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| 1 | Effect of Boschniakia rossica on expression of GSTP,p53 and p21^(ras)proteins in early stage of chemical hepatocarcinogenesis and its anti-inflammatory activities in rats显示文摘AIM To investigate the effect of Boschniakiarossica(BR)extract on expression of GST-P,p53 and p21rasproteins in early stage of chemicalhepatocarcinogenesis in rats and its anti-inflammatory activities.METHODS The expression of tumor marker-placental form glutathione S-transferase(GST-P),p53 and p21rasproteins were investigated byimmunohistochemical techniques and ABCmethod.Anti-inflammatory activities of BR werestudied by xylene and croton oil-induced mouseear edema,carrageenin,histamine and hotscald-induced rat pow edema,adjuvant-inducedrat arthritis and cotton pellet-induced mousegranuloma formation methods.RESULTS The 500 mg/kg of BR-H2O extractfractionated from BR-Methanol extract hadinhibitory effect on the formation of DEN-inducedGST-P-positive foci in rat liver(GST-P stainingwas 78% positive in DEN+AAF group vs 20%positive in DEN+AAF+BR group,P<0.05)andthe expression of mutant p53 and p21rasproteinwas lower than that of hepatic preneoplasticlesions(33% and 22% positive respectively inDEN+AAF group vs negative in DEN+AAF+BRgroup).Both CH2Cl2 and H2O extracts from BRhad anti-inflamatory effect in xylene and crotonoil-induced mouse ear edema(inhibitory rateswere 26%-29% and 35%-59%,respectively). BR-H2O extract exhibited inhibitory effect incarrageenin,histamine and hot scald-inducedhind paw edema and adjuvant-induced arthritis inrats and cotton pellet-induced granulomaformation in mice.CONCLUSION BR extract exhibited inhibitory effect on formation of preneoplastic hepatic foci in early stage of rat chemical hepato-carcinogenesis. Both CH2CI2 and H2O extracts from BR exerted anti-inflammatory effect in rats and mice. | Zong Zhu Yin Hai Ling Jin Xue Zhe Yin Tian Zhu Li Ji Shu Quan Zeng Nan Jin Institute for Cancer Research,Yanbian University College of Medicine,Yanji 133000,Jilin Province,China | 2000 | World Journal of Gastroenterology2000，6，6： | 33 |
| 2 | Calycosin improves cognitive function in a transgenic mouse model of Alzheimer's disease by activating the protein kinase C pathway显示文摘The major pathological changes in Alzheimer's disease are beta amyloid deposits and cognitive impairment. Calycosin is a typical phytoestrogen derived from radix astragali that binds to estrogen receptors to produce estrogen-like effects. Radix astragali Calycosin has been shown to relieve cognitive impairment induced by diabetes mellitus, suggesting calycosin may improve the cognitive function of Alzheimer's disease patients. The protein kinase C pathway is upstream of the mitogen-activated protein kinase pathway and exerts a neuroprotective effect by regulating Alzheimer's disease-related beta amyloid degradation. We hypothesized that calycosin improves the cognitive function of a transgenic mouse model of Alzheimer's disease by activating the protein kinase C pathway. Various doses of calycosin(10, 20 and 40 mg/kg) were intraperitoneally injected into APP/PS1 transgenic mice that model Alzheimer's disease. Calycosin diminished hippocampal beta amyloid, Tau protein, interleukin-1 beta, tumor necrosis factor-alpha, acetylcholinesterase and malondialdehyde levels in a dose-dependent manner, and increased acetylcholine and glutathione activities. The administration of a protein kinase C inhibitor, calphostin C, abolished the neuroprotective effects of calycosin including improving cognitive ability, and anti-oxidative and anti-inflammatory effects. Our data demonstrated that calycosin mitigated oxidative stress and inflammatory responses in the hippocampus of Alzheimer's disease model mice by activating the protein kinase C pathway, and thereby improving cognitive function. | Lei Song Xiaoping Li Xiao-xue Bai Jian Gao Chun-yan Wang | 2017 | Neural Regeneration Research2017，12，11： | 25 |
