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rat的相关文献在1993年到2023年内共计599篇,主要集中在肿瘤学、内科学、基础医学 等领域,其中期刊论文321篇、会议论文3篇、专利文献275篇;相关期刊132种,包括华中科技大学学报(医学)(英德文版)、国际肝胆胰疾病杂志(英文版)、神经科学通报:英文版等; 相关会议3种,包括首届中西部营养与健康、亚健康学术会议、CERNET第十届学术年会、中国计算机学会网络与数据通信学术会议等;rat的相关文献由1754位作者贡献,包括李国钧、S.瓦格、叶书苹等。

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期刊论文>

论文:321 占比:53.59%

会议论文>

论文:3 占比:0.50%

专利文献>

论文:275 占比:45.91%

总计:599篇

rat—发文趋势图

rat

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  • 李国钧
  • S.瓦格
  • 叶书苹
  • 张大伟
  • 朱京
  • 纳吉恩·海玛亚特
  • G·B·霍恩
  • S·巴拉苏布拉马尼安
  • A·V·桑塔纳姆
  • O.N.C.依玛兹
  • 期刊论文
  • 会议论文
  • 专利文献

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    • Zeina Msheik; Stephanie Durand; Emilie Pinault; Martial Caillaud; Laetitia Vignaud; Fabrice Billet; Mohamed El Massry; Alexis Desmoulière
    • 摘要: The sensorimotor and histological aspects of peripheral neuropathies were already studied by our team in two rat models:the sciatic nerve crush and the Charcot-Marie-Tooth-1A disease.In this study,we sought to highlight and compare the protein signature of these two pathological situations.Indeed,the identification of protein profiles in diseases can play an important role in the development of pharmacological targets.In fact,Charcot-Marie-Tooth-1A rats develop motor impairments that are more severe in the hind limbs.Therefore,for the first time,protein expression in sciatic nerve of Charcot-Marie-Tooth-1A rats was examined.First,distal sciatic nerves were collected from Charcot-Marie-Tooth-1A and uninjured wild-type rats aged 3 months.After protein extraction,sequential window acquisition of all theoretical fragment ion spectra liquid chromatography and mass spectrometry was employed.445 proteins mapped to Swiss-Prot or trEMBL Uniprot databases were identified and quantified.Of these,153 proteins showed statistically significant differences between Charcot-Marie-Tooth-1A and wild-type groups.The majority of these proteins were overexpressed in Charcot-Marie-Tooth-1A.Hierarchical clustering and functional enrichment using Gene Ontology were used to group these proteins based on their biological effects concerning Charcot-Marie-Tooth-1A pathophysiology.Second,proteomic characterization of wild-type rats subjected to sciatic nerve crush was performed sequential window acquisition of all theoretical fragment ion spectra liquid chromatography and mass spectrometry.One month after injury,distal sciatic nerves were collected and analyzed as described above.Out of 459 identified proteins,92 showed significant differences between sciatic nerve crush and the uninjured wild-type rats used in the first study.The results suggest that young adult Charcot-Marie-Tooth-1A rats(3 months old)develop compensatory mechanisms at the level of redox balance,protein folding,myelination,and axonogenesis.These mechanisms seem insufficient to hurdle the progress of the disease.Notably,response to oxidative stress appears to be a significant feature of Charcot-Marie-Tooth-1A,potentially playing a role in the pathological process.In contrast to the first experiment,the majority of the proteins that differed from wild-type were downregulated in the sciatic nerve crush group.Functional enrichment suggested that neurogenesis,response to axon injury,and oxidative stress were important biological processes.Protein analysis revealed an imperfect repair at this time point after injury and identified several distinguishable proteins.In conclusion,we suggest that peripheral neuropathies,whether of a genetic or traumatic cause,share some common pathological pathways.This study may provide directions for better characterization of these models and/or identifying new specific therapeutic targets.
    • Min Cai; Jian Shao; Bryant Yung; Yi Wang; Nan-Nan Gao; Xi Xu; Huan-Huan Zhang; Yu-Mei Feng; Deng-Bing Yao
