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Xiaoyu Li - One of the best experts on this subject based on the ideXlab platform.

  • Ginkgolide A b And huperzine A inhibit nitric oxide induced neurotoxicity
    International Immunopharmacology, 2002
    Co-Authors: Hongwei Zhao, Xiaoyu Li
    Abstract:

    AbstrAct Nitric oxide (NO) is believed to plAy importAnt roles in neuronAl degenerAtion. In this study, the effects of NO on cell growth And Apoptosis hAve been exAmined in humAn neuroblAstomA cell line SK–N–SH. Sodium nitroprusside (SNP), A NO donor, wAs found to significAntly inhibit cell growth And to induce Apoptosis. The inhibitory And Apoptotic Activities of SNP followed A dose- And time-dependent mAnner. Ginkgolide A, B (GA, B), And huperzine A (Hup A), the three compounds isolAted from Chinese herbs, blocked the inhibition of cell growth And Apoptosis induced by SNP. The results suggest thAt inhibition of NO-induced neurotoxicity mAy be one mechAnism of the Above three therApeutic Agents in neurodegenerAtive diseAses.

  • Ginkgolide A b And huperzine A inhibit nitric oxide production from rAt c6 And humAn bt325 gliomA cells
    Acta Pharmacologica Sinica, 1999
    Co-Authors: Hongwei Zhao, Xiaoyu Li
    Abstract:

    AIM: To study the effects of Ginkgolide A, B (Gin A, Gin B) And huperzine A (Hup A) on nitric oxide (NO) production from cultured Astrocytes. METHODS: Nitrites in supernAtAnts were meAsured with Griess AssAy. RESULTS: Hup A 0.001-100 mumol.L-1 time- And concentrAtion-dependently inhibited the NO production from rAt C6 AstrocytomA cells. The NO production from C6 cells wAs concentrAtion-dependently inhibited by the treAtment with Gin A or Gin B 0.001-10 micromol.L-1 for 24 h. The NO production from humAn BT325 AstrocytomA cells wAs concentrAtion-dependently inhibited by Hup A, Gin A, or Gin B 0.01-10 micromol.L-1 for 24 h. CONCLUSION: Gin A, Gin B, And Hup A inhibited Astrocytes producing NO.

Hongwei Zhao - One of the best experts on this subject based on the ideXlab platform.

  • Ginkgolide A b And huperzine A inhibit nitric oxide induced neurotoxicity
    International Immunopharmacology, 2002
    Co-Authors: Hongwei Zhao, Xiaoyu Li
    Abstract:

    AbstrAct Nitric oxide (NO) is believed to plAy importAnt roles in neuronAl degenerAtion. In this study, the effects of NO on cell growth And Apoptosis hAve been exAmined in humAn neuroblAstomA cell line SK–N–SH. Sodium nitroprusside (SNP), A NO donor, wAs found to significAntly inhibit cell growth And to induce Apoptosis. The inhibitory And Apoptotic Activities of SNP followed A dose- And time-dependent mAnner. Ginkgolide A, B (GA, B), And huperzine A (Hup A), the three compounds isolAted from Chinese herbs, blocked the inhibition of cell growth And Apoptosis induced by SNP. The results suggest thAt inhibition of NO-induced neurotoxicity mAy be one mechAnism of the Above three therApeutic Agents in neurodegenerAtive diseAses.

  • Ginkgolide A b And huperzine A inhibit nitric oxide production from rAt c6 And humAn bt325 gliomA cells
    Acta Pharmacologica Sinica, 1999
    Co-Authors: Hongwei Zhao, Xiaoyu Li
    Abstract:

    AIM: To study the effects of Ginkgolide A, B (Gin A, Gin B) And huperzine A (Hup A) on nitric oxide (NO) production from cultured Astrocytes. METHODS: Nitrites in supernAtAnts were meAsured with Griess AssAy. RESULTS: Hup A 0.001-100 mumol.L-1 time- And concentrAtion-dependently inhibited the NO production from rAt C6 AstrocytomA cells. The NO production from C6 cells wAs concentrAtion-dependently inhibited by the treAtment with Gin A or Gin B 0.001-10 micromol.L-1 for 24 h. The NO production from humAn BT325 AstrocytomA cells wAs concentrAtion-dependently inhibited by Hup A, Gin A, or Gin B 0.01-10 micromol.L-1 for 24 h. CONCLUSION: Gin A, Gin B, And Hup A inhibited Astrocytes producing NO.

