hours after surgery.The treatment group received intracoronary injection of tirofiban and nicorandil,and then intravenous infusion of tirofiban and nicorandil 36 hours after surgery.The following parameters were measured:TIMI grade,corrected TIMI frame count(c TFC),TIMI myocardial perfusion grade(TMPG),STsegment resolution(STR)rate 2 hours post-operatively,resolution of ST-segment elevation(STR)at 2 hours postoperatively,peak level of serum CK-MB,left ventricular end diastolic diameter(LVEDD)and left ventricular ejection fraction(LVEF)at 7–10 days postoperatively,and major adverse cardiac events(MACEs)in-hospital and within 30 days post-operatively.RESULTS:Compared with the control group,more patients in the treatment group had TIMI 3 and TMPG 3,and STR after PCI was significantly higher.The treatment group also had significantly lower c TFC,lower infarction relative artery(IRA),lower peak CK-MB,and no reflow ratio after PCI.The treatment group had significantly higher LVEDD and LVEF but lower incidence of MACEs than the control group.CONCLUSION:The intracoronary injection of nicorandil combined with tirofiban can effectively improve myocardial reperfusion in elderly STEMI patients after emergency PCI and improve shortterm prognoses. | Guo-xiong Chen Hong-na Wang Jin-lin Zou Xiao-xu Yuan | 2020 | World Journal of Emergency Medicine2020，11，3： | 27 |
| 3 | Calpain system and its involvement in myocardial ischemia and reperfusion injury显示文摘Calpains are ubiquitous non-lysosomal Ca2+-dependent cysteine proteases also present in myocardial cytosol and mitochondria.Numerous experimental studies reveal an essential role of the calpain system in myocardial injury during ischemia,reperfusion and postischemic structural remodelling.The increasing Ca2+-content and Ca2+-overload in myocardial cytosol and mitochondria during ischemia and reperfusion causes an activation of calpains.Upon activation they are able to injure the contractile apparatus and impair the energy production by cleaving structural and functional proteins of myocytes and mitochondria.Besides their causal involvement in acute myocardial dysfunction they are also involved in structural remodelling after myocardial infarction by the generation and release of proapoptotic factors from mitochondria.Calpain inhibition can prevent or attenuate myocardial injury during ischemia,reperfusion,and in later stages of myocardial infarction. | Christiane Neuhof Heinz Neuhof | 2014 | World Journal of Cardiology2014，6，7： | 23 |
| 4 | Sevoflurane postconditioning protects against myocardial ischemia/reperfusion injury by restoring autophagic flux via an NO-dependent mechanism显示文摘Volatile anesthetics improve postischemic cardiac function and reduce infarction even when administered for only a brief-time at the onset of reperfusion.A recent study showed that sevoflurane postconditioning (SPC)attenuated myocardial reperfusion injury, but the underlying mechanisms remain unclear,in this study,we examined the effects of sevoflurane on nitric oxide (NO)release and autophagic flux during the myocardial ischemia/reperfusion (I/R)injury in rats in vivo and ex vivo.Male rats were subjected to 30 min ischemia and 2 h reperfusion in the presence or absence of sevoflurane (1.0 minimum alveolar concentration)during the first 15 min of reperfusion.We found that SPC significantly improved hemodynamic performance after reperfusion,alleviated postischemic myocardial infarction,reduced nicotinamide adenine dinucleotide content loss,and cytochrome c.release in heart tissues.Furthermore,SPC significantly increased the phosphorylation of endothelial nitric oxide synthase (NOS)and neuronal nitric oxide synthase,and elevated myocardial NOS activity and NO production.All these effects were abolished by treatment with an NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME,10 mg/kg,i.v.).We also observed myocardial I/R-induced accumulation of autophagosomes in heart tissues,as evidenced by increased ratios of microtubule:associated protein 1 light chain 3 Ⅱ/Ⅰ,upregulation of Beclin 1 and P62,and reduced lysosome-assciated membrane protein-2 expression.SPC significantly attenuated I/R- impaired autophagic flux,which were blocked by L-NAME.Moreover,pretreatment with the autophagic flUX blocker chloroquine (10 mg/kg,i.p.)increased autophagosome accumulation in SPC-treated heart following I/R and blocked SPC-induced cardioprotection.The same results were also observed in a rat model of myocardial I/R injury ex vivo,suggesting that SPC protects rat hearts against myocardial reperfusion injury by restoring I/R-impaired autophagic flux yia an NO-dependent mechanism. | Shi-gang Qiao Ying Sun Bo Sun An Wang Jia Qiu Lei Hong Jian-zhong An Chen Wang Hui-ling Zhang | 2019 | Acta Pharmacologica Sinica2019，40，1： | 21 |
