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| 1 | Oxidative stress,insulin resistance,dyslipidemia and type 2 diabetes mellitus显示文摘Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus(T2DM) and this appears to underlie the development of cardiovascular disease,T2 DM and diabetic complications.Increased oxidative stress appears to be a deleterious factor leading toinsulin resistance,dyslipidemia,β-cell dysfunction,impaired glucose tolerance and ultimately leading to T2 DM.Chronic oxidative stress,hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant,have high oxidative energy requirements,decrease the gene expression of key β-cell genes and induce cell death.If β-cell functioning is impaired,it results in an under production of insulin,impairs glucose stimulated insulin secretion,fasting hyperglycemia and eventually the development of T2 DM. | Surapon Tangvarasittichai | 2015 | World Journal of Diabetes2015，6，3： | 95 |
| 2 | Gut microbiota imbalance and colorectal cancer显示文摘The gut microbiota acts as a real organ. The symbiotic interactions between resident micro-organisms and the digestive tract highly contribute to maintain the gut homeostasis. However, alterations to the microbiome caused by environmental changes(e.g., infection, diet and/or lifestyle) can disturb this symbiotic relationship and promote disease, such as inflammatory bowel diseases and cancer. Colorectal cancer is a complex association of tumoral cells, non-neoplastic cells and a large amount of micro-organisms, and the involvement of the microbiota in colorectal carcinogenesis is becoming increasingly clear. Indeed, many changes in the bacterial composition of the gut microbiota have been reported in colorectal cancer, suggesting a major role of dysbiosis in colorectal carcinogenesis. Some bacterial species have been identified and suspected to play a role in colorectal carcinogenesis, such as Streptococcus bovis, Helicobacter pylori, Bacteroides fragilis, Enterococcus faecalis, Clostridium septicum, Fusobacterium spp. and Escherichia coli. The potential pro-carcinogenic effects of these bacteria are now better understood. In this review, we discuss the possible links between the bacterial microbiota and colorectal carcinogenesis, focusing on dysbiosis and the potential pro-carcinogenic properties of bacteria, such as genotoxicity and other virulence factors, inflammation, host defenses modulation, bacterial derived metabolism, oxidative stress and anti-oxidative defenses modulation. We lastly describe how bacterial microbiota modifications could represent novel prognosis markers and/or targets for innovative therapeutic strategies. | Johan Gagnière Jennifer Raisch Julie Veziant Nicolas Barnich Richard Bonnet Emmanuel Buc Marie-Agnès Bringer Denis Pezet Mathilde Bonnet | 2016 | World Journal of Gastroenterology2016，22，2： | 76 |
| 3 | Oxidative stress as a crucial factor in liver diseases显示文摘Redox state constitutes an important background of numerous liver disorders. The redox state participates in the course of inflammatory, metabolic and proliferative liver diseases. Reactive oxygen species(ROS) are primarily produced in the mitochondria and in the endoplasmic reticulum of hepatocytes via the cytochrome P450 enzymes. Under the proper conditions, cells are equipped with special molecular strategies that control the level of oxidative stress and maintain a balance between oxidant and antioxidant particles. Oxidative stress represents an imbalance between oxidant and antioxidant agents. Hepatocytic proteins, lipids and DNA are among the cellular structures that are primarily affected by ROS and reactive nitrogen species. The process results in structural and functional abnormalities in the liver. Thus, the phenomenon of oxidative stress should be investigated for several reasons. First, it may explain the pathogenesis of various liver disorders. Moreover, monitoring oxidative markers among hepatocytes offers the potential to diagnose the degree of liver damage and ultimately to observe the response to pharmacological therapies. The present report focuses on the role of oxidative stress in selected liver diseases. | Halina Cichoz-Lach Agata Michalak | 2014 | World Journal of Gastroenterology2014，20，25： | 70 |
