排序方式: 共有17条查询结果,搜索用时 18 毫秒
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目的探讨柯里拉京对单纯疱疹病毒型脑炎(HSE)炎性因子分泌和神经元凋亡的影响。方法建立HSV-1接种BV2细胞模型,随机分为正常组、单纯疱疹病毒1型(HSV-1)感染组、柯里拉京干预组、地塞米松干预组、黄芪多糖干预组,采用ELISA法检测各组炎性因子白细胞介素1β(IL-1β)、肿瘤坏死因子(TNF-a)的表达水平;25只Balb/c小鼠按上述分组分成五组,除正常组外其它各组应用HSV-1感染小鼠建立病毒性脑炎模型,治疗4d后采用TUNEL法观察各组小鼠神经元凋亡的情况。结果与病毒感染组比较,柯里拉京和地塞米松干预组HSV-1感染后IL-1b和TNF-a的分泌(P<0.01)和神经元凋亡数(P<0.01)均明显减少。结论柯里拉京可能通过减少HSV-1感染后IL-1b和TNF-a的分泌,并同时抑制神经元的凋亡来发挥其脑保护作用。 相似文献
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Xi-Quan Zhang Hong-Mei Gu Xin-Zhu Li Zhong-Nan Xu Yu-Sheng Chen Yang Li 《Journal of ethnopharmacology》2013
Ethnopharmocological relevance
Geranium wilfordii Maxim has been extensively used in Chinese Herbal Medicine for treating gastrointestinal disorders, diarrhea and dysentery. In the current study we aimed to investigate the anti-Helicobacter pylori activity of ethanol extracts of Geranium wilfordii Maxim and its main active compounds, corilagin and 1,2,3,6-tetra-O-galloyl-β-d-glucose.Materials and methods
The plant materials were extracted three times with ethanol and the concentrated filtrate was successively fractioned into chloroform, ethyl acetate, and n-BuOH-soluble portions which were examined in vitro for the anti-Helicobacter. pylori activity. Employing a standard strain and five clinical isolates of Helicobacter pylori, the extract, fractions and compounds of Geranium wilfordii Maxim were assessed in vitro.Results
The ethanol fraction, ethyl acetate fraction, corilagin, and 1,2,3,6-tetra-O-galloyl-β-d-glucose were found to be strongly inhibitory to Helicobacter. pylori (MICs: 40, 30, 4, and 8 μg/ml respectively).Conclusions
The results of the present study showed that the ethanol and the ethyl acetate extracts from Geranium wilfordii Maxim displayed as well the most significant inhibition to the growth of Helicobacter. pylori, of which corilagin and 1,2,3,6-tetra-O-galloyl-β-d-glucose have been identified main anti-Helicobacter pylori active constituents. 相似文献4.
Chung SK Nam JA Jeon SY Kim SI Lee HJ Chung TH Song KS 《Archives of pharmacal research》2003,26(12):1024-1028
A prolyl endopeptidase inhibitor was isolated from the ethyl acetate soluble fraction of Phyllanthus ussurensis. The active compound was identified as an ellagitannin, corilagin. It was shown to non-competitively inhibit prolyl endopeptidase (PEP) with the IC50 value of 1.17x10(-6) microM. The Ki value was 6.70x10(-7) M. Corilagin was less inhibitory to other serine proteases such as chymotrypsin, trypsin, and elastase, indicating that it was relatively a specific inhibitor of PEP. Corilagin also effectively inhibited reactive oxygen species such as hydroxide and superoxide anion radical, hydrogen peroxide, and DPPH. Especially, corilagin showed potent scavenging activity on the superoxide anion radical in the ESR method (IC50 = 3.79x10(-6) M) as well as xanthine oxidase system. 相似文献
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目的 研究corilagin对氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)损伤人脐静脉血管内皮细胞(human umbilical vein endothelial ceils,HUVEC)增殖及细胞周期的影响,探索corilagin抗动脉粥样硬化(atherosclerosis,AS)的机理.方法 采用ox-LDL复制HUVEC的损伤模型,MTT法观察Corilagin对ox-LDL损伤HUVEC的保护作用.流式细胞术方法分析Corilagin对ox-LDL损伤HUVEC细胞周期的影响.结果 与模型对照组比较,Corilagin (6.25 μmol/L~ 50 μmol/L),作用12h、24 h、48 h对HUVEC有保护作用(P<0.05).与模型组比较,corilagin组S期细胞比例增加,G1、G2的变异系数减小,sub-G1减小,其各期细胞分布图趋于正常组的分布比例.结论 Corilagin呈浓度依赖性明显抑制ox-LDL对HUVEC的损伤,其机制可能是通过改善内皮细胞周期的G2/M期阻滞而发挥作用. 相似文献