    • 摘要: Wallerian degeneration is a complex biological process that occurs after nerve injury,and involves nerve degeneration and regeneration.Schwann cells play a crucial role in the cellular and molecular events of Wallerian degeneration of the peripheral nervous system.However,Wallerian degeneration regulating nerve injury and repair remains largely unknown,especially the early response.We have previously reported some key regulators of Wallerian degeneration after sciatic nerve injury.Baculoviral inhibitor of apoptosis protein repeat-containing protein 3(BIRC3)is an important factor that regulates apoptosis-inhibiting protein.In this study,we established rat models of right sciatic nerve injury.In vitro Schwann cell models were also established and subjected to gene transfection to inhibit and overexpress BIRC3.The data indicated that BIRC3 expression was significantly up-regulated after sciatic nerve injury.Both BIRC3 upregulation and downregulation affected the migration,proliferation and apoptosis of Schwan cells and affected the expression of related factors through activating c-fos and ERK signal pathway.Inhibition of BIRC3 delayed early Wallerian degeneration through inhibiting the apoptosis of Schwann cells after sciatic nerve injury.These findings suggest that BIRC3 plays an important role in peripheral nerve injury repair and regeneration.The study was approved by the Institutional Animal Care and Use Committee of Nantong University,China(approval No.2019-nsfc004)on March 1,2019.
    • Camilla Homans; Emine B. Yalcin; Ming Tong; Gina Gallucci; David Bautista; Natalia Moriel; Suzanne de la Monte
    • 摘要: Background & Objective: Chronic excessive alcohol consumption causes white matter degeneration with myelin loss and impaired neuronal conductivity. Subsequent rarefaction of myelin accounts for the sustained deficits in cognition, learning, and memory. Correspondingly, chronic heavy or repeated binge alcohol exposures in humans and experimental models alter myelin lipid composition leading to build-up of ceramides which can be neurotoxic and broadly inhibitory to brain functions. Methods: This study examined the effects of chronic + binge alcohol exposures (8 weeks) and intervention with myriocin, a ceramide inhibitor, on neurobehavioral functions (Open Field, Novel Object Recognition, and Morris Water Maze tests) and frontal lobe white matter myelin lipid biochemical pathology in an adult Long-Evans rat model. Results: The ethanol-exposed group had significant deficits in executive functions with increased indices of anxiety and impairments in spatial learning acquisition. Myriocin partially remediated these effects of ethanol while not impacting behavior in the control group. Ethanol-fed rats had significantly smaller brains with broadly reduced expression of sulfatides and reduced expression of two of the three sphingomyelins detected in frontal white matter. Myriocin partially resolved these effects corresponding with improvements in neurobehavioral function. Conclusion: Therapeutic strategies that support cerebral white matter myelin expression of sulfatide and sphingomyelin may help remediate cognitive-behavioral dysfunction following chronic heavy alcohol consumption in humans.
    • Li Zeng; Fangwei Zhong; Zhiliang Chen; Gengxi Li; Qi Zhu
    • 摘要: Polygonatum sibiricum is a traditional medicinal and dietary plant of the family Liliaceae. The main functional macromolecules of P. sibiricum are polysaccharides, which function in antioxidation and regulating immunity. Previous studies have shown that insulin resistance(IR), oxidative stress, and inflammation are important factors in the induction of lipid metabolic diseases such as obesity. Therefore, in this study, we established a high-fat diet-induced rat model of obesity and nonalcoholic fatty liver disease(NAFLD) to explore the potential protective effect of P. sibiricum polysaccharides(PSPs) and the mechanisms behind it. After 4 weeks of high-fat diet feeding to induce obesity, the rats were treated with different doses of PSP solution or distilled water for 6 weeks. Compared with untreated obese rats, PSP-treated obese rats showed a decrease in body weight, serum total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels, hepatic aspartate aminotransferase and alanine aminotransferase activity, hepatic malondialdehyde content, and hepatic levels of the pro-inflammatory factors tumor necrosis factor-α, interleukin-1β, and interleukin-6, as well as increased serum high-density lipoprotein cholesterol levels and hepatic superoxide dismutase, catalase, and glutathione peroxidase activity. Pathological analysis and immunoblotting of the liver tissues indicated that mechanistically, PSPs reduced obesity and NAFLD in rats by upregulating insulin receptor expression, increasing adenosine monophosphate-activated protein kinase phosphorylation, and downregulating sterol regulatory element-binding protein 2 and low-density lipoprotein receptor expression, thus promoting lipid metabolism, decreasing body weight, and reducing inflammation and oxidative stress caused by lipid accumulation. Based on these results, PSPs may have the potential to reduce obesity and NAFLD associated with a high-fat diet.