| 4 | Myocardial reperfusion injury and oxidative stress: Therapeutic opportunities显示文摘Acute myocardial infarction(AMI) is the leading cause of death worldwide. Its associated mortality, morbidity and complications have significantly decreased with the development of interventional cardiology and percutaneous coronary angioplasty(PCA) treatment, which quick-ly and effectively restore the blood flow to the area previously subjected to ischemia. Paradoxi-cally, the restoration of blood flow to the ischemic zone leads to a massive production of reactive oxygen species(ROS) which generate rapid and severe damage to biomolecules, generating a phenomenon called myocardial reperfusion injury(MRI). In the clinical setting, MRI is associated with multiple complications such as lethal reperfusion, no-reflow, myocardial stunning, and reperfusion arrhythmias. Despite significant advances in the understanding of the mechanisms accounting for the myocardial ischemia reperfusion injury, it remains an unsolved problem. Although promising results have been obtained in experimental studies(mainly in animal models), these benefits have not been translated into clinical settings. Thus, clinical trials have failed to find benefits from any therapy to prevent MRI. There is major evidence with respect to the contribution of oxidative stress to MRI in cardiovascular diseases. The lack- of consistency between basic studies and clinical trials is not solely based on the diversity inherent in epidemiology but is also a result of the methodological weak-nesses of some studies. It is quite possible that pharmacological issues, such as doses, active ingredients, bioavailability, routes of administration, co-therapies, startup time of the drug intervention,and its continuity may also have some responsibility for the lack- of consistency between different studies. Furthermore, the administration of high ascorbate doses prior to reperfusion appears to be a safe and rational therapy against the development of oxidative damage associated with myocardial reperfusion. In addition, the association with N-acetylcysteine(a glutathione donor) and deferoxamine(an iron chelator) could improve the antioxidant cardioprotection by ascorbate, mak-ing it even more effective in preventing myocardial reperfusion damage associated with PCA following AMI. | Jaime González-Montero Roberto Brito Abraham IJ Gajardo Ramón Rodrigo | 2018 | World Journal of Cardiology2018，10，9： | 56 |
| 5 | Oxidative stress, cardiolipin and mitochondrial dysfunction in nonalcoholic fatty liver disease显示文摘Nonalcoholic fatty liver disease(NAFLD) is today considered the most common form of chronic liver disease, affecting a high proportion of the population worldwide. NAFLD encompasses a large spectrum of liver damage, ranging from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. Obesity, hyperglycemia, type 2 diabetes and hypertriglyceridemia are the most important risk factors. The pathogenesis of NAFLD and its progression to fibrosis and chronic liver disease is still unknown. Accumulating evidence indicates that mitochondrial dysfunction plays a key role in the physiopathology of NAFLD, although the mechanisms underlying this dysfunction are still unclear. Oxidative stress is considered an important factor in producing lethal hepatocyte injury associated with NAFLD. Mitochondrial respiratory chain is the main subcellular source of reactive oxygen species(ROS), which may damage mitochondrial proteins, lipids and mitochondrial DNA. Cardiolipin, a phospholipid located at the level of the inner mitochondrial membrane, plays an important role in several reactions and processes involved in mitochondrial bioenergetics as well as in mitochondrial dependent steps of apoptosis. This phospholipid is particularly susceptible to ROS attack. Cardiolipin peroxidation has been associated with mitochondrial dysfunction in multiple tissues in several physiopathological conditions, including NAFLD. In this review, we focus on the potential roles played by oxidative stress and cardiolipin alterations in mitochondrial dysfunction associated with NAFLD. | Giuseppe Paradies Valeria Paradies Francesca M Ruggiero Giuseppe Petrosillo | 2014 | World Journal of Gastroenterology2014，20，39： | 50 |
| 6 | Protective effects of nitric oxide on salt stress-induced oxidative damage to wheat (Triticum aestivum L.)leaves显示文摘The changes of chlorophyll and malondialde-hyde (MDA) contents, plasma membrane permeability confirmed that 0.1 and 1 mmol/L sodium nitroprusside (SNP), a donor of nitric oxide (NO) in vivo, could markedly alleviate the oxidative damage to wheat (Triticum aestivum L.) leaves induced by 150 and 300 mmol/L NaCl treatments, respectively. Further results proved that NO significantly enhanced the activities of superoxide dismutase (SOD) and catalase (CAT), both of which separately contributed to the delay of O2- and H2O2 accumulation in wheat leaves under saltstress. Meanwhile, the accumulation of proline was apparently accelerated. Therefore, these results suggested that NO could strongly protect wheat leaves from oxidative damage caused by salt stress. | Haihua Ruan Wenbiao Shen Maobing Ye Langlai Xu | 2002 | Chinese Science Bulletin2002，47，8： | 37 |