| 3 | Glutathione S-transferases M1,T1 genotypes and the risk of gastric cancer:A case-control study显示文摘AIM Glutathione S-transferases (GSTs are involved in the detoxification of many potential carcinogens and appear to play a critical role in the protection from the effects of carcinogens. The contribution of glutathione Stransferases M1 and T1 genotypes to susceptibility to the risk of gastric cancer and their interaction with cigarette smoking are still unclear. The aim of this study was to determine whether there was any relationship between genetic polymorphisms of GSTM1 and GSTT1 and gastric cancer.METHODS A population based case - control study was carried out in a high-risk area, Changle County, Fujian Province, China. The epidemiological data were collected by a standard questionnaire and blood samples were obtained from 95 incidence gastric cancer cases and 94 healthy controls. A polymerase chain reaction method was used to detect the presence or absence of the GSTM1 and GSTT1 genes in genomic DNA. Logistic regression model was employed in the data analysis.RESULTS An increase in risk for gastric cancer was found among carriers of GSTM1 null genotype. The adjusted odds ratio (OR) was 2.63 [95% Confidence Interval (95% CI) 1.17-5.88], after controlling for age,gender, cigarette smoking, alcohol drinking, and fish sauce intake. The frequency of GSTT1 null genotype in cancer cases (43.16%) was not significantly different from that in controls (50.00%). However, the risk for gastric cancer in those with GSTM1 null and GSTT1 nonnull genotype was significantly higher than in those with both GSTM1 and GSTT1 non-null genotype (OR = 2.77,95% Cl 1.15- 6.77). Compared with those subjects who never smoked and had normal GSTM1 genotype, Ors were 1.60 (95% CI: 0.62- 4.19) for never smokers with GSTM1 null type, 2.33 (95% CI 0.88- 6.28) for smokers with normal GSTM1, and 8.06 (95% CI 2.83- 23.67) for smokers with GSTM1 null type.CONCLUSIONS GSTM1 gene polymorphisms may be associated with genetic susceptibility of stomach cancer and may modulate tobacco-related carcinogenesis of gastric cancer. | Lin Cai Shun-Zhang Yu Zuo-Feng Zhang Department of Epidemiology.Fujian Medical University,Fuzhou 350004,Fujian Province,ChinaDepartment of Epidemiology,Shanghai Medical University,Shanghai 200032,China Department of Epidemiology,UCLA School of Public Health,Los Angeles California,USA | 2001 | World Journal of Gastroenterology2001，7，4： | 22 |
| 4 | Ferrostatin-1 protects HT-22 cells from oxidative toxicity显示文摘Ferroptosis is a type of programmed cell death dependent on iron.It is different from other forms of cell death such as apoptosis,classic necrosis and autophagy.Ferroptosis is involved in many neurodegenerative diseases.The role of ferroptosis in glutamate-induced neuronal toxicity is not fully understood.To test its toxicity,glutamate(1.25–20 mM)was applied to HT-22 cells for 12 to 48 hours.The optimal experimental conditions occurred at 12 hours after incubation with 5 mM glutamate.Cells were cultured with 3–12μM ferrostatin-1,an inhibitor of ferroptosis,for 12 hours before exposure to glutamate.The cell viability was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Autophagy was determined by monodansylcadaverine staining and apoptosis by caspase 3 activity.Damage to cell structures was observed under light and by transmission electron microscopy.The release of lactate dehydrogenase was detected by the commercial kit.Reactive oxygen species were measured by flow cytometry.Glutathione peroxidase activity,superoxide dismutase activity and malondialdehyde level were detected by the appropriate commercial kit.Prostaglandin peroxidase synthase 2 and glutathione peroxidase 4 gene expression was detected by real-time quantitative polymerase chain reaction.Glutathione peroxidase 4 and nuclear factor erythroid-derived-like 2 protein expression was detected by western blot analysis.Results showed that ferrostatin-1 can significantly counter the effects of glutamate on HT-22 cells,improving the survival rate,reducing the release of lactate dehydrogenase and reducing the damage to mitochondrial ultrastructure.However,it did not affect the caspase-3 expression and monodansylcadaverine-positive staining in glutamate-injured HT-22 cells.Ferrostatin-1 reduced the levels of reactive oxygen species and malondialdehyde and enhanced superoxide dismutase activity.It decreased gene expression of prostaglandin peroxidase synthase 2 and increased gene expression of glutathione peroxidase 4 and protein expressions of glutathione peroxidase 4 and nuclear factor(erythroid-derived)-like 2 in glutamate-injured HT-22 cells.Treatment of cultured cells with the apoptosis inhibitor Z-Val-Ala-Asp(OMe)-fluoromethyl ketone(2–8μM),autophagy inhibitor 3-methyladenine(100–400μM)or necrosis inhibitor necrostatin-1(10–40μM)had no effect on glutamate induced cell damage.However,the iron chelator deferoxamine mesylate salt inhibited glutamate induced cell death.Thus,the results suggested that ferroptosis is caused by glutamate-induced toxicity and that ferrostatin-1 protects HT-22 cells from glutamate-induced oxidative toxicity by inhibiting the oxidative stress. | Jun Chu Chen-Xu Liu Rui Song Qing-Lin Li | 2020 | Neural Regeneration Research2020，15，3： | 16 |
