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| 1 | Th e role of ferroptosis in ionizing radiation-induced cell death and tumor suppression显示文摘Ferroptosis,a form of regulated cell death caused by lipid peroxidation,was recently identified as a natural tumor suppression mechanism.Here,we show that ionizing radiation(IR)induces ferroptosis in cancer cells.Mechanistically,IR induces not only reactive oxygen species(ROS)but also the expression of ACSL4,a lipid metabolism enzyme required for ferroptosis,resulting in elevated lipid peroxidation and ferroptosis.ACSL4 ablation largely abolishes IR-induced ferroptosis and promotes radioresistance.IR also induces the expression of ferroptosis inhibitors,including SLC7A11 and GPX4;as an adaptive response.IR-or KEAP1 deficiencyinduced SLC7A11 expression promotes radioresistance through inhibiting ferroptosis.Inactivating SLC7A11 or GPX4 with ferroptosis inducers(FINs)sensitizes radioresistant cancer cells and xenograft tumors to IR.Furthermore,radiotherapy induces ferroptosis in cancer patients,and increased ferroptosis correlates with better response and longer survival to radiotherapy in cancer patients.Our study reveals a previously unrecognized link between IR and ferroptosis and indicates that further exploration of the combination of radiotherapy and FINs in cancer treatment is warranted. | Guang Lei Yilei Zhang Pranavi Koppula Xiaoguang Liu Jie Zhang Steven HLin Jaffer AAjani Qin Xiao Zhongxing Liao Hui Wang Boyi Gan | 2020 | Cell Research2020，30，2： | 88 |
| 2 | Erianin,a novel dibenzyl compound in Dendrobium extract,inhibits lung cancer cell growth and migration via calcium/calmodulin-dependent ferroptosis显示文摘Ferroptosis,a novel form of programmed cell death,is characterized by iron-dependent lipid peroxidation and has been shown to be involved in multiple diseases,including cancer.Stimulating ferroptosis in cancer cells may be a potential strategy for cancer therapy.Therefore,ferroptosis-inducing drugs are attracting more attention for cancer treatment.Here,we showed that erianin,a natural product isolated from Dendrobium chrysotoxum Lindl,exerted its anticancer activity by inducing cell death and inhibiting cell migration in lung cancer cells.Subsequently,we demonstrated for the first time that erianin induced ferroptotic cell death in lung cancer cells,which was accompanied by ROS accumulation,lipid peroxidation,and GSH depletion.The ferroptosis inhibitors Fer-1 and Lip-1 but not Z-VAD-FMK,CQ,or necrostatin-1 rescued erianin-induced cell death,indicating that ferroptosis contributed to erianin-induced cell death.Furthermore,we demonstrated that Ca^(2+)/CaM signaling was a critical mediator of erianin-induced ferroptosis and that blockade of this signaling significantly rescued cell death induced by erianin treatment by suppressing ferroptosis.Taken together,our data suggest that the natural product erianin exerts its anticancer effects by inducing Ca^(2+)/CaMdependent ferroptosis and inhibiting cell migration,and erianin will hopefully serve as a prospective compound for lung cancer treatment. | Peng Chen Qibiao Wu Jiao Feng Lili Yan Yitian Sun Shuiping Liu Yu Xiang Mingming Zhang Ting Pan Xiaying Chen Ting Duan Lijuan Zhai Bingtao Zhai Wengang Wang Ruonan Zhang Bi Chen Xuemeng Han Yicong Li Liuxi Chen Ying Liu Xingxing Huang Ting Jin Wenzheng Zhang Hong Luo Xiaohui Chen Yongqiang Li Qiujie Li Guohua Li Qin Zhang Lvjia Zhuo Zuyi Yang Huifen Tang Tian Xie Xiaoping Ouyang Xinbing Sui | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 42 |