| 7 | A meta-analysis of oxidative stress markers in schizophrenia显示文摘Oxidative stress has been identified as a possible element in the neuropathological processes of schizophrenia(SCZ).Alteration of oxidative stress markers has been reported in SCZ studies,but with inconsistent results.To evaluate the risk of oxidative stress to schizophrenia,a meta-analysis was conducted,including five markers of oxidative stress [thiobarbituric reactive substances(TBARS),nitric oxide(NO),catalase(CAT),glutathione peroxidase(GP) and superoxide dismutase(SOD)] in SCZ patients versus healthy controls.This study showed that TBARS and NO significantly increased in SCZ,while SOD activity significantly decreased in the disorganized type of SCZ patients.No significant effect size was found for the activities of GP and CAT in SCZ patients(P>0.05).Egger’s regression test observed no significant publication bias across the oxidative stress markers,but found high heterogeneities in all the 5 markers.The subgroup analysis suggested that the ethnicity,sample size of patients and sample sources may contribute to the heterogeneity of the results for TBARS,NO and SOD.The result further demonstrated the involvement of oxidative stress in the pathophysiology of schizophrenia. | ZHANG Ming1,2,ZHAO ZhongMing3,HE Lin1,2,4 & WAN ChunLing1,2 1 Bio-X Center,Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders(Ministry of Education),Shanghai Jiao Tong University,Shanghai 200030,China 2 Institutes for Nutritional Sciences,Shanghai Institute of Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China 3 Departments of Biomedical Informatics,Psychiatry,and Cancer Biology,Vanderbilt University Medical Center,Nashville,TN 37232,USA 4 Institutes of Biomedical Sciences,Fudan University,Shanghai 200032,China | 2010 | Science China(Life Sciences)2010，53，1： | 32 |
| 8 | Dietary resveratrol improves antioxidant status of sows and piglets and regulates antioxidant gene expression in placenta by Keap1-Nrf2 pathway and Sirt1显示文摘Background: Resveratrol, a plant phenol, affords protection against inflammation and oxidative stress. The objective of this study was to investigate the effects of dietary resveratrol supplementation during pregnancy and lactation on the antioxidant status of sows and piglets and on antioxidant gene expression and pathway in placenta.Methods: Forty sows were allotted to 2 dietary treatments 20 d after breeding. Sows were fed a control diet and a control diet with 300 mg/kg resveratrol. Oxidative stress biomarkers and antioxidant enzymes were measured in the placenta, milk, and plasma of sows and piglets. Antioxidant gene expression and protein expression of Kelch-like ECH-associated protein 1-Nuclear factor E2-related factor 2(Keap1-Nrf2), nuclear factor kappa B-p65(NFκB-p65) and sirtuin1(Sirt1) were quantified in the placenta.Results: Dietary resveratrol increased the litter and piglets weaning weights. Antioxidant status in the milk, placenta and plasma of sows and piglets was partially improved by dietary resveratrol. In placenta, Nrf2 protein expression was increased and Keap1 protein expression was decreased by dietary resveratrol. The m RNA expression of antioxidant genes including catalase(CAT), glutathione peroxidase 1(GPX1), GPX4, superoxide dismutase 1(SOD1)and heme oxygenase 1(HO1), and phase 2 detoxification genes, including glutamate-cysteine ligase modifier(GCLM), microsomal glutathione S-transferase 1(MGST1) and UDP glucuronosyltransferase family 1 member A1(UGT1 A1), was increased by dietary resveratrol. Dietary resveratrol also increased Sirt1 and phosphorylated NFκB-p65 protein expression in the placenta. We failed to observe any influences of dietary resveratrol on pro-inflammatory cytokine levels, including those of interleukin 1β(IL-1β), IL-6, IL-8 and tumor necrosis factor α(TNF-α). However, we observed that the m RNA expression of IL-8 in placenta was reduced by maternal resveratrol. In addition, dietary resveratrol showed interactive effects with day of lactation on activities of SOD and CAT and levels of malonaldehyde(MDA) and hydrogen peroxide(H2 O2) in milk.Conclusions: Dietary resveratrol supplementation during pregnancy and lactation improves the antioxidant status of sows and piglets, which is beneficial to the reproductive performance of sows. Dietary resveratrol regulates placental antioxidant gene expression by the Keap1-Nrf2 pathway and Sirt1 in placenta. | Qingwei Meng Tao Guo Gaoqiang Li Shishuai Sun Shiqi He Baojing Cheng Baoming Shi Anshan Shan | 2018 | Journal of Animal Science and Biotechnology2018，9，3： | 33 |