| 5 | 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 |
| 6 | Role of ferroptosis in the process of diabetes-induced endothelial dysfunction显示文摘BACKGROUND Endothelial dysfunction,a hallmark of diabetes,is a critical and initiating contributor to the pathogenesis of diabetic cardiovascular complications.However,the underlying mechanisms are still not fully understood.Ferroptosis is a newly defined regulated cell death driven by cellular metabolism and irondependent lipid peroxidation.Although the involvement of ferroptosis in disease pathogenesis has been shown in cancers and degenerative diseases,the participation of ferroptosis in the pathogenesis of diabetic endothelial dysfunction remains unclear.AIM To examine the role of ferroptosis in diabetes-induced endothelial dysfunction and the underlying mechanisms.METHODS Human umbilical vein endothelial cells(HUVECs)were treated with high glucose(HG),interleukin-1β(IL-1β),and ferroptosis inhibitor,and then the cell viability,reactive oxygen species(ROS),and ferroptosis-related marker protein were tested.To further determine whether the p53-xCT(the substrate-specific subunit of system Xc-)-glutathione(GSH)axis is involved in HG and IL-1βinduced ferroptosis,HUVECs were transiently transfected with p53 small interfering ribonucleic acid or NC small interfering ribonucleic acid and then treated with HG and IL-1β.Cell viability,ROS,and ferroptosis-related marker protein were then assessed.In addition,we detected the xCT and p53 expression in the aorta of db/db mice.RESULTS It was found that HG and IL-1βinduced ferroptosis in HUVECs,as evidenced by the protective effect of the ferroptosis inhibitors,Deferoxamine and ferrostatin-1,resulting in increased lipid ROS and decreased cell viability.Mechanistically,activation of the p53-xCT-GSH axis induced by HG and IL-1βenhanced ferroptosis in HUVECs.In addition,a decrease in xCT and the presence of deendothelialized areas were observed in the aortic endothelium of db/db mice.CONCLUSION Ferroptosis is involved in endothelial dysfunction and p53-xCT-GSH axis activation plays a crucial role in endothelial cell ferroptosis and endothelial dysfunction. | Er-Fei Luo Hong-Xia Li Yu-Han Qin Yong Qiao Gao-Liang Yan Yu-Yu Yao Lin-Qing Li Jian-Tong Hou Cheng-Chun Tang Dong Wang | 2021 | World Journal of Diabetes2021，12，2： | 10 |
| 7 | Infection of Schistosomiasis japanicum is likely to enhance proliferation and migration of human breast cancer cells:mechanism of action of differential expression of MMP2 and MMP9显示文摘Objective:To study whether the infection of Schistosomiasis japanicum(S.japanicum) is related to enhanced proliferation and migration of cancer cells,and the molecular mechanism pertains to cancer cell metastasis in human host.Methods:The gene of S.japanicum glutathione transferase(sjGST) cloned from 5.japanicum was expressed,purified and applied in a series of assays to explore the effect of sjGST on proliferation and migration of MDA-MB-435S,and the expression of MMP2 and MMP9.Immunofluorescence assay for the binding of sjGST to MDA-MB-435S was also carried out.Results:Results showed that sjGST enhanced proliferation and migration in human breast cancer cell MDA-MB-435S signifycantly at 50-200 nM,but did not enhance them in human lung cancer cell A549.Immunofluorescence assay for the binding of sjGST to MDA-MB-435S and A549 showed that GST was readily hound to the breast cancer cells,but showed almost no binding to human lung cancer cells.The assays for gelatinase activity showed that both MMP2 and MMP9 activities were increased significantly in the presence of sjGST(50-200 nM) in MDA-MB-435S, but they were not significant in A549.Conclusions:Our current results show strongly that S. japanicum GST binds to MDA-MB-435S probably via its i'eceptor,and enhances proliferation and migration of the cancer cells by up-regulatory expression of MMP2 and MMP9. | Ya-Ling Lin Rakesh Ramanujum Shiping He | 2011 | Asian Pacific Journal of Tropical Biomedicine2011，1，1： | 9 |