| 5 | Inhibition of FOXO3a/BIM signaling pathway contributes to the protective effect of salvianolic acid A against cerebral ischemia/reperfusion injury显示文摘Salvianolic acid A(SalA) is an effective compound extracted from traditional Chinese medicine Salvia miltiorrhiza Bunge. The Forkhead box O3a(FOXO3a) signaling pathway plays crucial roles in the modulation of ischemia-induced cell apoptosis. However, no information about the regulatory effect of SalA on FoxO3a is available. To explore the anti-cerebral ischemia effect and clarify the therapeutic mechanism of SalA, SH-SY5Y cells and Sprague–Dawley rats were applied, which were exposed to oxygen glucose deprivation/reoxygenation(OGD/R) and middle cerebral artery occlusion/reperfusion(MCAO/R) injuries, respectively. The involved pathway was identified using the specific inhibitor LY294002. Results showed that SalA concentration-dependently inhibited OGD/R injury triggered cell viability loss. SalA reduced cerebral infarction, lowered brain edema, improved neurological function, and inhibited neuron apoptosis in MCAO/R rats, which were attenuated by the treatment of phosphatidylinositol-4,5-bisphosphate 3-kinase(PI3K) specific inhibitor LY294002. SalA time-and concentration-dependently upregulated the phosphorylation levels of protein kinase B(AKT) and its downstream protein FOXO3a. Moreover, the nuclear translocation of FOXO3a was inhibited by SalA both in vivo and in vitro, which was also reversed by LY294002. The above results indicated that SalA fought against ischemia/reperfusion damage at least partially via the AKT/FOXO3a/BIM pathway. | Junke Song Wen Zhang Jinhua Wang Haiguang Yang Qimeng Zhou Haigang Wang Li Li Guanhua Du | 2019 | Acta Pharmaceutica Sinica B2019，9，3： | 20 |
| 6 | Post reperfusion syndrome during liver transplantation:From pathophysiology to therapy and preventive strategies显示文摘This review aims at evaluating the existing evidence regarding post reperfusion syndrome, providing a description of the pathophysiologic mechanisms involved and possible management and preventive strategies. A Pub Med search was conducted using the Me SH database, 'Reperfusion' AND 'liver transplantation' were the combined Me SH headings; EMBASE and the Cochrane library were also searched using the same terms. 52 relevant studies and one ongoing trial were found. The concept of post reperfusion syndrome has evolved through years to a multisystemic disorder. The implications of the main organ, recipient and procedure related factors in the genesis of this complex syndrome are discussed in the text as the novel pharmacologic and technical approaches to reduce its incidence. However the available evidence about risk factors, physiopathology and preventive measures is still confusing, the presence of two main definitions and the numerosity of possible confounding factors greatly complicates the interpretation of the studies. | Antonio Siniscalchi Lorenzo Gamberini Cristiana Laici Tommaso Bardi Giorgio Ercolani Laura Lorenzini Stefano Faenza | 2016 | World Journal of Gastroenterology2016，22，4： | 20 |
| 7 | Mechanism of TLR-4/NF-κB pathway in myocardial ischemia reperfusion injury of mouse显示文摘Objective: To detect the expression of Toll-like receptor 4(TLR-4) and NF-κB and to discuss the mechanism of TLR-4/NF-κB pathway in the myocardial ischemia reperfusion injury of mouse. Methods: TLR-4 mutant mice and wild homozygous mice were divided into the model group and sham group. Mice in the model group were given the ligation of left anterior descending coronary artery for the modeling, while mice in the sham group were not given the ligation after threading. The cardiac muscle tissues were collected for the morphological observation. The immuno histochemistry was employed to detect the expression of NF-κB, Western blot was used to detect the expression of TLR-4 and ELISA to detect the expression of serum inflammatory factors. Results: The expression