| 9 | Ginsenoside Rgl protects against ischemic/reperfusioninduced neuronal injury through miR-144/Nrf2/ARE pathway显示文摘Ginsenoside Rg1 (Rg1),a saponin extracted from Panax ginseng,has been well documented to be effective against ischemic/ reperfusion (I/R)neuronal injury.However,the underlying mechanisms remain obscure.In the present study,we investigated the roles of Nrf2 and miR-144 in the protective effects of Rgl against I/R-induced neuronal injury.In OGD/R-treated PC12 cells,Rgl (0.01-1 μmol/L)dose-dependently attenuated the cell injury accompanied by prolonging nuclear accumulation of Nrf2,enhancing the transcriptional activity of Nrf2,as well as promoting the expression of ARE-target genes.The activation of the Nrf2/ARE pathway by Rgl was independent of disassociation with Keapl,but resulted from post-translational regulations.Knockdown of Nrf2 abolished all the protective changes of Rgl in OG-D/R-treated PC12 cells.Furthermore,Rgl treatment significantly decreased the expression of miR-144,which downregulated Nrf2 production by targeting its 3'-untranlated region after OGD/R.Knockdown of Nrf2 had no effect on the expression of miR-144,suggesting that miR-144 was an upstream regulator of Nrf2.We revealed that there was a direct binding between Nrf2 and miR-144 in PC12 cells.Application of anti-miR-144 occluded the activation of the Nrf2/ ARE pathway by Rgl in OGD/R-treated PC12 cells.In tMCAO rats,administration of Rgl (20 mg/kg).significantly alleviated ischemic injury,and activated Nff2/ARE pathway.The protective effects of Rgl were abolished by injecting of AAV-HIF-miR-144-shRNA into the predicted ischemic penumbra.In conclusion,our results demonstrate that Rgl alleviates oxidative,stress after I/R through inhibiting miR-144 activity and subsequently promoting the Nrf2/ARE pathway at the post-translational-level. | Shi-feng Chu Zhao Zhang Xin Zhou Wen-bin He Chen Chen Piao Luo Dan-dan Liu Qi-di Ai Hai-fan Gong Zhen-zhen Wang Hong-shuo Sun Zhong-ping Feng Nai-hong Chen | 2019 | Acta Pharmacologica Sinica2019，40，1： | 30 |
| 10 | From fatty liver to fibrosis:A tale of “second hit”显示文摘Although much is known about how fat accumulates in the liver,much remains unknown about how this causes sustained hepatocellular injury.The consequences of injury are recognized as nonalcoholic steatohepatitis(NASH) and progressive fibrosis.The accumulation of fat within the hepatocytes sensitizes the liver to injury from a variety of causes and the regenerative capacity of a fatty liver is impaired.An additional stressor is sometimes referred to as a 'second hit' in a paradigm that identifies the accumulation of fat as the 'first hit'.Possible candidates for the second hit include increased oxidative stress,lipid peroxidation and release of toxic products such as malondialdehyde and 4-hydroxynonenal,decreased antioxidants,adipocytokines,transforming growth factor(TGF)-β,Fas ligand,mitochondrial dysfunction,fatty acid oxidation by CYPs(CYP 2E1,4A10 and 4A14),and peroxisomes,excess iron,small intestinal bacterial overgrowth,and the generation of gut-derived toxins such as lipopolysaccharide and ethanol.Oxidative stress is one of the most popular proposed mechanisms of hepatocellular injury.Previous studies have specifically observed increased plasma and tissue levels of oxidative stress markers and lipid peroxidation products,with reduced hepatic and plasma levels of antioxidants.There is also some indirect evidence of the benefit of antioxidants such as vitamin E,S-adenosylmethionine,betaine,phlebotomy to remove iron,and N-acetylcysteine in NASH.However,a causal relationship or a pathogenic link between NASH and oxidative stress has not been established so far.A number of sources of increased reactive oxygen species production have been established in NASH that include proinflammatory cytokines such as tumor necrosis factor(TNF)-α,iron overload,overburdened and dysfunctional mitochondria,CYPs,and peroxisomes.Briefly,the pathogenesis of NASH is multifactorial and excess intracellular fatty acids,oxidant stress,ATP depletion,and mitochondrial dysfunction are important causes of hepatocellular injury in the steatotic liver. | Metin Basaranoglu Gkcen Basaranoglu Hakan Sentürk | 2013 | World Journal of Gastroenterology2013，19，8： | 28 |