| 8 | Salvianolic acid B modulates the expression of drug-metabolizing enzymes in HepG2 cells显示文摘BACKGROUND: Enzymes involved in drug and xenobiotic metabolism have been considered to exist in two groups: phase I and phase II enzymes. Cytochrome P450 isoenzymes (CYPs) are the most important phase I enzymes in the metabolism of xenobiotics. The products of phase I metabolism are then acted upon by phase II enzymes, including glutathione S-transferases (GSTs). Herbs that inhibit CYPs such as CYP3A4 or that induce GSTs may have the potential to protect against chemical carcinogenesis since the mutagenic effects of carcinogens are often mediated through an excess of CYP-generated reactive intermediates. This study was designed to investigate the effects of salvianolic acid B (Sal B), a pure compound extracted from Radix Salviae Miltiorrhizae, a Chinese herb, on cell proliferation and CYP1A2 and CYP3A4 mRNA expression in the presence or absence of rifampicin, a potent inducer of CYPs and GST protein expression in HepG2 cells. METHODS: HepG2 cells were incubated with different concentrations of Sal B. Cell proliferation was determined by SYTOX-Green nucleic acid staining. CYP3A4 and CYP1A2 mRNA expression was assayed by real-time PCR. GST protein expression was analyzed by Western blotting. RESULTS: Low concentrations of Sal B (0-20 μmol/L) had no significant effects on cell proliferation, while higher concentrations (100-250 μmol/L) significantly inhibited proliferation in a concentration-dependent manner. Ten μmol/L Sal B, but not 1 μmol/L, down-regulated CYP3A4 and CYP1A2 mRNA expression after 24 hours of incubation, whereas both 1 and 10 μmol/L Sal B down-regulated CYP3A4mRNA expression after 96 hours of incubation; moreover, 1 and 10 μmol/L Sal B inhibited CYP3A4 mRNA expression induced by rifampicin. Both 1 μmol/L and 10 μmol/L Sal B increased GST expression. CONCLUSION: Sal B inhibits CYP3A4 and CYP1A2 mRNA expression and induces GST expression in HepG2 cells. | Hani El-Nezami | 2011 | Hepatobiliary & Pancreatic Diseases International2011，10，5： | 9 |
| 9 | Enzymatic antioxidant system in vascular inflammation and coronary artery disease显示文摘In biological systems there is a balance between the production and neutralization of reactive oxygen species(ROS). This balance is maintained by the presence of natural antioxidants and antioxidant enzymes suchas superoxide dismutase(SOD), catalase and glutathione peroxidase. The enhancement of lipid peroxidation or the decrease of antioxidant protection present in metabolic diseases or bad lifestyle can induce endothelial dysfunction and atherosclerosis.Clinical studies have shown that oxidative stress can increase ROS reducing the formation of antioxidant defences, especially in subjects with coronary artery disease(CAD). Some observation indicated that in the early stages of the disease there is a homeostatic upregulation of the antioxidant enzyme system in response to increased free radicals to prevent vascular damage.As soon as free radicals get to chronically elevated levels, this compensation ceases. Therefore, SOD and the other enzymes may represent a good therapeutic target against ROS, but they are not useful markers for the diagnosis of CAD. In conclusion antioxidant enzymes are reduced in presence of metabolic disease and CAD. However the existence of genes that promote their enzymatic activity could contribute to create new drugs for the treatment of damage caused by metabolic diseases or lifestyle that increases the plasma ROS levels. | Valter Lubrano Silvana Balzan | 2015 | World Journal of Experimental Medicine2015，5，4： | 7 |
| 10 | A silybin-phospholipids complex counteracts rat fatty liver degeneration and mitochondrial oxidative changes显示文摘AIM:To investigate the effectiveness of antioxidant compounds in modulating mitochondrial oxidative alterations and lipids accumulation in fatty hepatocytes.METHODS:Silybin-phospholipid complex containing vitamin E(Realsil) was daily administered by gavage(one pouch diluted in 3 mL of water and containing 15 mg vitamin E and 47 mg silybin complexed with phospholipids) to rats fed a choline-deprived(CD) or a high fat diet [20% fat,containing 71% total calories as fat,11% as carbohydrate,and 18% as protein,high fat diet(HFD)] for 30 d and 60 d,respectively.The control group was fed a normal semi-purified diet containing adequate levels of choline(35% total calories as fat,47% as carbohydrate,and 18% as protein).Circulating and hepatic redox active and nitrogen regulating molecules(thioredoxin,glutathione,glutathione peroxidase),NO metabolites(nitrosothiols,nitrotyrosine),lipid peroxides [malondialdehyde-thiobarbituric(MDA-TBA)],and pro-inflammatory keratins(K-18) were measured on days 0,7,14,30,and 60.Mitochondrial respiratory chain proteins and the extent of hepatic fatty infiltration were evaluated.RESULTS:Both diet regimens produced liver steatosis(50% and 25% of liver slices with CD and HFD,respectively) with no signs of necro-inflammation:fat infiltration ranged from large droplets at day 14 to disseminated and confluent vacuoles resulting in microvesicular steatosis at day 30(CD) and day 60(HFD).In