of NF-κB in TLR-4 null mice after the myocardial ischemia reperfusion was significantly lower than that in wild homozygous mice. For the model group and sham group, the expression of TLR-4 in wild homozygous mice was all significantly higher than that in TLR-4 null mice, while the expression of TLR-4 in TLR-4 null mice in the model group was significantly higher than that in sham group, with the statistical difference(P<0.05). The expression of inflammatory factors in TLR-4 null mice and wild homozygous mice in the model group was significantly higher than that in sham group. The expression of all factors in group A with TLR-4 null was significantly lower than that in group B with wild homozygous type, with the statistical difference(P<0.05). Conclusions: TLR-4/NF-κB pathway is closely related to the myocardial ischemia reperfusion injury, which plays its role through the release of inflammatory cytokines. | Hao Chen Ruo-Qing Zhang Xiao-Gang Wei Xiao-Min Ren Xiao-Qian Gao | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，5： | 19 |
| 8 | Cardioprotection and pharmacological therapies in acute myocardial infarction: Challenges in the current era显示文摘In patients with an acute ST-segment elevation myocardial infarction, timely myocardial reperfusion using primary percutaneous coronary intervention is the most effective therapy for limiting myocardial infarct size, preserving left-ventricular systolic function and reducing the onset of heart failure. Within minutes after the restoration of blood flow, however, reperfusion itself results in additional damage, also known as myocardial ischemia-reperfusion injury. An improved understanding of the pathophysiological mechanisms underlying reperfusion injury has resulted in the identification ofseveral promising pharmacological(cyclosporin-A, exenatide, glucose-insulin-potassium, atrial natriuretic peptide, adenosine, abciximab, erythropoietin, metoprolol and melatonin) therapeutic strategies for reducing the severity of myocardial reperfusion injury. Many of these agents have shown promise in initial proofof-principle clinical studies. In this article, we review the pathophysiology underlying myocardial reperfusion injury and highlight the potential pharmacological interventions which could be used in the future to prevent reperfusion injury and improve clinical outcomes in patients with coronary heart disease. | Alberto Dominguez-Rodriguez Pedro Abreu-Gonzalez Russel J Reiter | 2014 | World Journal of Cardiology2014，6，3： | 18 |
| 9 | Neuroprotective effect of ethyl acetate extract from gastrodia elata against transient focal cerebral ischemia in rats induced by middle cerebral artery occlusion显示文摘OBJECTIVE: To investigate the protective effect of neuroprotection against transient focal cerebral ischemia of the extract from Tianma(Rhizoma Gastrodiae) and the possible mechanisms underlying the action.METHODS: Cerebral ischemia-reperfusion injury was induced through middle cerebral artery occlusion(MCAO). Adult male Sprague-Dawley rats were randomly divided into four groups: sham-operated,ischemia-reperfusion model, 102.6 mg/kg extract treated and 11.4 mg/kg extract treated groups. The extract was prepared from gastrodia elata with ethyl acetate. The effect of the extract tested on rat neurological de fi cits and Cerebral index, cerebral infarct volume, brain injury, terminal dexynucleotidyl transferase-mediated d UTP nick end labeling(TUNEL) and B-cell lymphoma-2(Bcl-2) positive cells.RESULTS: The extract was able to reduce neurological scores, cerebral index and cerebral infarction rate. The brain injury was also relieved by the extract. The results of immunofluorescence staining analysis indicated that the extract increased the expression of Bcl-2 and reduced TUNEL-positive cells significantly in the extract treated groups.CONCLUSION: These results suggested that the extract relieved ischemic injury induced by transient focal cerebral ischemia in rats, and this neuroprotective effect might be partially due to the attenuated apoptosis pathway. | Duan Xiaohua Wang Weili Liu Xiaoqing Yan Hanwen Dai Rong Lin Qing | 2015 | Journal of Traditional Chinese Medicine2015，35，6： | 18 |