| 11 | Ginsenoside Rb1,a Panoxadiol Saponin against Oxidative Damage and Renal Interstitial Fibrosis in Rats with Unilateral Ureteral Obstruction显示文摘Objective:To investigate the possible protective effect and mechanism of ginsenoside Rb1 against oxidative damage and renal interstitial fibrosis on rats with unilateral ureteral obstruction(UUO). Methods:In total,80 male rats were randomly divided into 4 groups,20 in each group:the sham operated group (SOR),UUO group,UUO with ginsenoside Rb1 treatment group(treated with intraperitoneal injection of 50 mg/ kg daily) and UUO with Losartan treatment group(as the positive control,treated with 20 mg/kg by ga... | 谢席胜 刘衡川 杨满 左川 邓尧 樊均明 | 2009 | Chinese Journal of Integrative Medicine2009，15，2： | 25 |
| 12 | Up-Regulation of Trem2 Inhibits Hippocampal Neuronal Apoptosis and Alleviates Oxidative Stress in Epilepsy via the PI3K/Akt Pathway in Mice显示文摘Epilepsy is a chronic and severe neurological disorder that has negative effects on the autonomous activities of patients. Functionally, Trem2(triggering receptor expressed on myeloid cells-2) is an immunoglobulin receptor that affects neurological and psychiatric genetic diseases. Based on this rationale, we aimed to assess the potential role of Trem2 integration with the PI3 K/Akt pathway in epilepsy. We used microarray-based gene expression profiling to identify epilepsy-related differentially-expressed genes. In a mouse hippocampal neuron model of epilepsy, neurons were treated with lowMg^2+ extracellular fluid, and the protein and mRNA expression of Trem2 were determined. Using a gain-offunction approach with Trem2, neuronal apoptosis and its related factors were assessed by flow cytometry, RT-qPCR,and Western blot analysis. In a pilocarpine-induced epileptic mouse model, the malondialdehyde(MDA) and8-hydroxy-20-deoxyguanosine(8-OHdG) content and superoxide dismutase(SOD) and glutathione-peroxidase(GSH-Px) activity in the hippocampus were determined,and the protein expression of Trem2 was measured. In addition, the regulatory effect of Trem2 on the PI3 K/Akt pathway was analyzed by inhibiting this pathway in both the cell and mouse models of epilepsy. Trem2 was found to occupy a core position and was correlated with epilepsy.Trem2 was decreased in the hippocampus of epileptic miceand epileptic hippocampal neurons. Of crucial importance,overexpression of Trem2 activated the PI3 K/Akt pathway to inhibit neuronal apoptosis. Moreover, activation of the PI3 K/Akt pathway through over-expression of Trem2 alleviated oxidative stress, as shown by the increased expression of SOD and GSH-Px and the decreased expression of MDA and 8-OHdG. The current study defines the potential role of Trem2 in inhibiting the development of epilepsy, indicating that Trem2 up-regulation alleviates hippocampal neuronal injury and oxidative stress, and inhibits neuronal apoptosis in epilepsy by activating the PI3 K/Akt pathway. | Ai-Hua Liu Min Chu Yu-Ping Wang | 2019 | Neuroscience Bulletin2019，35，3： | 25 |
| 13 | Matrine attenuates oxidative stress and cardiomyocyte apoptosis in doxorubicin-induced cardiotoxicity via maintaining AMPKα/UCP2 pathway显示文摘Oxidative stress and cardiomyocyte apoptosis are involved in the pathogenesis of doxorubicin(DOX)-induced cardiotoxicity. Matrine is well-known for its powerful anti-oxidant and anti-apoptotic capacities. Our present study aimed to investigate the effect of matrine on DOX-induced cardiotoxicity and try to unearth the underlying mechanisms. Mice were exposed with DOX to generate DOX-induced cardiotoxicity or normal saline as control. H9 C2 cells were used to verify the effect of matrine in vitro.DOX injection triggered increased generation of reactive oxygen species(ROS) and excessive cardiomyocyte apoptosis, which were significantly mitigated by matrine. Mechanistically, we found that matrine ameliorated DOX-induced uncoupling protein 2(UCP2) downregulation, and UCP2 inhibition bygenipin could blunt the protective effect of matrine on DOX-induced oxidative stress and cardiomyocyte apoptosis. Besides, 50-AMP-activated protein kinase α2(Ampkα2) deficiency inhibited matrine-mediated UCP2 preservation and abolished the beneficial effect of matrine in mice. Besides, we observed that matrine incubation alleviated DOX-induced H9 C2 cells apoptosis and oxidative stress level via activating AMPKα/UCP2, which were blunted by either AMPKα or UCP2 inhibition with genetic or pharmacological methods. Matrine attenuated oxidative stress and cardiomyocyte apoptosis in DOX-induced cardiotoxicity via maintaining AMPKα/UCP2 pathway, and it might be a promising therapeutic agent for the treatment of DOX-induced cardiotoxicity. | Can Hu Xin Zhang Wenying Wei Ning Zhang Haiming Wu Zhenguo Ma Lingli Li Wei Deng Qizhu Tang | 2019 | Acta Pharmaceutica Sinica B2019，9，4： | 25 |