plasma,thioredoxin and nitrosothiols were not significantly changed,while MDA-TBA,nitrotyrosine(from 6 ± 1 nmol/L to 14 ± 3 nmol/L day 30 CD,P < 0.001,and 12 ± 2 nmol/L day 60 HFD,P < 0.001),and K-18(from 198 ± 20 to 289 ± 21 U/L day 30 CD,P < 0.001,and 242 ± 23 U/L day 60 HFD,P < 0.001) levels increased significantly with ongoing steatosis.In the liver,glutathione was decreased(from 34.0 ± 1.3 to 25.3 ± 1.2 nmol/mg prot day 30 CD,P < 0.001,and 22.4 ± 2.4 nmol/mg prot day 60 HFD,P < 0.001),while thioredoxin and glutathione peroxidase were initially increased and then decreased.Nitrosothiols were constantly increased.MDA-TBA levels were five-fold increased from 9.1 ± 1.2 nmol/g to 75.6 ± 5.4 nmol/g on day 30,P < 0.001(CD) and doubled with HFD on day 60.Realsil administration significantly lowered the extent of fat infiltration,maintained liver glutathione levels during the first half period,and halved its decrease during the second half.Also,Realsil modulated thioredoxin changes and the production of NO derivatives and significantly lowered MDA-TBA levels both in liver(from 73.6 ± 5.4 to 57.2 ± 6.3 nmol/g day 30 CD,P < 0.01 and from 27.3 ± 2.1 nmol/g to 20.5 ± 2.2 nmol/g day 60 HFD,P < 0.01) and in plasma.Changes in mitochondrial respiratory complexes were also attenuated by Realsil in HFD rats with a major protective effect on Complex Ⅱ subunit CII-30.CONCLUSION:Realsil administration effectively contrasts hepatocyte fat deposition,NO derivatives formation,and mitochondrial alterations,allowing the liver to maintain a better glutathione and thioredoxin antioxidant activity. | Ignazio Grattagliano Catia V Diogo Maria Mastrodonato Ornella de Bari Michele Persichella David QH Wang Adriana Liquori Domenico Ferri Maria Rosaria Carratù Paulo J Oliveira Piero Portincasa | 2013 | World Journal of Gastroenterology2013，19，20： | 6 |
| 11 | 谷胱甘肽过氧化物酶1基因C594T多态性与急性脑梗死的关系显示文摘目的探讨谷胱甘肽过氧化物酶1(GPx-1)基因C594T多态性与急性脑梗死的关系。方法用聚合酶链反应-限制性片段长度多态性分析法(PCR-RFLP)检测急性脑梗死患者(脑梗死组,128例)和健康体检者(正常对照组,111例)GPx-1基因C594T的基因型和等位基因频率。根据是否存在急性脑梗死的危险因素(高龄,高血压病,2型糖尿病,吸烟史)将脑梗死组分为8个亚组,计算各亚组急性脑梗死的OR值,并与正常对照组比较。结果急性脑梗死组患者GPx-1基因C594T的基因型和等位基因频率与正常对照组相比差异无统计学意义(P=0.24,P=0.28);经分层分析后,脑梗死组各亚组急性脑梗死的OR值与正常对照组相比差异无统计学意义。结论 GPx-1基因C594T多态性与急性脑梗死的发生无相关性。急性脑梗死的相关危险因素(高龄,高血压病,2型糖尿病,吸烟史)与GPx-1 C594T基因多态性共同作用时,对急性脑梗死的发生影响不显著。 | 刘榕 黄东雅 安荷娣 Rajeev Ohja 堵翠 朱雯霞 沈楠 涂志兰 | 2014 | 临床神经病学杂志2014，27，3： | 6 |
| 12 | Etomidate affects the anti-oxidant pathway to protect retinal ganglion cells after optic nerve transection显示文摘Our previous studies revealed that etomidate, a non-barbiturate intravenous anesthetic agent, has protective effects on retinal ganglion cells within 7 days after optic nerve transection. Whether this process is related to anti-oxidative stress is not clear. To reveal its mechanism, we established the optic nerve transection injury model by transecting 1 mm behind the left eyeball of adult male Sprague-Dawley rats. The rats received an intraperitoneal injection of etomidate(4 mg/kg) once per day for 7 days. The results showed that etomidate significantly enhanced the number of retinal ganglion cells retrogradely labeled with Fluorogold at 7 days after optic nerve transection. Etomidate also significantly reduced the levels of nitric oxide and malonaldehyde in the retina and increased the level of glutathione at 12 hours after optic nerve transection. Thus, etomidate can protect retinal ganglion cells after optic nerve transection in adult rats by activating an anti-oxidative stress response. The study was approved by the Animal Ethics Committee at Air Force Medical University, China(approval No. 20180305) on March 5, 2018. | Xuan Zhao Fang Kuang Yi-Yan You Ming-Mei Wu Si-Wei You | 2019 | Neural Regeneration Research2019，14，11： | 6 |
| 13 | INHIBITORY EFFECT OF BOSCHNIAKIA ROSSICA ON DEN-INDUCED PRECANCEROUS HEPATIC FOCI AND ITS ANTIOXIDATIVE ACTIVITIES IN RATS显示文摘Objective: To investigate the inhibitory effect ofBoschniakia rossica(BR) on rat precancerous hepatic fociinduced by diethylnitrosamine (DEN) and its antioxidativeaedvities. Methods: The expression of tumor markerPlacental form glutathione S-transferase (GST-P), p53 andp21 protein were investigated by immunohistochendstrytechniques using ABC method. TNF-α was measured byELISA and antioxidative activities of SOD, MDA, GSH-Px,GST and CAT were investigated by colorimetric method inrat serum and mitochondria of liver cells. Results: The500mg/kg of BR-H2O extract fraction from BR-methanolextract had inhibitory effect on the formation of DENinduced GST-P-positive foci in rat liver and the expressionof mutant p53 and p21 protein was