| 3 | A study on relationship of nitric oxide,oxidation,peroxidation,lipoperoxidation with chronic cholecystitis显示文摘AIM To study relationship of injury induced bynitric oxide,oxidation,peroxidation,lipoperoxidation with chronic cholecystitis.METHODS The values of plasma nitric oxide(P-NO),plasma vitamin C(P-VC),plasma vitamin E(P-VE),plasma β-carotene(P-β-CAR),plasmalipoperoxides(P-LPO),erythrocyte superoxidedismutase(E-SOD),erythrocyte catalase(E-CAT),erythrocyte glutathione peroxidase(E-GSH-Px)activities and erythrocyte lipoperoxides(E-LPO)level in 77 patients with chronic cholecystitisand 80 healthy control subjects were determined,differences of the above average values betweenthe patient group and the control group anddifferences of the average values betweenpreoperative and postoperative patients wereanalyzed and compared,linear regression andcorrelation of the disease course with the abovedetermination values as well as the stepwiseregression and correlation of the course with thevalues were analyzed.RESULTS Compared with the control group,theaverage values of P-NO,P-LPO,E-LPO weresignificantly increased(P<0.01),and of P-VC, P-VE,P-β-CAR,E-SOD,E-CAT and E-GSH-Pxdecreased(P<0.01)in the patient group.Theanalysis of the linear regression and correlationshowed that with prolonging of the course,thevalues of P-NO,P-LPO and E-LPO in the patientswere gradually ascended and the values of P-VC,P-VE,P-β-CAR,E-SOD,E-CAT and E-GSH-Pxdescended(P<0.01).The analysis of thestepwise regression and correlation indicated thatthe correlation of the course with P-NO,P-VE andP-β-CAR values was the closest.Compared withthe preoperative patients,the average values of P-NO,P-LPO and E-LPO were significantlydecreased(P<0.01)and the average values of P-VC,E-SOD,E-CAT and E-GSH-Px in postoperativepatients increased(P<0.01)in postoperativepatients.But there was no significant difference inthe average values of P-VE,P-β-CAR preoperativeand postoperative patients.CONCLUSION Chronic cholecystitis could inducethe increase of nitric oxide,oxidation,peroxidation and lipoperoxidation. | Jun Fu Zhou Dong Cai You Gen Zhu Jin Lu Yang Cheng Hong Peng Yang Hai Yu | 2000 | World Journal of Gastroenterology2000，6，4： | 36 |
| 4 | Deferoxamine promotes recovery of traumatic spinal cord injury by inhibiting ferroptosis显示文摘Ferroptosis is an iron-dependent novel cell death pathway. Deferoxamine, a ferroptosis inhibitor, has been reported to promote spinal cord injury repair. It has yet to be clarified whether ferroptosis inhibition represents the mechanism of action of Deferoxamine on spinal cord injury recovery. A rat model of Deferoxamine at thoracic 10 segment was established using a modified Allen's method. Ninety 8-week-old female Wistar rats were used. Rats in the Deferoxamine group were intraperitoneally injected with 100 mg/kg Deferoxamine 30 minutes before injury. Simultaneously, the Sham and Deferoxamine groups served as controls. Drug administration was conducted for 7 consecutive days. The results were as follows:(1) Electron microscopy revealed shrunken mitochondria in the spinal cord injury group.(2) The Basso, Beattie and Bresnahan locomotor rating score showed that recovery of the hindlimb was remarkably better in the Deferoxamine group than in the spinal cord injury group.(3) The iron concentration was lower in the Deferoxamine group than in the spinal cord injury group after injury.(4) Western blot assay revealed that, compared with the spinal cord injury group, GPX4, xCT, and glutathione expression was markedly increased in the Deferoxamine group.(5) Real-time polymerase chain reaction revealed that, compared with the Deferoxamine group, mRNA levels of ferroptosis-related genes Acyl-CoA synthetase family member 2(ACSF2) and iron-responsive element-binding protein 2(IREB2) were up-regulated in the Deferoxamine group.(6) Deferoxamine increased survival of neurons and inhibited gliosis. These findings confirm that Deferoxamine can repair spinal cord injury by inhibiting ferroptosis. Targeting ferroptosis is therefore a promising therapeutic approach for spinal cord injury. | Xue Yao Yan Zhang Jian Hao Hui-Quan Duan Chen-Xi Zhao Chao Sun Bo Li Bao-You Fan Xu Wang Wen-Xiang Li Xuan-Hao Fu Yong Hu Chang Liu Xiao-Hong Kong Shi-Qing Feng | 2019 | Neural Regeneration Research2019，14，3： | 35 |
| 5 | 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 |