| 10 | Combined bone marrow stromal cells and oxiracetam treatments ameliorates acute cerebral ischemia/reperfusion injury through TRPC6显示文摘Ischemic stroke has become one of the leading causes of deaths and disabilities all over the world.In this study,we investigated the therapeutic effects of combined bone marrow stromal cells(BMSCs)and oxiracetam treatments on acute cerebral ischemia/reperfusion(I/R)injury.A rat model of middle cerebral artery occlusion(MCAO)followed by complete reperfusion,as well as a cortex neuron oxygen-glucose deprivation(OGD)model was established.When compared with BMSCs or oxiracetam monotherapy,combination therapy significantly improved functional restoration with decreased infarct volume in observed ischemic brain.We propose that it may occur through the transient receptor potential canonical(TRPC)6 neuron survival pathway.The increased expression of TRPC6 along with the reduction of neuronal cell death in the OGD cortex neurons and combination therapy group indicated that the TRPC6 neuron survival pathway plays an important role in the combined BMSCs and oxiracetam treatments.We further tested the activity of the calpain proteolytic system,and the results suggested that oxiracetam could protect the integrity of TRPC6 neuron survival pathway by inhibiting TRPC6 degradation.The protein levels of phospho-cAMP response element binding protein(p-CREB)were tested.It was found that BMSCs play a role in the activation of the TRPC6 pathway.Our study suggests that the TRPC6 neuron survival pathway plays a significant role in the protective effect of combined BMSCs and oxiracetam treatments on acute cerebral I/R injury.Combined therapy could inhibit the abnormal degradation of TRPC6 via decreasing the activity of calpain and increasing the activation of TRPC6 neuron survival pathway. | Jing Wang Ruohan Sun Zhenzhu Li Yujun Pan | 2019 | Acta Biochimica et Biophysica Sinica2019，51，8： | 17 |
| 11 | Current status and recent advances of liver transplantation from donation after cardiac death显示文摘The last decade saw increased organ donation activity from donors after cardiac death (DCD). This contributed to a signif icant proportion of transplant activity. Despite certain drawbacks, liver transplantation from DCD donors continues to supplement the donor pool on the backdrop of a severe organ shortage. Understanding the pathophysiology has provided the basis for modulation of DCD organs that has been proven to be effective outside liver transplantation but remains experimental in liver transplantation models. Research continues on how best to further increase the utility of DCD grafts. Most of the work has been carried out exploring the use of organ preservation using machine assisted perfusion. Both ex-situ and in-situ organ perfusion systems are tested in the liver transplantation setting with promising results. Additional techniques involved pharmacological manipulation of the donor, graft and the recipient. Ethical barriers and end-of-life care pathways are obstacles to widespread clinical application of some of the recent advances to practice. It is likely that some of the DCD offers are in fact probably 'prematurely' of-fered without ideal donor management or even prior to brain death being established. The absolute benef its of DCD exist only if this form of donation supplements the existing deceased donor pool; hence, it is worthwhile revisiting organ donation process enabling us to identify counter remedial measures. | M Thamara PR Perera Simon R Bramhall | 2011 | World Journal of Gastrointestinal Surgery2011，3，11： | 16 |
| 12 | Effect of peroxisome proliferator-activated receptor gamma agonist on heart of rabbits with acute myocardial ischemia/reperfusion injury显示文摘Objective:To explore protective effect of rosiglitazone on myocardial ischemia reperfusion injury.Methods:A total of 48 male SD rats were randomly divided into control group(A),I/R group(B),high dose of rosiglitazone(C),low dose of rosiglitazone(D).Plasm concentration of creatine kinase(CK),CK-MB,hsCRP,Superoxide dismutase(SOD),malondialdehyde(MDA),glutathione peroxidase(GSH-Px),nitric oxide(NO)and endothelin(ET)were measured 1 h later after I/R.24 h after I/R hearts were harvested to observe pathological and ultrastructural changes.Immunohistochemistry and western blotting was used to test CD40 expression in myocardial tissue.Area of myocardial infarction were tested,arrhythmia rate during I/R was recorded.Results:Plasm concentration of creatine kinase(CK),CK-MB,hsCRP,NO,MDA and ET were decreased in group C,D compared with group B.Plasm concentration of T-SOD and GSHPx was increased significantly in group C,D compared with group B.Compared with group B,pathological and ultrastructural changes in group C,D were slightly.Myocardial infarction area and arrhythmia rate were lower in group C,D compare with group B.Conclusions:Rosiglitazone can protect myocardium from I/R injury by enhancing T-SOD and GSH-Px concentration,inhibit inflammatory reaction,improve endothelial function,reduce oxidative stress and calcium overload. | Qian Hu Jiong Chen Chao Jiang Heng-Fang Liu | 2014 | Asian Pacific Journal of Tropical Medicine2014，7，4： | 14 |
