ライフサイエンスコーパス: NDGA

1 NDGA decreased sterol regulatory element binding protein

2 NDGA inhibited very low-density lipoprotein (VLDL) secre

3 NDGA negated the HCV-induced alteration of host lipid ho

4 NDGA seemed to be the most potent of the phenolic antiox

5 NDGA was able to inhibit FGFR3 autophosphorylation both

6 NDGA-mediated alterations of host lipid metabolism, LD m

7 ralizing ROS with nordihydroguaiaretic acid (NDGA) abrogated cell death induced by AF-TUSC2-erlotinib

8 and investigated nordihydroguaiaretic acid (NDGA) derivatives and have established that the reductiv

9 MP (8-Br-cAMP) or nordihydroguaiaretic acid (NDGA) had no effect on the relative level of channel act

10 Nordihydroguaiaretic acid (NDGA) was also characterized as an inhibitor of carboxyl

11 Nordihydroguaiaretic acid (NDGA) was observed by Ono et al. to decrease the fluores

12 COX enzymes; and nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor on human lung cancer cel

13 lo-oxygenase, nor nordihydroguaiaretic acid (NDGA), an inhibitor of the lipoxygenase pathway.

14 the antioxidants nordihydroguaiaretic acid (NDGA), catechol, glutaryl probucol, and N-acetylcysteine

15 olipidemic agent, nordihydroguaiaretic acid (NDGA), on host lipid/fatty acid synthesis and HCV life c

16 Indomethacin and nordihydroguaiaretic acid (NDGA), potent inhibitors of the cyclooxygenase (COX) and

17 genase inhibitor, nordihydroguaiaretic acid (NDGA), the 5-lipoxygenase inhibitor, AA861, the epoxygen

18 tory properties of nordihydroguaiartic acid (NDGA), which blocks protein transport through the Golgi,

19 Neither nordihydroquararetic acid (NDGA), which inhibits metabolism of ArA by cyclooxygenas

20 oprevention (exisulind +/- retinoic acid +/- NDGA) and therapeutic (exisulind +/- paclitaxel +/- cisp

21 Although NDGA failed to disaggregate Abeta protofibrils, it did i

22 tent with the promoter studies, curcumin and NDGA, inhibitors of AP-1 activation, markedly inhibited

23 actions for sulindac sulfide, exisulind, and NDGA with paclitaxel, cisplatin, and 13-cis-retinoic aci

24 gnalling inhibitors Wortmannin, LY294002 and NDGA, and concluded that the four invasive pathogenic sp

25 gest that inhibitory small molecules such as NDGA that target a specific subcellular compartment may

26 Both NDGA and AA861 inhibited progesterone production and StA

27 ated protein kinase (MAPK) were inhibited by NDGA treatment.

28 nM total carboxylesterases was unaffected by NDGA.

29 when protofibrils were incubated with excess NDGA.

30 l lines expressing activated forms of FGFR3, NDGA generally resulted in a decrease in MAPK activation

31 ddition, we have determined that hydrophobic NDGA derivatives activate 15-HLO, suggesting a hydrophob

32 njection of the phospholipase A(2) inhibitor NDGA partially suppressed the induction of immediate ear

33 eline and in the presence of LOX inhibitors (NDGA, AA-861, CDC, baicalein, and PD146176) vs. vehicle-

34 In addition, the binding of NDGA to Abeta protofibrils increased their nonspecific a

35 teration of thioflavin T upon the binding of NDGA to these aggregates.

36 This effect of NDGA was enhanced by nonphenolic antioxidants such as N-

37 This effect of NDGA was not due to inhibition of lipoxygenase because c

38 The effects of NDGA on activated FGFR3 derivatives targeted either to t

39 The antiviral effects of NDGA resulted in reduced HCV replication and secretion.

40 hdrawing substituents on the phenyl rings of NDGA.

41 C50 = 0.003-0.150 microM); sulindac sulfide, NDGA, and 13-cis-retinoic acid had intermediate potency

42 They concluded that NDGA could disaggregate Abeta fibrils into aggregates th

43 In the current study, we confirmed that NDGA induces a decrease in the fluorescence of thioflavi

44 Nuclear run-on studies indicated that NDGA increased eNOS transcription.

45 These results suggest that NDGA might bind along the lateral surface of Abeta proto

46 lic hydroxyl groups completely inhibited the NDGA effect on eNOS mRNA levels.

47 Exposure of BAECs to NDGA enhanced NO production, as measured by electron par

48 and perinuclear distribution of LDs, whereas NDGA most notably reduced the overall number and increas

49 re observed regardless of the order in which NDGA, thioflavin T, and Abeta protofibrils were added to

50 BAECs or human aortic endothelial cells with NDGA.