    • Qi Li; Bo Wang; Kai-Wen Lin; Tang Deng; Qi-Feng Huang; Shuang-Qin Xu; Hang-Fei Wang; Xin-Xin Wu; Nan Li; Yang Yi; Ji-Chao Peng; Yue Huang; Jin Qian; Xiao-Ran Liu
    • 摘要: Objective:To explore the protective effects of anthrahydroquinone-2,6-disulfonate(AH_(2)QDS)on the kidneys of paraquat(PQ)poisoned rats via the apelin-APJ pathway.Methods:Male Sprague Dawley rats were divided into four experimental groups:control,PQ,PQ+sivelestat,and PQ+AH_(2)QDS.The PQ+sivelestat group served as the positive control group.The model of poisoning was established via intragastric treatment with a 20%PQ pesticide solution at 200 mg/kg.Two hours after poisoning,the PQ+sivelestat group was treated with sivelestat,while the PQ+AH_(2)QDS group was given AH_(2)QDS.Six rats were selected from each group on the first,third,and seventh days after poisoning and dissected after anesthesia.The PQ content of the kidneys was measured using the sodium disulfite method.Hematoxylin-eosin staining of renal tissues was performed to detect pathological changes.Apelin expression in the renal tissues was detected using immunofluorescence.Western blotting was used to detect the expression levels of the following proteins in the kidney tissues:IL-6,TNF-α,apelin-APJ(the apelin-angiotensin receptor),NF-κB p65,caspase-1,caspase-8,glucose-regulated protein 78(GRP78),and the C/EBP homologous protein(CHOP).In in vitro study,a PQ toxicity model was established using human tubular epithelial cells treated with standard PQ.Twenty-four hours after poisoning,sivelestat and AH_(2)QDS were administered.The levels of oxidative stress in human renal tubular epithelial cells were assessed using a reactive oxygen species fluorescence probe.Results:The PQ content in the kidney tissues of the PQ group was higher than that of the PQ+AH_(2)QDS group.Hematoxylin-eosin staining showed extensive hemorrhage and congestion in the renal parenchyma of the PQ group.Vacuolar degeneration of the renal tubule epithelial cells,deposition of crescent-like red staining material in renal follicles,infiltration by a few inflammatory cells,and a small number of cast formation were also observed.However,these pathological changes were less severe in the PQ+sivelestat group and the PQ+AH_(2)QDS group(P<0.05).On the third day after poisoning,immunofluorescence assay showed that the level of apelin in the renal tissues was significantly higher in the PQ+AH_(2)QDS group than in the PQ group.Western blotting analysis results showed that IL-6,TNF-α,NF-κB p65,caspase-1,caspase-8,GRP78,and CHOP protein levels in the PQ group were higher than in the PQ+AH_(2)QDS group(P<0.05).The expression of apelin-APJ proteins in the PQ+AH_(2)QDS group was higher than in the PQ+sivelestat and PQ groups(P<0.05);this difference was significant on Day 3 and Day 7.The level of oxidative stress in the renal tubular epithelial cells of the PQ+AH_(2)QDS group and the PQ+sivelestat group was significantly lower than in the PQ group(P<0.05).Conclusions:This study confirms that AH_(2)QDS has a protective effect on PQ-poisoned kidneys and its positive effect is superior to that of sivelestat.The mechanism of the protective effects of AH_(2)QDS may be linked to reduction in cellular oxidative stress,PQ content of renal tissue,inflammatory injury,endoplasmic reticulum stress,and apoptosis.AH_(2)QDS may play a role in the treatment of PQ poisoning by upregulating the expression of the apelin-APJ.
    • Masud Eneji Sadiq; Chibuzo Egwuenu; Rabiu Saidu Umar Wasagu; Usman Zayyanu Umar; Bello Usman