| 13 | Hepatic ischemia-reperfusion injury in liver transplant setting:mechanisms and protective strategies显示文摘Hepatic ischemia-reperfusion injury is a major cause of liver transplant failure,and is of increasing significance due to increased use of expanded criteria livers for transplantation.This review summarizes the mechanisms and protective strategies for hepatic ischemia-reperfusion injury in the context of liver transplantation.Pharmacological therapies,the use of pre-and post-conditioning and machine perfusion are discussed as protective strategies.The use of machine perfusion offers significant potential in the reconditioning of liver grafts and the prevention of hepatic ischemia-reperfusion injury,and is an exciting and active area of research,which needs more study clinically. | Sanketh Rampes Daqing Ma | 2019 | The Journal of Biomedical Research2019，33，4： | 14 |
| 14 | Heme oxygenase-1 protects rat liver against warm ischemia/reperfusion injury via TLR2/TLR4-triggered signaling pathways显示文摘AIM:To investigate the efficacy and molecularmechanisms of induced heme oxygenase(HO)-1 in protecting liver from warm ischemia/reperfusion(I/R)injury.METHODS:Partial warm ischemia was produced in the left and middle hepatic lobes of SD rats for 75min,followed by 6 h of reperfusion.Rats were treated with saline,cobalt protoporphyrin(Co PP)or zinc protoporphyrin(Zn PP)at 24 h prior to the ischemia insult.Blood and samples of ischemic lobes subjected to ischemia were collected at 6 h after reperfusion.Serum transaminases level,plasma lactate dehydrogenase and myeloperoxidase activity in liver were measured.Liver histological injury and inflammatory cell infiltration were evaluated by tissue section and liver immunohistochemical analysis.We used quantitative reverse transcription polymerase chain reaction to analyze liver expression of inflammatory cytokines and chemokines.The cell lysates were subjected to immunoprecipitation with anti-Toll-IL-1R-containing adaptor inducing interferon-β(TRIF)and anti-myeloid differentiation factor 88(My D88),and then the immunoprecipitates were analyzed by SDS-PAGE and immunoblotted with the indicated antibodies.RESULTS:HO-1 protected livers from I/R injury,as evidenced by diminished liver enzymes and wellpreserved tissue architecture.In comparison with Zn PP livers 6 h after surgery,Co PP treatment livers showed a significant increase inflammatory cell infiltration of lymphocytes,plasma cells,neutrophils and macrophages.The Toll-like receptor(TLR)-4 and TANK binding kinase1 protein levels of rats treated with Co PP significantly reduced in TRIF-immunoprecipitated complex,as compared with Zn PP treatment.In addition,pretreatment with Co PP reduced the expression levels of TLR2,TLR4,IL-1R-associated kinase(IRAK)-1 and tumor necrosis factor receptor-associated factor 6 in My D88-immunoprecipitated complex.The inflammatory cytokines and chemokines m RNA expression rapidly decreased inCo PP-pretreated liver,compared with the Zn PP-treated group.However,the expression of negative regulators Tollinteracting protein,suppressor of cytokine signaling-1,IRAK-M and Src homology 2 domain-containing inositol-5-phosphatase-1 in Co PP treatment rats were markedly up-regulated as compared with Zn PP-treated rats.CONCLUSION:HO-1 protects liver against I/R injury by inhibiting TLR2/TLR4-triggered My D88-and TRIFdependent signaling pathways and increasing expression of negative regulators of TLR signaling in rats. | Han-Fei Huang Zhong Zeng Kun-Hua Wang Hai-Yan Zhang Shuai Wang Wen-Xiang Zhou Zhan-Bo Wang Wang-Gang Xu Jian Duan | 2015 | World Journal of Gastroenterology2015，21，10： | 12 |