| 6 | Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage显示文摘Intracerebral haemorrhage (ICH) is a devastating type of stroke with high mortality and morbidity. However, we have few options for ICH therapy and limited knowledge about post-ICH neuronal death and related mechanisms. In the aftermath of ICH, iron overload within the perihaematomal region can induce lethal reactive oxygen species (ROS) production and lipid peroxidation, which contribute to secondary brain injury. Indeed, iron chelation therapy has shown efficacy in preclinical ICH studies. Recently, an iron-dependent form of non-apoptotic cell death known as ferroptosis was identified. It is characterised by an accumulation of iron-induced lipid ROS, which leads to intracellular oxidative stress. The ROS cause damage to nucleic acids, proteins and lipid membranes, and eventually cell death. Recently, we and others discovered that ferroptosis does occur after haemorrhagic stroke in vitro and in vivo and contributes to neuronal death. Inhibition of ferroptosis is beneficial in several in vivo and in vitro ICH conditions. This minireview summarises current research on iron toxicity, lipid peroxidation and ferroptosis in the pathomechanisms of ICH, the underlying molecular mechanisms of ferroptosis and the potential for combined therapeutic strategies. Understanding the role of ferroptosis after ICH will provide a vital foundation for cell death-based ICH treatment and prevention. | Jieru Wan Honglei Ren Jian Wang | 2019 | Stroke & Vascular Neurology2019，4，2： | 32 |
| 7 | Targeting ferroptosis suppresses osteocyte glucolipotoxicity and alleviates diabetic osteoporosis显示文摘Diabetic osteoporosis(DOP) is the leading complication continuously threatening the bone health of patients with diabetes. A key pathogenic factor in DOP is loss of osteocyte viability. However, the mechanism of osteocyte death remains unclear. Here, we identified ferroptosis, which is iron-dependent programmed cell death, as a critical mechanism of osteocyte death in murine models of DOP. The diabetic microenvironment significantly enhanced osteocyte ferroptosis in vitro, as shown by the substantial lipid peroxidation, iron overload, and aberrant activation of the ferroptosis pathway. RNA sequencing showed that heme oxygenase-1(HO-1) expression was notably upregulated in ferroptotic osteocytes. Further findings revealed that HO-1 was essential for osteocyte ferroptosis in DOP and that its promoter activity was controlled by the interaction between the upstream NRF2 and c-JUN transcription factors. Targeting ferroptosis or HO-1 efficiently rescued osteocyte death in DOP by disrupting the vicious cycle between lipid peroxidation and HO-1 activation, eventually ameliorating trabecular deterioration. Our study provides insight into DOP pathogenesis, and our results provide a mechanism-based strategy for clinical DOP treatment. | Yiqi Yang Yixuan Lin Minqi Wang Kai Yuan Qishan Wang Pei Mu Jingke Du Zhifeng Yu Shengbing Yang Kai Huang Yugang Wang Hanjun Li Tingting Tang | 2022 | Bone Research2022，10，3： | 19 |
| 8 | Cuproptosis:a copper-triggered modality of mitochondrial cell death显示文摘Various heavy metals can induce regulated cell death through different subroutines.A recent study published in Science found that intracellular copper accumulation triggers the aggregation of mitochondrial lipoylated proteins and the destabilization of Fe–S cluster proteins,leading to a unique type of cell death termed cuproptosis.Beyond classical apoptosis,several forms of regulated cell death(RCD)have been identified.These RCD subroutines differ in the initiating stimuli,intermediate activation events,and end effectors.1 Heavy metal ions are essential micronutrients,but either insufficient or excessive abundance of metals can trigger cell death.For example,ferroptosis has been defined as an iron-dependent form of oxidative cell death caused by unrestricted lipid peroxidation.2 Surprisingly,a recent study by Tsvetkov and colleagues showed that intracellular copper(Cu)induces a novel form of RCD that is different from oxidative stress-related cell death(e.g.,apoptosis,ferroptosis,and necroptosis)and has been termed“cuproptosis”.3 In contrast,mitochondrial stress,especially the aggregation of lipoylated mitochondrial enzymes and the loss of Fe–S cluster proteins,ignites cuproptosis(Fig.1). | Daolin Tang Xin Chen Guido Kroemer | 2022 | Cell Research2022，32，5： | 19 |
