ライフサイエンスコーパス: probucol

1 with tauroursodeoxycholic acid but not with probucol.

2 ive oxygen species generation was reduced by probucol.

3 administering the cholesterol-lowering drug probucol.

4 qual reductions by vitamin E+selenium and by probucol.

5 tamin E+selenium (with or without vitamin C)>probucol.

6 Dietary administration of probucol (0.5%, wt/wt) efficiently reduced total plasma

7 been designed and synthesized starting from probucol (1).

8 tamin C, 791 mg/d; selenium, 22 microg/d; or probucol, 406 mg/d.

9 th FH at 3 and 6 months after treatment with probucol, a cholesterol-lowering agent.

10 Even more effective was probucol, a PPAR-activating anti-lipid drug that we show

11 In SR-BI knockout mice, probucol also substantially reduced HDL-C but significan

12 el and these processes could be inhibited by probucol and L-thyroxine.

13 h classical phenolic antioxidants as BHT and probucol and rivals the antioxidant potency of Vitamin E

14 containing the lipophilic antioxidant drug, probucol, and macrophages derived from the human monocyt

15 roguaiaretic acid (NDGA), catechol, glutaryl probucol, and N-acetylcysteine increased eNOS expression

16 ucol (pCRLPs) when compared to CRLPs without probucol, and this was because of increases in triacylgl

17 ted with pCRLPs as compared to CRLPs without probucol, but phospholipid and cholesteryl ester formati

18 ly as an equally hypocholesterolemic dose of probucol by a mechanism(s) that is in part independent o

19 e timing of administration and withdrawal of probucol could control the onset of death and suggested

20 tely 3 (weaning) and 5 weeks of age and that probucol delayed heart failure even after development of

21 y now suggests that the protective effect of probucol depends not on its ability to inhibit lipid oxi

22 In WT mice, probucol, despite decreasing HDL-C by >80%, effectively

23 a reduction in plasma cholesterol caused by probucol does not necessarily lead to an antiatherogenic

24 antiatherosclerosis, and antioxidation drug probucol extended life to as long as 60 weeks (mean 36 w

25 njury model that vitamins C and E as well as probucol had beneficial effects on the vessel response t

26 Patients treated with lovastatin and probucol had prolongation of the lag phase (263 +/- 64 m

27 , alpha-carotene, beta-carotene, lutein, and probucol in octane:butyronitrile (9:1, v/v) were determi

28 Probucol inhibited ABCA1-dependent cholesterol efflux fr

29 lase, superoxide dismutase) and antioxidant (probucol) inhibited these events.

30 resent study was to test the hypothesis that probucol inhibits hepatic ABCA1 activity, thereby reduci

31 Probucol is a compound that reduces HDL-C levels but als

32 tyramine (seven patients), or lovastatin and probucol (nine patients).

33 se results explain the beneficial effects of probucol on atherosclerosis and xanthomas despite its HD

34 as shown to be responsible for the effect of probucol on increasing the fecal excretion of HDL-derive

35 ut mice were fed a chow diet containing 0.5% probucol or normal chow for 2 weeks.

36 s not observed with the similar antioxidants probucol or Trolox, suggesting that the alpha-tocopherol

37 lability and plasma lipid-lowering effect of probucol (PB) by constructing a combined drug delivery s

38 n of THP-1 macrophages with CRLPs containing probucol (pCRLPs) when compared to CRLPs without probuco

39 in E+selenium, vitamins E and C+selenium, or probucol (positive control).

40 al inhibition of hepatic ABCA1 activity with probucol reduced HDL-C levels but promoted RCT through d

41 sistent with this idea, the antioxidant drug probucol reduces the risk of restenosis, a form of cardi

42 Furthermore, probucol significantly enhanced the excretion of HDL-der

43 antioxidants catalase, N-acetylcysteine, and probucol significantly reduced proliferation in primary

44 as also partially rescued by the antioxidant probucol, the mitochondrial complex II activator, D-beta

45 Thus, the enhanced atherosclerosis in the probucol-treated animals is unlikely to be caused by the

46 wever, aortic atherosclerotic plaques in the probucol-treated apoE-/- mice formed more rapidly than i

47 sma lipoprotein profiles very similar to the probucol-treated apoE-/- mice, but do not have accelerat

48 nger protected from oxidation, compared with probucol-treated LDL, which remained protected.

49 Histologically, lesions in probucol-treated mice contained increased fibrous materi

50 FR was significantly higher after AGBM-Ab in probucol-treated versus untreated rats.

51 Probucol treatment also accelerated lesion development i

52 The ability of probucol treatment to modulate pathophysiology in the do

53 on in LpA after AGBM-Ab was not prevented by probucol treatment.

54 antioxidant pretreatment with water-soluble probucol would improve glomerular hemodynamics 60 to 90