lower than that ofhepatic precancerous lesions. The serum TNF-α wasincreased by the administration of BR extract in the earlystage of chemical hepatocarcinogenesis in rat livers. Thesertun and liver cells mitochondria activities of SOD andGSH-Px rose again in rats administered with BR-H2Oextract and the increasing activity 0f GST and content ofMDA in the hepatic precancerous were decreased by theBR-H2O extract. Conclusion: These results indicated thatBR-H2O extract has inhibitory effect on DEN-inducedprecancerous hepatic foci in rats and induced TNF-αproduction in rats. The antioxidative action was exhibitedby the administration of BR-H2O extract in the early stageof chemical bepatocarcinogenesis in rat livers. | 尹宗柱 金海玲 沈明花 李天洙 全吉淑 | 1999 | Chinese Journal of Cancer Research1999，11，3： | 6 |
| 14 | Exogenous glutathione exerts a therapeutic effect in ischemic stroke rats by interacting with intrastriatal dopamine显示文摘We previously showed that oral administration of exogenous glutathione(GSH)exerted a direct and/or indirect therapeutic effect on ischemic stroke rats,but the underlying mechanisms remain elusive.In the current study,we conducted a quantitative proteomic analysis to explore the pathways mediating the therapeutic effect of GSH in cerebral ischemia/reperfusion(I/R)model rats.Rats were subjected to middle cerebral artery occlusion(MCAO)for 2 h followed by reperfusion.The rats were treated with GSH(250 mg/kg,ig)or levodopa(L-dopa,100 mg/kg,ig)plus carbidopa(10 mg/kg,ig).Neurologic deficits were assessed,and the rats were sacrificed at 24 h after cerebral I/R surgery to measure brain infarct sizes.We conducted a proteomic analysis of the lesion side striatum samples and found that tyrosine metabolism and dopaminergic synapse were involved in the occurrence of cerebral stroke and the therapeutic effect of GSH.Western blot assay revealed that tyrosine hydroxylase(TH)mediated the occurrence of I/R-induced ischemic stroke and the therapeutic effect of GSH.We analyzed the regulation of GSH on endogenous small molecule metabolites and showed that exogenous GSH had the most significant effect on intrastriatal dopamine(DA)in I/R model rats by promoting its synthesis and inhibiting its degradation.To further explore whether DA-related alterations were potential targets of GSH,we investigated the therapeutic effect of DA accumulation on ischemic brain injury.The combined administration of the precursor drugs of DA(L-dopa and carbidopa)significantly ameliorated neurological deficits,reduced infarct size,and oxidative stress,and decreased pro-inflammatory cytokines levels in the striatum of I/R injury rats.More interestingly,exogenous L-dopa/carbidopa could also greatly enhance the exposure of intracerebral GSH by upregulating GSH synthetases and enhancing homocysteine(HCY)levels in the striatum.Thus,administration of exogenous GSH exerts a therapeutic effect on ischemic stroke by increasing intrastriatal DA,and the accumulated DA can,in turn,enhance the exposure of GSH and its related substances,thus promoting the therapeutic effect of GSH. | He Wang Yi-sha Du Wen-shuo Xu Chang-jian Li Hong Sun Kang-rui Hu Yuan-zhuo Hu Teng-jie Yu Hui-min Guo Lin Xie Guang-ji Wang Yan Liang | 2022 | Acta Pharmacologica Sinica2022，43，3： | 5 |
| 15 | Protective effects of oral glutathione on fasting-induced intestinal atrophy through oxidative stress显示文摘AIM To determine whether oral glutathione(GSH)administration can alleviate the effects of fasting-induced intestinal atrophy in the small intestinal mucosa. METHODS Rats were divided into eight groups.One group was fed ad libitum,another was fed ad libitum and received oral GSH,and six groups were administrated saline(SA)or GSH orally during fasting.Mucosal height,apoptosis,and cell proliferation in the jejunum were histologically evaluated.i NOS protein expression(by immunohistochemistry),nitrite levels(by high performance liquid chromatography,as a measure of NO production),8-hydroxydeoxyguanosine formation(by ELISA,indicating ROS levels),glutathione/oxidized glutathione(GSH/GSSG)ratio(by enzymatic colorimetric detection),andγ-glutamyl transpeptidase(Ggt1)mR NA levels in the jejunum(by semi-quantitative RT-PCR)were also estimated. RESULTS O r a l G S H a d m i n i s t r a t i o n w a s d e m o n s t r a t e d t o drastically reduce fasting-induced intestinal atrophy in the jejunum.In particular,jejunal mucosal height was enhanced in GSH-treated animals compared to SA-treated animals[527.2±6.9 for 50 mg/kg GSH,567.6±5.4 for 500 mg/kg GSH vs 483.1±4.9(μm),P<0.01at 72 h].This effect was consistent with decreasing