| 15 | Plasma D(-)-lactate as a new marker for diagnosis of acute intestinal injury following ischemia-reperfusion显示文摘PlasmaD()lactateasanewmarkerfordiagnosisofacuteintestinalinjuryfolowingischemiareperfusionYAOYongMing1,YUYan1,WUYe2,LUL... | YAO YongMing1, YU Yan1, WU Ye2, LU LianRong1 and SHENG ZhiYong1 | 1997 | World Journal of Gastroenterology1997，3，4： | 12 |
| 16 | Danshensu Ameliorates Cardiac Ischaemia Reperfusion Injury through Activating Sirt1/Fox01/Rab7 Signal Pathway显示文摘Objective:To explore the specific molecular mechanisms of Danshensu(DSS)in the treatment of ischemia reperfusion injury(IRI).Methods:IRI model was established with isolated rat hearts by performing global ischaemia for 30 min,and then followed by 60 min reperfusion.Also,H9C2 cells were subjected to 4-h hypoxia followed by 3-h reoxygenation.Then 10|i mol/L DSS were added in the reperfusion/reoxygenation step to intervene IRI.Cardiac function,structural change and apoptosis were respectively tested by Langendorff System,hematoxylin and eosin(HE)and terminal-deoxynucleotidyl transferase mediated nick endabeling(TUNEL)stainings.Then lactate dehydrogenase(LDH),cardiac troponin T(cTnT),reactive oxygen species(ROS),superoxide dismutase(SOD)and glutathione peroxidase(GSH-PX)were detected by enzyme-linked immunosorbent assay(ELISA).Sirt1/FoxO1/Rab7 Signal Pathway was monitored at both protein and mRNA levels.Results:The results showed that IRI not only greatly attenuated cardiac function(LVDP and±dp/dtmax,P<0.01,P<0.05)and increased the level of the marker enzymes(cTnT,LDH,P<0.01)from the coronary effluents,but also markedly induced changes in the structure of cardiomyocytes and contributed to apoptosis,which were mediated by boosted en doge nous ROS.However,after treatment with DSS all above indexes were improved,which was related to activating Sirt1/FoxO1/Rab7 signal pathway accompanied with the enhancement of antioxidant defense system,such as SOD and GSH-PX.Conclusion:DSS is able to protect hearts from IRI,which may be attributable to inhibiting excessive ROS through Sirt1/FoxO1/Rab7 signaling. | SUN Da-wei GAO Qing QI Xin | 2020 | Chinese Journal of Integrative Medicine2020，26，4： | 11 |
| 17 | Brain-derived neurotrophic factor mediates macrophage migration inhibitory factor to protect neurons against oxygen-glucose deprivation显示文摘Macrophage migration inhibitory factor(MIF)is a chemokine that plays an essential role in immune system function.Previous studies suggested that MIF protects neurons in ischemic conditions.However,few studies are reported on the role of MIF in neurological recovery after ischemic stroke.The purpose of this study is to identify the molecular mechanism of neuroprotection mediated by MIF.Human neuroblastoma cells were incubated in Dulbecco’s modified Eagle’s medium under oxygen-glucose deprivation(OGD)for 4 hours and then returned to normal aerobic environment for reperfusion(OGD/R).30 ng/mL MIF recombinant(30 ng/mL)or ISO-1(MIF antagonist;50μM)was administered to human neuroblastoma cells.Then cell cultures were assigned to one of four groups:control,OGD/R,OGD/R with MIF,OGD/R with ISO-1.Cell viability was analyzed using WST-1 assay.Expression levels of brain-derived neurotrophic factor(BDNF),microtubule-associated protein 2(MAP2),Caspase-3,Bcl2,and Bax were detected by western blot assay and immunocytochemistry in each group to measure apoptotic activity.WST-1 assay results revealed that compared to the OGD/R group,cell survival rate was significantly higher in the OGD/R with MIF group and lower in the OGD/R with ISO-1 group.Western blot assay and immunocytochemistry results revealed that expression levels of BDNF,Bcl2,and MAP2 were significantly higher,and expression levels of Caspase-3 and Bax were significantly lower in the MIF group than in the OGD/R group.Expression levels of BDNF,Bcl2,and MAP2 were significantly lower,and expression levels of Caspase-3 and Bax were significantly higher in the ISO-1 group than in the OGD/R group.MIF administration promoted neuronal cell survival and induced high expression levels of BDNF,MAP2,and Bcl2(anti-apoptosis)and low expression levels of Caspase-3 and Bax(pro-apoptosis)in an OGD/R model.These results suggest that MIF administration is effective for inducing expression of BDNF and leads to neuroprotection of neuronal cells against hypoxic injury. | Su Hwan Bae Mi Ran Yoo Ye Yeong Kim In Kyung Hong Mi Hee Kim Seung Hak Lee Dae Yul Kim | 2020 | Neural Regeneration Research2020，15，8： | 11 |