| 9 | Neuroprotection of Cyperus esculentus L. orientin against cerebral ischemia/reperfusion induced brain injury显示文摘Orientin is a flavonoid monomer.In recent years,its importance as a source of pharmacological active substance is growing rapidly due to its properties such as anti-myocardial ischemia,anti-apoptosis,anti-radiation,anti-tumor,and anti-aging.However,the neuroprotective effects of Orientin on stroke injury have not been comprehensively evaluated.The aim of the present study was thus to investigate the neuroprotective capacity and the potential mechanisms of Cyperus esculentus L.orientin(CLO)from Cyperus esculentus L.leaves against ischemia/reperfusion(I/R)injury using standard orientin as control.For in vitro studies,we treated HT22 cells with CoCl2 as an in vitro ischemic injury model.HT22 cells in the control group were treated with CoCl2.For in vivo studies,we used rat models of middle cerebral artery occlusion,and animals that received sham surgery were used as controls.We found that CLO protected CoCl2-induced HT22 cells against ischemia/reperfusion injury by lowering lipid peroxidation and reactive oxygen species formation as well as decreasing protein oxidation.However,CLO did not reduce the release of lactate dehydrogenase nor increase the activity of superoxide dismutase.Results showed that CLO could decrease neurological deficit score,attenuate brain water content,and reduce cerebral infarct volume,leading to neuroprotection during cerebral ischemia-reperfusion injury.Our studies indicate that CLO flavonoids can be taken as a natural antioxidant and bacteriostastic substance in food and pharmaceutical industry.The molecular mechanisms of CLO could be at least partially attributed to the antioxidant properties and subsequently inhibiting activation of casepase-3.All experimental procedures and protocols were approved on May 16,2016 by the Experimental Animal Ethics Committee of Xinjiang Medical University of China(approval No.IACUC20160516-57). | Si-Qun Jing Sai-Sai Wang Rui-Min Zhong Jun-Yan Zhang Jin-Zi Wu Yi-Xian Tu Yan Pu Liang-Jun Yan | 2020 | Neural Regeneration Research2020，15，3： | 16 |
| 10 | Ferroptosis:mechanisms and links with diseases显示文摘Ferroptosis is an iron-dependent cell death,which is different from apoptosis,necrosis,autophagy,and other forms of cell death.The process of feroptotic cell death is defined by the accumulation of lethal lipid species derived from the peroxidation of lipids,which can be prevented by iron chelators(e.g.deferiprone,deferoxamine)and small lipophilic antioxidants(e.g,ferrostatin,liproxstatin).This review summarizes current knowledge about the regulatory mechanism of ferroptosis and its association withseveral pathways,including iron,lipid,and cysteine metabolism.We have further discussed the contribution of ferroptosis to thepathogenesis of several diseases such as cancer,ischemia/reperfusion,and various neurodegenerative diseases(e.g.Alzheimersdisease and Parkinson's disease),and evaluated the therapeutic applications of ferroptosis inhibitors in clinics. | Hong-fa Yan Ting Zou Qing-zhang Tuo Shuo Xu Hua Li Abdel Ali Belaidi Peng Lei | 2021 | Signal Transduction and Targeted Therapy2021，6，3： | 16 |
| 11 | Protective actions of salvianolic acid A on hepatocyte injured by peroxidation in vitro显示文摘INTRODUCTION Salvianolic radix,one of the most commonly usedtraditional Chinese herbs,was widely studied aboutits actions against liver injury and fibrosis,and wasone of the focuses of recent research.Salvianolic acid-A(SA-A)was an aqueous solublecomponent of Salvianolic radix.In our | Hu YY Liu CH Wang RP Liu C Liu P Zhu DY | 2000 | World Journal of Gastroenterology2000，6，3： | 15 |
| 12 | Proline accumulation in rice seedlings exposed to hydroxyl radical stress in relation to antioxidation显示文摘PROLINE(Pro)is an essential amino acid for proteins and free Pro extensively exists in plants.Pro accumulates in plant cells in response to water stress,salinity,low temperature,air pollu-tants,etc.and has been mainly studied for its role in the osmotic adjustment of plants subject-ed to drought and salinity.In addition to acting as a cytoplasmic osmoticum,Pro | Jiang, MY Guo, SC Zhang, XM | 1997 | Chinese Science Bulletin1997，42，10： | 14 |