| 14 | Coronary microvascular dysfunction in diabetes mellitus:A review显示文摘The exploration of coronary microcirculatory dysfunction in diabetes has accelerated in recent years.Cardiac function is compromised in diabetes.Diabetic patients manifest accelerated atherosclerosis in coronary arteries.These data are confirmed in diabetic animal mod-els,where lesions of small coronary arteries have been described.These concepts are epitomized in the classic microvascular complications of diabetes,i.e.blindness,kidney failure and distal dry gangrene.Most importantly,accumulating data indicate that insights gained from the link between inflammation and diabetes can yield predictive and prognostic information of considerable clinical utility.This review summarizes the evidence for the predisposing factors and the mechanisms involved in diabetes,and assesses the current state of knowledge regarding the triggers for inflammation in this disease.We evaluate the roles of hyperglycemia,oxidative stress,polyol pathway,protein kinase C,advanced glycation end products,insulin resistance,peroxisome proliferator-activated receptor-γ,inflammation,and diabetic cardiomyopathy as a 'stem cell disease'.Furthermore,we discuss the mechanisms responsible for impaired coronary arteriole function.Finally,we consider how new insights in diabetes may provide innovative therapeutic strategies. | Andrea Picchi Stefano Capobianco Marta Focardi | 2010 | World Journal of Cardiology2010，2，11： | 24 |
| 15 | AtHsfA2 modulates expression of stress responsive genes and enhances tolerance to heat and oxidative stress in Arabidopsis显示文摘There is increasing evidence for considerable interlinking between the responses to heat stress and oxidative stress, and recent researches suggest heat shock transcription factors (Hsfs) play an important role in linking heat shock with oxidative stress signals. In this paper, we present evidence that AtHsfA2 modulated expression of stress responsive genes and enhanced tolerance to heat and oxidative stress in Arabidopsis. Using Northern blot and quantitative RT-PCR analysis, we demonstrated that the expression of AtHsfA2 was induced by not only HS but also oxidative stress. By functional analysis of AtHsfA2 knockout mutants and AtHsfA2 overexpressing transgenic plants, we also demonstrated that the mutants displayed reduced the basal and acquired thermotolerance as well as oxidative stress tolerance but the overexpression lines displayed increased tolerance to these stress. The phenotypes correlated with the expres-sion of some Hsps and APX1, ion leakage, H2O2 level and degree of oxidative injuries. These results showed that, by modulated expression of stress responsive genes, AtHsfA2 enhanced tolerance to heat and oxidative stress in Arabidopsis. So we suggest that AtHsfA2 plays an im-portant role in linking heat shock with oxidative stress signals. | LI Chunguang1,2, CHEN Qijun1, GAO Xinqi1,3, QI Bishu1, CHEN Naizhi1, XU Shouming1, CHEN Jia1 & WANG Xuechen1 1. State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100094, China 2. Department of Industry Engineering, Zhengzhou Institute of Aeronautic Industry Management, Zhengzhou 450015, China 3. College of Life Science, Qufu Normal University, Qufu Shandong 273165, China | 2005 | Science China(Life Sciences)2005，48，6： | 23 |
| 16 | Oxidative stress:New insights on the association of nonalcoholic fatty liver disease and atherosclerosis显示文摘Non-alcoholic fatty liver disease(NAFLD) represents the most common and emerging chronic liver disease worldwide. It includes a wide spectrum of liver diseasesranging from simple fatty liver to non-alcoholic steatohepatitis(NASH),which may progress to fibrosis and more severe liver complications such as cirrhosis,hepatocellular carcinoma and liver mortality. NAFLD is strongly associated with obesity,insulin resistance,hypertension,and dyslipidaemia,and is now regarded as the liver manifestation of the metabolic syndrome. The increased mortality of patients with NAFLD is primarily a result of cardiovascular disease and,to a lesser extent,to liver related diseases. Increased oxidative stress has been reported in both patients with NAFLD and patient with cardiovascular risk factors. Thus,oxidative stress represents a