Lin Huimin - One of the best experts on this subject based on the ideXlab platform.

  • study on isolAtion And purificAtion of Ginkgolide A from ginkgo leAves
    Progress in Pharmaceutical Sciences, 2011
    Co-Authors: Lin Huimin
    Abstract:

    Objective:To estAblish A simple method of extrAction,isolAtion And purificAtion for GinkgolideA from ginkgo leAves.Methods:The GinkgolideA in ginkgo leAves wAs extrActed,isolAted And purified by extrActing with Alcohol-wAter solution And ethyl AcetAte,by mAcroporous resin′s Adsorption And elution,As well As by crystAllizAtion And recrystAllizAtion.The optimum conditions of the process were studied by tAking the yield And purity of GinkgolideA As index.Results:The optimum conditions of the process were confirmed As follows:the pH vAlue of ethAnol extrAct from ginkgo leAves wAs Adjusted to 3 before extrAction with ethyl AcetAte;the pH vAlue of ethyl AcetAte extrAct wAs Adjusted to 3 And then NM100 mAcroporous resin wAs used to Adsorb the ethyl AcetAte extrAct,with the flow rAte of 1 mL ·min-1;The column wAs eluted with 30% And 50% ethAnol respectively,And then the 50% ethAnol eluAnt wAs collected And concentrAted;The 50% ethAnol eluAnt wAs crystAllized At 4 ℃,And then the mAcrocrystAl wAs recrystAllized in ethAnol-wAter system with the rAtio of 2:1.The purity of the Ginkgolide A prepAred in this process wAs Above 99%,with the yield of 60%.Conclusion:The process is stAble And feAsible.It cAn be Applied to industriAl production.

Changyi Chen - One of the best experts on this subject based on the ideXlab platform.

  • Ginkgolide A gold nAnopArticles inhibit vAsculAr smooth muscle proliferAtion And migrAtion in vitro And reduce neointimAl hyperplAsiA in A mouse model
    Journal of Surgical Research, 2011
    Co-Authors: Sarah M Weakley, Xinwen Wang, Hong Mu, Jianming Lu, Changyi Chen
    Abstract:

    BAckground NeointimAl formAtion is mediAted by phenotypic chAnges in vAsculAr smooth muscle cells (SMC) And is An importAnt mediAtor of restenosis following ArteriAl reconstruction. We conjugAted AntioxidAnt Ginkgolide A (GA) to gold nAnopArticles (GNP) to determine the effect of GA delivery on neointimAl formAtion. MAteriAls And Methods GA wAs conjugAted to 80 nm GNP in An overnight incubAtion. Mouse P53LMAC01 vAsculAr SMC were treAted with vArious doses of GA-GNP, GA Alone, GNP Alone, And no treAtment control. Cell proliferAtion And migrAtion were AnAlyzed, And superoxide Anion levels And the phosphorylAtion stAtus of ERK1/2 were determined. Mice underwent ligAtion of the common cArotid Artery Along with locAl treAtment with GNP (control) or GA-GNP. The cArotid Artery wAs hArvested And subjected to immunohistochemicAl AnAlysis. Results GA-GNP treAtment significAntly inhibited SMC proliferAtion And migrAtion in vitro in compArison to GNP treAtment Alone, And the effect persisted for up to 72 h After treAtment. TreAtment with GA-GNP Also reduced superoxide Anion levels in vitro . PDGF-BB substAntiAlly induced ERK1/2 phosphorylAtion in GNP control cells; this PDGE-BB induced ERK1/2 phosphorylAtion wAs significAntly inhibited in GA-GNP-treAted cells compAred with GNP only. GA-GNP significAntly reduced neointimAl hyperplAsiA After injury in mice, And proliferAting cell nucleAr Antigen (PCNA) stAining wAs reduced substAntiAlly in the Arteries of mice treAted with GA-GNP. Conclusions GA-GNP reduce vAsculAr SMC proliferAtion And migrAtion in vitro through reduced ActivAtion of ERK1/2. LocAl treAtment with GA-GNP in AreAs of ArteriAl injury reduced neointimAl hyperplAsiA And subsequent stenosis.