changes in GSH-treated animals compared to SA-treated animals for iN OS protein staining[0.337±0.016for 50 mg/kg GSH,0.317±0.017 for 500 mg/kg GSH vs 0.430±0.023(area of staining part/area of tissue),P<0.01 at 72 h]and NO[2.99±0.29 for 50 mg/kg GSH,2.88±0.19 for 500 mg/kg GSH vs 5.34±0.35(nmol/g tissue),P<0.01 at 72 h]and ROS[3.92±0.46for 50 mg/kg GSH,4.58±0.29 for 500 mg/kg GSH vs6.42±0.52(8-OHdG pg/μg DNA),P<0.01,P<0.05at 72 h,respectively]levels as apoptosis mediators in the jejunum.Furthermore,oral GSH administration attenuated cell proliferation decreases in the fasting jejunum[182.5±1.9 for 500 mg/kg GSH vs 155.8±3.4(5-Brd U positive cells/10 crypts),P<0.01 at 72h].Notably,both GSH concentration and Ggt1 m RNA expression in the jejunum were also attenuated in rats following oral administration of GSH during fasting as compared with fasting alone[0.45±0.12 vs 0.97±0.06(nmol/mg tissue),P<0.01;1.01±0.11 vs 2.79±0.39(Ggt1 m RNA/Gapdh m RNA),P<0.01 for 500 mg/kg GSH at 48 h,respectively]. CONCLUSION Oral GSH administration during fasting enhances jejunal regenerative potential to minimize intestinal mucosal atrophy by diminishing fasting-mediated ROS generation and enterocyte apoptosis and enhancing cell proliferation. | Hiroyuki Uchida Yukari Nakajima Kazuo Ohtake Junta Ito Masahiko Morita Ayako Kamimura Jun Kobayashi | 2017 | World Journal of Gastroenterology2017，23，36： | 5 |
| 16 | Two Distinct Fluorescent Quantum Clusters of Gold Starting from Metallic Nanoparticles by pH-Dependent Ligand Etching显示文摘Two fl uorescent quantum clusters of gold,namely Au25 and Au8,have been synthesized from mercaptosuccinic acid-protected gold nanoparticles of 45 nm core diameter by etching with excess glutathione.While etching at pH~3 yielded Au_(25),that at pH 7-8 yielded Au_(8).This is the fi rst report of the synthesis of two quantum clusters starting from a single precursor.This simple method makes it possible to synthesize well-defined clusters in gram quantities.Since these clusters are highly fl uorescent and are highly biocompatible due to their low metallic content,they can be used for diagnostic applications. | Madathumpady Abubaker Habeeb Muhammed Subramani Ramesh Sudarson Sekhar Sinha Samir Kumar Pal Thalappil Pradeep | 2008 | Nano Research2008，1，4： | 5 |
| 17 | Comparison of physiological responses to oxidative and heavy metal stress in seedlings of rice paddy, Oryza sativa L.显示文摘Physiological responses on the bases of activities of antioxidant enzymes: peroxidase, catalase, superoxide dismutase and glutathione reductase as well as estimation of total protein, lipid peroxidation and thiols in the form of protein, non\|protein, glutathione and phytochelatin measured in growing seedlings of paddy, Oryza sativa L., from day 2 to 8 were compared following treatment of seeds for 5h with oxidative agents, paraquat 5 × 10 -5 , 10 -4 , 10 -3 mol/L, H 2O 2 10 -3 , 5×10 -3 , 10 -2 mol/L, and CdCl 2 10 -5 , 10 -4 , 5×10 -3 mol/L. A significant induction of all antioxidant enzymes along with an increase in the levels of protein, lipid peroxidation and glutathione was noted in response to oxidative stress, CdCl 2 induced significant peroxidase and catalase activities but not superoxide dismutase. In a marked contrast from oxidative stress, CdCl 2 decreased glutathione reductase activity as well as glutathione levels but increased phytochelatin level. The different physiological responses thus underlined the crucial involvement of glutathione and phytochelatin in the oxidative and heavy metal\|linduced adaptive responses respectively. | YU Guo\|ying, WANG Guo\|ping, HE Chi\|quan (Lab for Wetland Process and Environment, Changchun Institute of Geography, The Chinese Academy of Sciences, Changchun 130021,China E\|mail: yuguoying@mail.ccig.ac.cn) | 2000 | Journal of Environmental Sciences2000，12，4： | 5 |
| 18 | Impact of SNP-SNP interactions of DNA repair gene ERCC5 and metabolic gene GSTP1 on gastric cancer/atrophic gastritis risk in a Chinese population显示文摘AIM To investigate the interactions of the DNA repair gene excision repair cross complementing group 5(ERCC5) and the metabolic gene glutathione S-transferase pi 1(GSTP1) and their effects on atrophic gastritis(AG) and gastric cancer(GC) risk.METHODS Seven ERCC5 single nucleotide polymorphisms(SNPs)(rs1047768, rs2094258, rs2228959, rs4150291, rs4150383, rs751402, and rs873601) and GSTP1 SNP rs1695 were detected using the Sequenom MassA RRAY platform in 450 GC patients, 634 AG cases, and 621 healthy control subjects in a Chinese population.RESULTS Two pairwise combinations(ERCC5 rs2094258 and rs873601 with