shared pathophysiological disorder between the two conditions. Several therapeutic strategies targeting oxidative stress reduction in patients with NAFLD have been proposed,with conflicting results. In particular,vitamin E supplementation has been suggested for the treatment of non-diabetic,non-cirrhotic adults with active NASH,although this recommendation is based only on the results of a single randomized controlled trial. Other antioxidant treatments suggested are resveratrol,silybin,L-carnitine and pentoxiphylline. No trial so far,has evaluated the cardiovascular effects of antioxidant treatment in patients with NAFLD. New,large-scale studies including as end-point also the assessment of the atherosclerosis markers are needed. | Licia Polimeni Maria Del Ben Francesco Baratta Ludovica Perri Fabiana Albanese Daniele Pastori Francesco Violi Francesco Angelico | 2015 | World Journal of Hepatology2015，7，10： | 23 |
| 17 | Redox imbalance stress in diabetes mellitus: Role of the polyol pathway显示文摘In diabetes mellitus, the polyol pathway is highly active and consumes approximately 30% glucose in the body. This pathway contains 2 reactions catalyzed by aldose reductase(AR) and sorbitol dehydrogenase, respectively. AR reduces glucose to sorbitol at the expense of NADPH, while sorbitol dehydrogenase converts sorbitol to fructose at the expense of NAD+, leading to NADH production. Consumption of NADPH, accumulation of sorbitol, and generation of fructose and NADH have all been implicated in the pathogenesis of diabetes and its complications. In this review, the roles of this pathway in NADH/NAD+redox imbalance stress and oxidative stress in diabetes are highlighted. A potential intervention using nicotinamide riboside to restore redox balance as an approach to fighting diabetes is also discussed. | Liang-jun Yan | 2018 | Animal Models and Experimental Medicine2018，1，1： | 22 |
| 18 | Contribution of oxidative stress to pulmonary arterial hypertension显示文摘Recent data implicate oxidative stress as a mediator of pulmonary hypertension (PH) and of the associated pathological changes to the pulmonary vasculature and right ventricle (RV). Increases in reactive oxygen species (ROS), altered redox state, and elevated oxidant stress have been demonstrated in the lungs and RV of several animal models of PH, including chronic hypoxia, monocrotaline toxicity, caveolin-1 knock-out mouse, and the transgenic Ren2 rat which overexpresses the mouse renin gene. Generation of ROS in these models is derived mostly from the activities of the nicotinamide adenine dinucleotide phosphate oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase. As disease progresses circulating monocytes and bone marrow-derived monocytic progenitor cells are attracted to and accumulate in the pulmonary vasculature. Once established, these inflammatory cells generate ROS and secrete mitogenic and fibrogenic cytokines that induce cell proliferation and fibrosis in the vascular wall resulting in progressive vascular remodeling. Deficiencies in antioxidant enzymes also contribute to pulmonary hypertensive states. Current therapies were developed to improve endothelial function, reduce pulmonary artery pressure, and slow the progression of vascular remodeling in the pulmonary vasculature by targeting deficiencies in either NO (PDE-type 5 inhibition) or PGI 2 (prostacyclin analogs), or excessive synthesis of ET-1 (ET receptor blockers) with the intent to improve patient clinical status and survival. New therapies may slow disease progression to some extent, but long term management has not been achieved and mortality is still high. Although little is known concerning the effects of current pulmonary arterial hypertension treatments on RV structure and function, interest in this area is increasing. Development of therapeutic strategies that simultaneously target pathology in the pulmonary vasculature and RV may be beneficial in reducing mortality associated with RV failure. | Vincent G DeMarco Adam T Whaley-Connell James R Sowers Javad Habibi Kevin C Dellsperger | 2010 | World Journal of Cardiology2010，2，10： | 21 |