  • Ginkgolide A AttenuAtes homocysteine induced endotheliAl dysfunction in porcine coronAry Arteries
    Journal of Vascular Surgery, 2006
    Co-Authors: Wei Zhou, Hong Chai, Andy Courson, Alan B Lumsden, Changyi Chen
    Abstract:

    BAckground Homocysteine is An independent risk fActor for Atherosclerosis. The objective of this study wAs to investigAte whether Ginkgolide A (GA), A mAjor constituent of Ginkgo bilobA , could block homocysteine-induced endotheliAl dysfunction in porcine coronAry Arteries. Methods Porcine coronAry Artery rings were Assigned to six treAtment groups: control; homocysteine (50 μmol/L); low-dose (50 μmol/L) or high-dose (100 μmol/L) GA; And homocysteine plus low-dose or high-dose GA. After 24 hours' incubAtion, the rings were AnAlyzed for vAsomotor function in response to A thromboxAne A2 AnAlogue (U46619), brAdykinin, And sodium nitroprusside. EndotheliAl nitric oxide synthAse (eNOS) wAs studied by using reAl-time polymerAse chAin reAction And immunohistochemistry AnAlysis. Superoxide Anion production wAs Assessed by chemoluminescence AnAlysis. Results Endothelium-dependent relAxAtion (brAdykinin) wAs significAntly reduced in ring segments treAted with homocysteine As compAred with the control ( P P Conclusions Homocysteine significAntly impAirs endothelium-dependent vAsorelAxAtion through oxidAtive stress And downregulAtion of eNOS in porcine coronAry Arteries. GA effectively prevents homocysteine-induced endotheliAl dysfunction And moleculAr chAnges in porcine coronAry Arteries. This study underscores the potentiAl clinicAl benefits And ApplicAtions of GA in controlling homocysteine-AssociAted vAsculAr injury And cArdiovAsculAr diseAse.

Seiji Nishino - One of the best experts on this subject based on the ideXlab platform.

  • intrAperitoneAl injection of Ginkgolide b A mAjor Active compound of ginkgo bilobA dose dependently increAses the Amount of wAke And decreAses non rApid eye movement sleep in c57bl 6 mice
    Neuroscience Letters, 2020
    Co-Authors: Shohei Nishimon, Mai Yamaguchi, Hisae Muraki, Noriaki Sakai, Seiji Nishino
    Abstract:

    AbstrAct The terpene lActones of Ginkgo bilobA extrAct, nAmely Ginkgolides (A, B, And C) And bilobAlide, possess AntioxidAnt, Anti-inflAmmAtory, And neuroprotective effects. They Are widely prescribed for the treAtment of cerebrAl dysfunctions And neurologicAl impAirments. In Addition, they demonstrAte AntAgonistic Action At the gAmmA-Aminobutyric Acid type A And glycine receptors, which Are members of the ligAnd-gAted ion chAnnel superfAmily. In the present study, the effects of Ginkgolides (A, B, And C) And bilobAlide on sleep in C57BL/6 mice were investigAted. Ginkgolide B wAs found to dose-dependently increAse the Amount of wAke And decreAse thAt of non-rApid eye movement sleep without chAnges in the electroencephAlogrAphy power density of eAch sleep/wAke stAge, core body temperAture And locomotor Activity for the first 6 h After intrAperitoneAl injection. Of note, the Amount of wAke After injection of 5 mg/kg of Ginkgolide B showed A significAnt increAse (14.9 %) compAred with thAt of vehicle (P = 0.005). In contrAst, there were no significAnt differences in the Amount of sleep, core body temperAture, And locomotor Activity in the mice injected with Ginkgolide A And C. BilobAlide briefly induced A decreAse in locomotor Activity but did not exert significAnt effects on the Amounts of sleep And wAke. The modes of Action of the wAke-enhAncing effects of Ginkgolide B Are unknown. However, it mAy Act through the AntAgonism of gAmmA-Aminobutyric Acid type A And glycine receptors becAuse it is estAblished thAt these inhibitory Amino Acids mediAte sleep And sleep-relAted physiology. It is of interest to further evAluAte the stimulAnt And AwAking Actions of Ginkgolide B on the centrAl nervous system in clinicAl And bAsic reseArch studies.