    • 摘要: Objective:To investigate the role of Mirabilis jalapa root extracts in restoration of glucose homeostasis in alloxan-induced hyperglycemic Wistar albino rats.Methods:Experimental hyperglycemic rats were treated daily with 200 and 400 mg/kg of Mirabilis jalapa extracts after initial fasting for 6 h.Two-hour postprandial glucose and changes in body weight were monitored during treatment.After 14 d,the rats were sacrificed and blood was collected for biochemical assessment of serum glucose and insulin levels,lipid profile,and oxidative stress markers.Histopathological examinations of harvested pancreas were also carried out.Results:Mirabilis jalapa root extracts at 200 and 400 mg/kg increased the body weight of hyperglycemic rats.Postprandial glucose levels of the extract-treated hyperglycemic groups progressively declined during treatment compared with the untreated hyperglycemic control group(P<0.05).The lipid profile indices of the untreated negative control group were significantly elevated(P<0.05),which were reversed by treatment with Mirabilis jalapa extracts.The remarkable increases in antioxidant enzyme activities and a significant decrease in malondialdehyde levels were observed in the hyperglycemic group treated with Mirabilis jalapa extracts.Mirabilis jalapa extracts also significantly increased serum insulin levels(P<0.05).In addition,histopathological examinations of the pancreas revealed a significant cell population within the islet nests of the extract-treated hyperglycemic groups.Conclusions:Mirabilis jalapa extract can restore glucose homeostasis and show hypoglycemic and hypolipidemic effects in hyperglycemic rats.Further studies are needed to verify the active components of the plant and the underlying mechanism of action in the future.
    • Shi-Meng Li; Jian Zhou; Qi-Ping Wei; Jun Wang; Wu Sun; Yan Wang; Jie Wang; Yan-Ting Xia
    • 摘要: Objective:To investigate the effect of Wei’s triple nine needling therapy on the N2-P2 wave of the flash visual evoked potential(FVEP)in rats of the of the transverse directional pulling model.Methods:Thirty-six Wistar rats were randomly grouped,nine were in normal control group without any treatment,and the remaining 27 were surgically modelled in the right eyes.Eighteen of these rats were randomly divided into a Wei’s triple nine needling therapy group and a model group of nine rats each after the TON model was made using the transverse quantitative retraction method.The other 9 rats were sham-operated,and only the optic nerve was exposed without retraction.On the next day of modelling,the Wei’s triple nine needling therapy group was treated with Wei’s triple nine needling therapy for 20 minutes/1 time/1 day for 14 days.The model group,sham-operated group and normal control group were not intervened.Wei's triple nine acupoints were represented as follows:1st link:"Jingming"(BL1)and"Chengqi"(ST1);2nd link:"Sizhukong"(SJ23)penetrating"Taiyang"(EX-HN5);and the third:"Fengchi"(GB 20)and"Taichong"(LV3).The FVEP of each group was observed on 1d,7d and 14d.The FVEP of each group was observed on 1d,7d and 14d.Results:Compared with the model group,the N2 wave latency and P2 wave latency were shortened in the Wei’s triple nine needling therapy on 1d(P0.05).The delayed N2 and P2 wave latencies in the model group did not improve from 1d to 14d(P>0.05)and the amplitude decreased throughout,showing a significant difference on 14d compared to 1d(P0.05).There was also no significant decrease in N2-P2 wave amplitude between 1d and 14d in Wei’s triple nine needling therapy group(P>0.05).Conclusion:In this experiment,the TON rat model was successfully established by the transverse quantitative retraction method,and the treatment of TON rats with Wei’s triple nine needling therapy reduced the P2 wave delay of the FVEP electrophysiological signal and increased the N2-P2 amplitude,which had a certain positive effect on the repair of optic nerve injury,probably related to its effect of improving the conduction function of the optic nerve and protecting the retinal ganglion cells that had not been degenerated and necrosed.
    • Ahmed M.Fatani; Othman A.S.Baothman; Lobna S Shash; Huda A.Abuaraki; Mustafa A Zeyadi; Salman B.Hosawi; Hisham N.Altayb; Mohamed K.Abo-Golayel