| 19 | Mitophagy links oxidative stress conditions and neurodegenerative diseases显示文摘Mitophagy is activated by a number of stimuli, including hypoxia, energy stress, and increased oxidative phosphorylation activity. Mitophagy is associated with oxidative stress conditions and central neurodegenerative diseases. Proper regulation of mitophagy is crucial for maintaining homeostasis; conversely, inadequate removal of mitochondria through mitophagy leads to the generation of oxidative species, including reactive oxygen species and reactive nitrogen species, resulting in various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. These diseases are most prevalent in older adults whose bodies fail to maintain proper mitophagic functions to combat oxidative species. As mitophagy is essential for normal body function, by targeting mitophagic pathways we can improve these disease conditions. The search for effective remedies to treat these disease conditions is an ongoing process, which is why more studies are needed. Additionally, more relevant studies could help establish therapeutic conditions, which are currently in high demand. In this review, we discuss how mitophagy plays a significant role in homeostasis and how its dysregulation causes neurodegeneration. We also discuss how combating oxidative species and targeting mitophagy can help treat these neurodegenerative diseases. | Ulfuara Shefa Na Young Jeong In Ok Song Hyung-Joo Chung Dokyoung Kim Junyang Jung Youngbuhm Huh | 2019 | Neural Regeneration Research2019，14，5： | 21 |
| 20 | Protective effect of naringenin on acetic acid-induced ulcerative colitis in rats显示文摘AIM:To evaluate the ameliorative effect of naringenin(NG)during ulcerative colitis(UC)in rats.METHODS:Rats were treated with three different doses(25,50 and 100 mg/kg per day)of NG and a single dose of mesalazine(MES,300 mg/kg per day)for seven days prior to ulcerative colitis induction by4%acetic acid(AA).Twenty four hours after AA rectal administration,animals were scarified and the colonic tissues were dissected.Colonic mucus content was estimated using Alcian blue dye binding technique.In colon tissues,levels of total glutathione sulphadryls(T-GSH),non-protein sulphadryls(NP-SH)and thiobarbituric acid reactive substances(TBARS)were evaluated.The activities of the antioxidant enzymes,catalase(CAT)and superoxide dismutase(SOD)were measured.Concentrations of nucleic acids(DNA and RNA)and total protein were also estimated in colon tissues.Colonic levels of tumor necrosis factor-(TNF-),interleukin-1(IL-1),interleukin-6(IL-6),prostaglandin E2(PGE2)and nitric oxide(NO)were estimated.In cross section of colitis tissue the histopathological changes were observed.RESULTS:Colonic mucus content was decreased in AA compared to controls(587.09±65.59 mg/kg vs941.78±68.41 mg/kg,P<0.001).AA administration markedly reduced T-GSH(5.25±0.37 nmol/L vs 3.04±0.24 nmol/L,P<0.01),NP-SH(3.16±0.04 nmol/L vs 2.16±0.30 nmol/L,P<0.01),CAT(6.77±0.40 U/mg vs 3.04±0.2 U/mg,P<0.01)and SOD(3.10±0.11U/mg vs 1.77±0.18 U/mg,P<0.01)while TBARS,TNF-,IL-1,IL-6,PGE2 and NO levels(15.09±3.84nmol/L vs 59.90±16.34 nmol/L,P<0.01;113.56±1.91 pg/mg vs 134.24±4.77 pg/mg,P<0.01;209.20±36.38 pg/mg vs 422.19±31.47 pg/mg,P<0.01;250.83±25.09 pg/mg vs 638.58±115.9 pg/mg,P<0.01;248.19±36.98 pg/mg vs 541.74±58.34 pg/mg,P<0.01 and 81.26±2.98 mmol/g vs 101.90±10.73 mmol/g,P<0.001)were increased in colon of rats with UC compared controls respectively.Naringenin supplementation,significantly and dose dependently increased the colonic mucus content.The elevated TBARS levels were significantly decreased(39.35±5.86nmol/L,P<0.05;26.74±3.17 nmol/L,P<0.01 nmol/L and 17.74±2.69 nmol/L,P<0.01)compared to AA(59.90±16.34 nmol/L)group while the decreased levels of T-GSH and NP-SH and activities of CAT and SOD found increased by NG treatments in dose dependent manner.The decreased values of nucleic acids and total protein in AA group were also significantly(P<0.01)increased in all three NG supplemented groupsrespectively.NG pretreatment inhibited the TNF-levels(123.76±3.76 pg/mg,122.62±3.41 pg/mg and121.51±2.61 pg/mg vs 134.24±4.78 pg/mg,P<0.05)compared to AA group,respectively.Interleukins,IL-1 and IL-6 levels were also decreased in NG50+AA(314.37±16.31 pg/mg and 292.58±23.68 pg/mg,P<0.05)and NG100+AA(416.72±49.62 pg/mg and 407.96±43.87 pg/mg,P<0.05)when compared to AA(352.46±8.58 pg/mg and 638.58±115.98pg/mg)group.Similar decrease(P<0.05)was seen in PGE2and NO values when compared to AA group.The group pretreated with MES,as a reference drug,showed significant(P<0.01)protection against the changes induced in colon tissue by AA administration respectively.CONCLUSION:In present study,NG produced antioxidant and anti-inflammatory effects demonstrating protective effect in inflammatory bowel disease. | Salim S Al-Rejaie Hatem M Abuohashish Maher M Al-Enazi Abdullah H Al-Assaf Mihir Y Parmar Mohammed M Ahmed | 2013 | World Journal of Gastroenterology2013，19，34： | 20 |
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