| 18 | Expression of Bcl-2 and NF-κB in brain tissue after acute renal ischemia-reperfusion in rats显示文摘Objective:To investigate the effect of acute renal ischemia reperfusion on brain tissue.Methods:Fourty eight rats were randomly divided into four groups(n=12):sham operation group,30 min ischemia 60 min reperfusion group,60 min ischemia 60 min reperfusion group,and120 min ischemia 60 min reperfusion group.The brain tissues were taken after the experiment.TUNEL assay was used to detect the brain cell apoptosis,and western blot was used to detect the expression of apoptosis-related proteins and inflammatory factors.Results:Renal ischemiareperiusion induced apoptosis of brain tissues,and the apoptosis increased with prolongation of ischemia time.The detection at the molecular level showed decreased Bcl-2 expression,increased Bax expression,upreguiated expression of NF- κB and its downstream factor COX-2/PGE2.Conclusions:Acute renal ischemia-reperfusion can cause brain tissue damage,manifested as induced brain tissues apoptosis and inflammation activation. | Na Zhang Gen-Yang Cheng Xian-Zhi Liu Feng-Jiang Zhang | 2014 | Asian Pacific Journal of Tropical Medicine2014，7，5： | 11 |
| 19 | Anisodamine protects against neuronal death following cerebral ischemia in gerbils显示文摘To study the effect of anisodamine on neuronal death and hydroxyl radical (OH·) production during forebrain ischemia reperfusion in gerbils Methods The tested gerbils were divided into 3 groups, including sham operated, control and anisodamine groups. In each group, there were 8 animals for biochemical examination and 6 animals for histologic study. Forebrain ischemia was induced by occlusion the bilateral common carotid arteries for 10 min in gerbils. 2,3 and 2,5 DHBA outputs were determined by high performance hiquid chromatography coupled with electrochemical detection. Behavioral change was tested by open field test and neuronal death was assessed by histological examination.Results The exploratory activities of gerbils in the control group were significantly higher than those in the anisodamine group on all test days The amount of viable looking neurons in the medial, middle and lateral CA1 sectors in anisodamine group were 41%±12%, 50%±21% and 67%±15% of the sham operated gerbils, respectively, being significantly higher than those in the control group (3%±2%, 4%±3% and 7%±4% of sham, P <0 01) The 2,3 DHBA outputs in the control group increased by 5 fold of the sham operated gerbils after reperfusion for 60 min, but the 2,3 DHBA outputs in the anisodamine group were only 2 4 fold of sham operated gerbils, being significantly lower than that in the control group ( P <0 01) The 2,5 DHBA outputs in the control group were significantly higher than those in the sham operated group ( P <0 05) Conclusion Anisodamine has inhibitory effects on neuronal death and OH·production during cerebral ischemia reperfusion in | 陈群 曾因明 | 2000 | Chinese Medical Journal2000，，7： | 10 |
| 20 | Role of P-selectin and anti-P-selectin monoclonal antibody in apoptosis during hepatic/renal ischemia-reperfusion injury显示文摘AIM To evaluale the potential role of P-selectinand anti-P-selectin monoclonal antibody(mAb)in apoptosis during hepatic/renal ischemia-reperfusion injury.METHODS Plasma P-selectin level,hepatic/renal P-selectin expression and cell apoptosiswere detected in rat model of hepatic/ renalischemia-reperfusion injury.ELISA,immunohist-ochemistry and TUNEL were used.Someischemia-reperfusion rats were treated with anti-P-selectin mAb.RESULTS Hepatic/renal function insuffic-iency,up-regulated expression of P-selectin inplasma and hepatic/renal tissue,hepatic/renalhistopathological damages and cell apoptosiswere found in rats with hepatic/renal ischemia-reperfusion injury,while these changes becameless conspicuous in animals treated with anti-P-selectin mAb.CONCLUSION P-selectin might mediateneutrophil infiltration and cell apoptosis andcontribute to hepatic/renal ischemia-reperfusioninjury,anti-P-selectin mAb might be an efficientapproach for the prevention and treatment ofhepatic/renal ischemia-reperfusion injury. | Pei Wu Xiao Li Tong Zhou Ming Jun Zhang Jin Lian Chen Wei Ming Wang Nan Chen De Chang Dong | 2000 | World Journal of Gastroenterology2000，6，2： | 10 |
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