| 13 | Effect of medium-chain triglycerides on growth performance, nutrient digestibility,plasma metabolites and antioxidant capacity in weanling pigs显示文摘The aim of this study was to investigate the effect of medium-chain triglycerides(MCTs) on growth performance, nutrient digestibility, plasma metabolites and antioxidant capacity in weanling pigs. A total of 160 weanling(Duroc × Landrace x Yorkshire) pigs(age: 21 ± 1 d; body weight: 7.50 ± 0.28 kg) were randomly allotted to 4 treatments, receiving the following diets for 28 d: control diet [containing 3.5%soybean oil(SO)], MCT1 diet(containing 0.7% MCTs and 2.8% SO), MCT2 diet(containing 1.4% MCTs and2.1% SO) and MCT3 diet(containing 2.1% MCTs and 1.4% SO). Dietary inclusion of MCTs improved the average daily gain and feed efficiency(FE) of pigs compared with the control during the first 2 weeks post-weaning(P < 0.05). A similar positive effect was also observed for the overall FE in MCT2 group(P < 0.05). Compared with the control, apparent total tract digestibility(ATTD) of ether extract was improved by MCT2 and MCT3 treatment from day 12-14 post-weaning(P < 0.05). In addition, MCT2 treatment also exerted a beneficial effect on the ATTD of dry matter(P < 0.05). The increased total protein concentration and decreased urea nitrogen and malondialdehyde levels of plasma were observed in both MCT2 and MCT3 groups on day 14 post-weaning(P < 0.05). In conclusion, MCTs could improve growth performance, nutrients utilization, and antioxidant ability of weanling piglets. | Yue Li Hao Zhang Li Yang Lili Zhang Tian Wang | 2015 | Animal Nutrition2015，，1： | 13 |
| 14 | Modulatory effect of pineapple peel extract on lipid peroxidation,catalase activity and hepatic biomarker levels in blood plasma of alcoholinduced oxidative stressed rats显示文摘Objective:To investigate the ability of the methanolic extract of pineapple peel to modulate alcohol-induced lipid peroxidation,changes in catalase activities and hepatic biochemical marker levels in blood plasma.Methods:Oxidative stress was induced by oral administration of ethanol(20%w/v) at a dosage of 5 niL/kg bw in rats.After 28 days of treatment,the rats were fasted overnight and sacrificed by cervical dislocation.Blood was collected with a 2 mL syringe by cardiac puncture and was centrifuged at 3000 rpm for 10 min.The plasma was analyzed to evaluate malondialdehyde(MDA),catalase activity,aspartate aminotransferase(AST),alkaline phosphatase(ALP) and alanine aminotransferase(ALT) concentrations.Results:Administration of alcohol caused a drastic increase(87.74%) in MDA level compared with the control.Pineapple peel extract significantly reduced the MDA level by 60.16%at 2.S mL/kg bw.Rats fed alcohol only had the highest catalase activity,treatment with pineapple peel extract at 2.5 mL/kg bw however, reduced the activity.Increased AST,ALP and ALT activities were observed in rats fed alcohol only respectively,treatment with pineapple peel extract drastically reduced their activities. Conclusions:The positive modulation of lipid peroxidation,catalase activities as well as hepatic biomarker levels of blood plasma by the methanolic extract of pineapple peels under alcoholinduced oxidative stress is an indication of its protective ability in the management of alcoholinduced toxicity. | Okafor OY Erukainure OL Ajiboye JA Adejobi RO Owolabi FO Kosoko SB | 2011 | Asian Pacific Journal of Tropical Biomedicine2011，1，1： | 13 |
| 15 | In vitro inhibition activity of polyphenol-rich extracts from Syzygium aromaticum(L.)Merr.& Perry(Clove)buds against carbohydrate hydrolyzing enzymes linked to type 2 diabetes and Fe^(2+)-induced lipid peroxidation in rat pancreas显示文摘Objective:To investigate and compare the inhibitor)'properties)of free and bound phenolic extracts of clove bud against carbohydrate hydrolyzing enzymes(alpha-amylase&alphaglucosidase)and Fe^(2+)-induced lipid peroxidation in rat pancreas in vitro.Methods:The free phenolics were extracted with 80%.