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柯里拉京杀伤人喉癌Hep-2细胞的体外实验研究 总被引:1,自引:0,他引:1
目的 观察柯里拉京(Corilagin)对人喉癌细胞系Hep-2的杀伤作用。方法 在体外细胞培养的基础上,通过倒置显微镜、肼比色法、流式细胞仪观察Corilagin作用后Hep-2细胞的形态学、增殖率和细胞周期的改变。结果 Corilagin作用后的Hep-2细胞形态发生了明显变化;其抑制增殖作用呈量效、时效关系;Corilagin可阻肿瘤滞细胞于S期,并可诱导细胞凋亡。结论 Corilagin能显著抑制Hep-2细胞增殖,可能与阻滞细胞于S期和诱导凋亡有关,Corilagin抗肿瘤作用值得进一步研究。 相似文献
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Anti-hyperalgesic activity of corilagin,a tannin isolated from Phyllanthus niruri L. (Euphorbiaceae)
Jeverson Moreira Luiz Carlos Klein-Júnior Valdir Cechinel Filho Fátima de Campos Buzzi 《Journal of ethnopharmacology》2013
Ethnopharmacological relevance
Corilagin (β-1-O-galloyl-3,6-(R)-hexahydroxydiphenoyl-d-glucose) is a tannin isolated from Phyllanthus niruri (Euphorbiaceae). This plant is well known for their therapeutic purposes to treat several diseases associated with dolorous process and are used in several ethno-medicines in tropical and subtropical countries.Aim of the study
This study was designed to evaluate the anti-hyperalgesic activity of corilagin using chemically and thermally based nociception models in mice.Materials and methods
Corilagin was isolated from Phyllanthus niruri (Euphorbiaceae) by extraction and chromatographic procedures and the anti-hyperalgesic activity was evaluated by using writhing, formalin, capsaicin, glutamate and hot plate tests in mice.Results
Corilagin presented activity in acetic acid model with the ID50 calculated value of 6.46 (3.09–13.51) being about 20.6 fold more potent than acetylsalicylic acid. It also exhibited activity against the first phase of formalin test with ID50 value of 18.38 (15.15–22.59) μmol/kg. In the capsaicin and glutamate models, corilagin demonstrated significant activity at the 3 mg/kg.Conclusion
The experimental data demonstrated that corilagin exhibits anti-hyperalgesic activity that may be due to interaction with the glutamatergic system. 相似文献8.
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【摘要】目的 探讨柯里拉京能否通过下调NOTCH1信号通路抑制胃癌SGC 7901细胞的增殖, 以及对Hes1表达的影响。方法〓使用不同浓度的柯里拉京(0μg/ml、10μg/ml和100μg/ml)对胃癌SGC 7901细胞进行干预。在不同时间点(0、24和48h)使用MTT法对SGC 7901细胞活性进行检测。干预48h后, 使用qPCR和western blot对在不同浓度(0μg/ml、10μg/ml和100μg/ml)柯里拉京干预后,细胞NOTCH1、Hes1 mRNA和蛋白的表达水平进行分析。结果〓使用不同浓度柯里拉京(0μg/ml、10μg/ml和100μg/ml)对胃癌SGC 7901细胞进行干预后, 细胞活性呈时间依赖性和剂量依赖性下降, 差异均有统计学意义(P<005)。不同浓度柯里拉京(0μg/ml、10μg/ml和100μg/ml)干预48 h后, 胃癌SGC 7901细胞NOTCH1及Hes1 mRNA和蛋白的表达水平呈剂量依赖性降低, 差异均有统计学意义(P<005)。结论〓柯里拉京可通过下调NOTCH1/Hes1信号通路抑制胃癌SGC 7901细胞增殖, 同时为柯里拉京用于临床治疗胃癌等恶性肿瘤奠定了实验基础。 相似文献
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目的 研究抗炎药物Corilagin抑制放射引起小胶质细胞(BV-2)炎性反应的作用及其防护的分子机制。方法 细胞抑制实验(MTT)检测Corilagin对BV-2细胞的抑制率;Corilagin预处理小胶质细胞,12 h后,以0和32 Gy 2个放射剂量照射BV-2细胞,Real-time PCR检测小胶质细胞照射后不同时间点炎性反应因子IL-1β、TNF-α表达水平;硝酸还原酶法检测细胞上清液中一氧化氮(NO)的含量;Western blot检测各组细胞核转录因子NF-κB p65蛋白表达;激光共聚焦显微镜观察各组细胞标志物Iba-1的表达、NF-κB p65核转位及Nemo的表达。结果 1~10 μg/ml浓度范围内Corilagin对BV-2细胞增殖几乎无影响;照射后小胶质细胞表面标志物Iba-1表达明显,提示小胶质细胞激活,且炎性反应因子NO、TNF-α、IL-1β表达上调,而Corilagin(5μg/ml)可以显著抑制上述炎性反应因子的表达(tIL-1β=6.341, tTNF-α=3.411, tNO=3.134, P <0.05);Corilagin可抑制NF-κB活化蛋白Nemo,并显著抑制NF-κB p65的转位。结论 Corilagin可能通过NF-κB信号转导途径抑制照射后小胶质细胞的活化,从而下调炎性反应因子表达,保护神经元。 相似文献