    • 摘要: Objective:To investigate the prophylactic efficacy of date palm fruit extract against doxorubicin-induced hepatotoxicity in Wistar albino rats.Methods:The rats were equally and randomly assigned to 6 groups:group 1(untreated control),group 2 and 3 given daily oral administration of prophylactic aqueous extract of date palm fruit at 0.75 and 1.5 mg/kg body weight,respectively,and group 4,5 and 6 intraperitoneally injected with doxorubicin at 15 mg/kg on day 30.Rats in group 5 and 6 received daily oral administration of aqueous extract of date palm fruit at 0.75 and 1.5 mg/kg body weight,respectively,for 30 d.The phytochemicals identified by GC-MS analysis were analyzed using in silico study.Antioxidant enzymes,liver enzymatic,biochemical parameters and histopathological analysis were determined to evaluate hepatoprotective activity of date extract.Results:Aqueous extract of date palm fruit significantly mitigated doxorubicin-induced changes in activities of liver enzymes,reduced reactive oxygen species levels,and suppressed lipid peroxidation and DNA damage.Moreover,aqueous extract of date palm fruit reduced doxorubicin-induced hepatic lesions.Molecular docking studies showed that most compounds of aqueous extract of date palm fruit identified via GC-MS had good interaction with proteins of human pregnane X receptor,oxygenase-1,and CYP2C9.Conclusions:The aqueous extract of date palm fruit mitigates doxorubicin-mediated DNA damage and hepatotoxicity,and restores normal liver function and may be a promising agent against the deleterious effects of doxorubicin.
    • Nabilah Ibnat; Rahela Zaman; Mohammad Borhan Uddin; Ezharul Chowdhury; Chooi Yeng Lee
    • 摘要: BACKGROUND Glucagon-like peptide-1(GLP1)is an endogenous peptide that regulates blood glucose level.But its susceptibility to rapid metabolic degradation limits its therapeutic use.AIM To prepare GLP1-encapsulated nanosize particle with controlled release property to improve the systemic half-life of GLP1.METHODS GLP1 nanoparticles were prepared by complexation of GLP1 with carbonate apatite nanoparticles(CA NPs).The physicochemical properties of the CA NPs,the effects of GLP1-loaded CA NPs on cell viability,and the systemic bioavailability of GLP1 after CA NPs administration were determined.RESULTS The GLP1-loaded CA NPs was within 200 nm in size and stable in fetal bovine serum.The formulation did not affect the viability of human cell lines suggesting that the accumulation of CA NPs in target tissues is safe.In Sprague Dawley rats,the plasma GLP1 Levels as measured from the GLP1-loaded CA NPs-treated rats,were significantly higher than that of the control rats and free GLP1-treated rats at 1 h post-treatment(P<0.05),and the level remained higher than the other two groups for at least 4 h.CONCLUSION The GLP1-loaded CA NPs improved the plasma half-life of GLP1.The systemic bioavailability of GLP1 is longer than other GLP1 nanoparticles reported to date.
    • Berzan Haznedar; Engin Deveci; Ertuğrul Gök
    • 摘要: Background: Mancozeb, (ethylene-bis-dithiocarbamate), is an important fungicide useful against a wide range of fungus affecting ornamental plants, crops, and fruits. We aimed to evaluate the changes in the olfactory mucosa due to mancozeb toxicity and, if cytokine is active, IL-6 immunoactivity. Material and Method: In experimental group, the mancozeb (500 mg/kg) was administered with inhalation to 10 male Wistar Albino rats for five days a week. The control group (n = 10) received distilled water with spray at the same time period. The experiment was terminated after three weeks. Samples were placed in 10% formaldehyde for fixation and placed in paraffin, sections of 5 μm were prepared from paraffin blocks and stained with Hematoxylin-Eosin. Interleukin-6 (IL-6) primary antibody were used for immunohistochemical analysis. Result: In the mancozeb group, olfactory epithelial cell degeneration and apoptosis, inflammation, dilatation and congestion in the vessels were observed. IL-6 expression was increased in vascular endothelium and inflammatory cells. Conclusions: Mancozeb was thought that the increase in IL-6 expression due to the increase in cell degeneration signal was thought to affect the development of cell apoptosis and angiogenesis, and that the use of mancozeb might adversely affect the olfactory mechanism.
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