GSTP1 rs1695) influenced AG risk(P_(interaction) = 0.008 and 0.043, respectively), and the ERCC5 rs2094258-GSTP1 rs1695 SNP pair demonstrated an antagonistic effect, while ERCC5 rs873601-GSTP1 rs1695 showed a synergistic effect on AG risk OR = 0.51 and 1.79, respectively). No pairwise combinations were observed in relation to GC risk. There were no cumulative effects among the pairwise interactions(ERCC5 rs2094258 and rs873601 with GSTP1 rs1695) on AG susceptibility(P_(trend) > 0.05). When the modification effect of Helicobacter pylori(H. pylori) infection was evaluated, the cumulative effect of one of the aforementioned pairwise interactions(ERCC5 rs873601-GSTP1 rs1695) was associated with an increased AG risk in the case of negative H. pylori status(P_(trend)= 0.043).CONCLUSION There is a multifarious interaction between the DNA repair gene ERCC5 SNPs(rs2094258 and rs873601) and the metabolic gene GSTP1 rs1695, which may form the basis for various inter-individual susceptibilities to AG. | Liang Sang Zhi Lv Li-Ping Sun Qian Xu Yuan Yuan | 2018 | World Journal of Gastroenterology2018，24，5： | 4 |
| 19 | Glutathione S-transferase M1 polymorphism and esophagealcancer risk:An updated meta-analysis based on 37 studies显示文摘AIM: To evaluate the relationship between glutathione S-transferase M1(GSTM1) polymorphism and susceptibility to esophageal cancer(EC).METHODS: A comprehensive search of the United States National Library of Medicine Pub Med database and the Elsevier, Springer, and China National Knowledge Infrastructure databases for all relevant studies was conducted using combinations of the following terms: 'glutathione S-transferase M1', 'GSTM1', 'polymorphism', and 'EC'(until November 1, 2014). The statistical analysis was performed using the SAS software(v.9.1.3; SAS Institute, Cary, NC, United States) and the Review Manager software(v.5.0; Oxford, England); crude odds ratios(ORs) with 95% confidence intervals(CIs) were used to assess the association between the GSTM1 null genotype and the risk of EC.RESULTS: A total of 37 studies involving 2236 EC cases and 3243 controls were included in this metaanalysis. We observed that the GSTM1 null genotype was a significant risk factor for EC in most populations(OR = 1.33, 95%CI: 1.12-1.57, P_(heterogeneity) < 0.000001, and I2 = 77.0%), particularly in the Asian population(OR = 1.53, 95%CI: 1.26-1.86, P_(heterogeneity)< 0.000001, and I2 = 77.0%), but not in the Caucasian population(OR = 1.02, 95%CI: 0.87-1.19, P_(heterogeneity) = 0.97, and I2 = 0%).CONCLUSION: The GSTM1 null polymorphism may be associated with an increased risk for EC in Asian but not Caucasian populations. | Quan-Jun Lu Ya-Cong Bo Yan Zhao Er-Jiang Zhao Wolde Bekalo Sapa Ming-Jie Yao Dan-Dan Duan Yi-Wei Zhu Wei-Quan Lu Ling Yuan | 2016 | World Journal of Gastroenterology2016，22，5： | 4 |
| 20 | Emblica officinalis improves glycemic status and oxidative stress in STZ induced type 2 diabetic model rats显示文摘Objective:To evaluate the antidiabetic and antioxidant potential of Emblica officinalis(E.officinalis)fruit on normal and type 2 diabetic rats.Methods:Type 2 diabetes was induced into the male Long-Evans rats.The rats were divided into nine groups including control groups receiving water,type 2 diabetic controls,type 2 diabetic rats treated with glibenclamide(T2GT)and type 2diabetic rats treated with aqueous extract of fruit pulp of E.officinalis.They were fed orally for8 weeks with a single feeding.Blood was collected by cutting the tail tip on 0 and 28 days and by decapitation on 56 day.Packed red blood cells and serum were used for evaluating different biochemical parameters.Results:Four weeks administration of aqueous extract of E.officinalis improved oral glucose tolerance in type 2 rats and after 8 weeks it caused significant(P<0.007)reduction in fasting serum glucose level compared to 0 day.Triglycerides decreased by 14%but there was no significant change in serum ALT,creatinine,cholesterol and insulin level in any group.Furthermore,reduced erythrocyte malondialdehyde level showed no significant change(P<0.07)but reduced glutathione content was found to be increased significantly(P<0.05).Conclusions:The aqueous extract of E.officinalis has a promising antidiabetic and antioxidant properties and may be considered for further clinical studies in drug development. | Aneesa Ansari Md.Shahed Zaman Shahriar Md.Mehedi Hassan Shukla Rani Das Begum Rokeya Md.Anwarul Haque Md.Enamul Haque Nirupam Biswas Tama Sarkar | 2014 | Asian Pacific Journal of Tropical Medicine2014，7，1： | 4 |
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