(v/v)acetone,while bound phenolics were extracted from the alkaline and acid hydrolyzed residue with ethyl acetate.Then,the interaction of the extracts with alpha-amylase and alpha-glucosidase was subsequently assessed.Thereafter,the total phenolic contents and antioxidant activities of the extracts were determined.Results:The result revealed that both extracts inhibited alpha-amylase and alpha-glucosidase in a dose-dependent manner.However,the alpha-glucosidase inhibitory activity of the extracts were significantly(P<0.05)higher than their alpha-amylase inhibitory activity.The free phenolics(31.67 mg/g)and flavonoid(17.28 mg/g)contents were significantly(P<0.05)higher than bound phenolic(23.52 mg/g)and flavonoid(13.70 mg/g)contents.Both extracts also exhibited high antioxidant activities as typified by their high reducing power,LI diphenyl-2-picrylhydrazyl(DPPH)and 2,2-azinobis-3-ethylbenzo-thiazoline-6-sulfonate(ABTS)radical scavenging abilities,as well as inhibition of Fe^(2+)-induced lipid peroxidation in rat pancreas in vitro.Conclusions:This study provides a biochemical rationale by which clove elicits therapeutic effect on type 2 diabetes. | Stephen Adeniyi Adefegha Ganiyu Oboh | 2012 | Asian Pacific Journal of Tropical Biomedicine2012，2，10： | 11 |
| 16 | Prevention of Cistanche salsa Extract on Hepatic Fibrosis Induced by Carbon Tetrachloride in Rats显示文摘Objective To explore the antifibrotic effect of echinacoside on carbon tetrachloride(CCl4)-induced hepatic fibrosis in rats.Methods Male Wistar rats were randomly divided into normal control(n=8),model(n=14),and echinacoside treatment(n=14)groups.The hepatic fibrosis model was induced by CCl4compositor.The rats were ig administered with echinacoside at a daily dose of 50 mg/kg.The anti-oxidant status,liver function parameters,and hepatic hydroxyproline content were detected by chromatometry.The serum levels of hyaluronic acid(HA),type IV collagen(CIV),type III precollagen(PIIIP),and laminin(LN)were assayed with radioimmunoassay.The hpatic injury was detected by haematoxylin-eosine staining.The deposition of collagen was observed with Masson staining.Results Echinacoside increased the superoxide dismutase activity and reduced the levels of malondialdehyde,aspartate aminotransferase,alanine aminotransferase,HA,CIV,PIIIP,and LN in serum.Echinacoside could also reduce the hydroxyproline content in liver,alleviate hepatic injury,and inhibit collagen deposition.Conclusion Echinacoside possesses antihepatic fibrosis effect. | YANG Feng-rui WEN Du-su FANG Bu-wu LOU Jian-shi MENG Lin | 2013 | Chinese Herbal Medicines2013，5，3： | 10 |
| 17 | 氧自由基脂质过氧化反应对肺部组织细胞损伤的初步探讨显示文摘肺组织中低浓度的氧自由基(oxygen free radicals,OFRs)参与机体免疫功能、抵抗外来病原菌,当肺组织发生病变或物理条件下氧自由基产生过多时,氧自由基便成为损害肺组织细胞的重要角色。氧自由基可启动膜脂质过氧化(lipid peroxidation)的链式反应,造成膜的流动性及通透性改变,并生成脂质过氧化物(LPO),丙二醛(MOD)为LPO代表物之一[1]。 | 蒋慧 顾玉海 | 2014 | 临床肺科杂志2014，19，8： | 9 |
| 18 | Studies on antioxidative activities of methanol extract from Murraya paniculata显示文摘Murraya paniculata(L.),a well-known medical plant,has widely been used to treat inflammation,stomach ache,internal and external injuries,and for other purposes.In this study,we determined the reducing,lipid peroxidation inhibition,1,1-diphenyl-2-picryl-hydrazil radical(DPPH•)scavenging,superoxide anion radical(O2−•)scavenging,hydroxyl radical(HO•)scavenging and hydrogen peroxide(H2O2)scavenging activities of the methanolic extract of M.paniculata(MPE)by UV–vis spectrophotometer.The results showed that M.paniculata was rich in flavonoids(375 mg RE/g of extract).Reducing,lipid peroxidation inhibition and HO•scavenging activities of the extract were 0.26 mg/mL,0.023 mg/mL and 0.302 mg/mL,respectively,these activities were significantly higher than those of trolox.Other antioxidative behavior indicators,i.e.,DPPH•scavenging,O2−•scavenging and H2O2 scavenging activities of MPE were 0.93 mg/mL,0.581 mg/mL and 0.47 mg/mL,respectively,and were comparable to those exhibited by trolox.These results indicate that the methanolic extract of M.paniculata exhibited strong antioxidative and radical scavenging activities. | Chao-hua Zhu Zhen-lin Lei Yan-ping Luo | 2015 | Food Science and Human Wellness2015，4，3： | 8 |
| 19 | Antioxidant,lipid peroxidation inhibition and free radical scavenging efficacy of a diterpenoid compound sugiol isolated from Metasequoia glyptostroboides显示文摘Objective:To investigate the antioxidant enicacy of a biologically active dilerpenoid compound sugiol isolated from Metasequoia glyptostroboides(M.glyptostroboides)in various antioxidant models.Methods:An abietane type diterpenoid sugiol,isolated from ethyl acetate extract of M.glyptostroboides cones,was analyzed for its antioxidant efficacy as reducing power ability and lipid peroxidation inhibition as well as its ability to scavenge free radicals such as 1,1-diphenyl-2-picryl hydrazyl,nitric oxide,superoxide and hydroxyl radicals.Results:The sugiol showed significant and concentration-dependent antioxidant and free radical scavenging activities.Consequently,the sugiol exerted lipid peroxidation inhibitory effect by 76.3%as compared to a-tocopherol(80.13%)and butylaled hydroxyanisole(76.59%).In addition,the sugiol had significant scavenging activities of l,l-diphenyl-2-picryl hydrazyl,nitric oxide,superoxide and hydroxyl free radicals in a concentration-dependent manner by 78.83%,72.42%,72.99%and 85.04%,when compared to the standard compound ascorbic acid(81.69%,74.62%,73.00%and 73.79%)and a-tocopherol/butylated hydroxyanisole(84.09%,78.61%,74.45%and 70.02%),respectively.Conclusions:These findings justify the biological and traditional uses of M.glyptostroboides or its secondary metabolites as confirmed by its promising antioxidant efficacy. | Vivek K.Bajpai Ajay Sharma Sun Chul Kang Kwang-Hyun Baek | 2014 | Asian Pacific Journal of Tropical Medicine2014，7，1： | 8 |
| 20 | Glutamine prevents oxidative stress in a model of mesenteric ischemia and reperfusion显示文摘AIM: To evaluate preventative effects of glutamine in an animal model of gut ischemia/reperfusion(I/R).METHODS: Male Wistar rats were housed in a controlled environment and allowed access to food and water ad libitum. Twenty male Wistar rats were divided into four experimental groups:(1) control group(control)- rats underwent exploratory laparotomy;(2) control + glutamine group(control-GLU)- rats were subjected to laparotomy and treated intraperitoneally with glutamine 24 and 48 h prior to surgery;(3) I/R group- rats were subjected to occlusion of the superior mesenteric artery for 30 min followed by 15 min of reperfusion; and(4) ischemia/reperfusion + glutamine group(G + I/R)- rats were treated intraperitoneally with glutamine 24 and 48 h before I/R. Local and systemic injuries were determined by evaluating intestinal and lung segments for oxidative stress using lipid peroxidation and the activity of superoxide dismutase(SOD), interleukin-6(IL-6) and nuclear factor kappa beta(NFkB) after mesenteric I/R. RESULTS: Lipid peroxidation of the membrane was increased in the animals subjected to I/R(P < 0.05). However, the group that received glutamine 24 and 48 h before the I/R procedure showed levels of lipid peroxidation similar to the control groups(P < 0.05). The activity of the antioxidant enzyme SOD was decreased in the gut of animals subjected to I/R when compared with the control group of animals not subjected to I/R(P < 0.05). However, the group that received glutamine 24 and 48 h before I/R showed similar SOD activity to both control groups not subjected to I/R(P < 0.05). The mean area of NF-kB staining for each of the control groups was similar. The I/R group showed the largest area of staining for NF-kB. The G + I/R group had the second highest amount of staining, but the mean value was much lower than that of the I/R group(P < 0.05). For IL-6, control and control-GLU groups showed similar areas of staining. The I/R group contained the largest area of IL-6 staining, followed by the G + I/R animals; however, this area was significantly lower than that of the group that underwent I/R without glutamine(P < 0.05). CONCLUSION: These results demonstrate that pretreatment with glutamine prevents mucosal injury and improves gut and lung recovery after I/R injury in rats. | Gilmara Pandolfo Zabot Gustavo Franco Carvalhal Norma Possa Marroni Renata Minuzzo Hartmann Vinícius Duval da Silva Henrique Sarubbi Fillmann | 2014 | World Journal of Gastroenterology2014，20，32： | 7 |
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