ライフサイエンスコーパス: bezafibrate

1 P2C8 mRNA and protein levels were induced by bezafibrate.

2 as had previously been noted in a trial with bezafibrate.

3 y ameliorated in the BACHD mice treated with bezafibrate.

4 gulated in opposite manners by ritonavir and bezafibrate, a hypolipidemic agonist of the peroxisome p

5 DF rats were treated for 6 weeks with either bezafibrate, a lipid-lowering drug that does not affect

6 cently, we showed that the administration of bezafibrate, a pan-PPAR agonist, increases the expressio

7 ntion of intracellular 4-HNE accumulation by bezafibrate, a peroxisome proliferator-activated recepto

8 l as activation of fatty acid oxidation with bezafibrate also protected Akt-expressing cells from glu

9 A redeployed drug combination of bezafibrate and medroxyprogesterone acetate (BaP) has sh

10 The redeployed drug combination of bezafibrate and medroxyprogesterone acetate (designated

11 nscription factor PPARalpha with the ligands bezafibrate and Wyeth-14,643.

12 n HepG2 cells, with a further increase after bezafibrate ( approximately 18-fold), 4-chloro-6-(2,3-xy

13 Fenofibrate and bezafibrate are reasonable second-line therapies for dys

14 Fenofibrate and bezafibrate are reasonable second-line therapies for dys

15 Bezafibrate (BEZ), a pan activator of peroxisome prolife

16 For 5 of the chemicals (bezafibrate, climbazole, diclofenac, furosemide, and hyd

17 r concentrations than ionic PCs (metoprolol, bezafibrate, clofibric acid, diclofenac, gemfibrozil, ib

18 thology had developed, our data suggest that bezafibrate exerts a preventive effect on both tau patho

19 provide strong evidence that treatment with bezafibrate exerts neuroprotective effects which may be

20 ighlight the strong therapeutic potential of bezafibrate for treatment of HD.

21 mouse model of HD, we tested the efficacy of bezafibrate in a 'full-length' Htt mouse model, the BACH

22 Our data demonstrate the efficacy of bezafibrate in ameliorating both neuropathological featu

23 We found that administration of bezafibrate in the diet restored levels of PGC-1alpha, P

24 ed 15 355 patients who were screened for the Bezafibrate Infarction Prevention (BIP) trial.

25 analyses of the Helsinki Heart Study and the Bezafibrate Infarction Prevention Study.

26 n Trial, results of other studies, e.g., the Bezafibrate Intervention Program and the Diabetes Athero

27 Moreover, as bezafibrate is a well-tolerated clinically approved drug

28 Bezafibrate is therefore a promising agent for the treat

29 te that treatment with a PPAR-alpha agonist, bezafibrate, is able to reverse the miR-27b-induced lipi

30 Hypolipidemic drugs, such as bezafibrate, known activators of the peroxisome prolifer

31 -lives (DT50) of diclofenac (<0.1-1.4 days), bezafibrate (<0.1-4.8 days), sulfamethoxazole (2-33 days

32 studied the effects of the pan-PPAR agonist bezafibrate on tau pathology, inflammation, lipid metabo

33 human macrophages with the PPARalpha ligands bezafibrate or WY14643 inhibited OPN expression.

34 n the presence of inositol hexaphosphate and bezafibrate (or derivatives), liganded Hb at low pH (pH

35 roliferator-activated receptor-alpha agonist bezafibrate, or the nonsteroidal anti-inflammatory drug

36 L35, a bezafibrate-related compound, is one of the more potent

37 Finally, bezafibrate rescued lipid accumulation and apparent vacu

38 , treatment of type 2 diabetic patients with bezafibrate significantly decreased OPN plasma levels.

39 oglitazone), but not a PPAR-alpha activator (bezafibrate), strikingly diminished Egr-1 mRNA and prote

40 Bezafibrate therefore exerts neuroprotective effects in

41 Bezafibrate treatment also diminished microglial activat

42 Bezafibrate treatment lessened the rise in plasma TAG ob

43 pha to this PPARalpha response element after bezafibrate treatment of human hepatocytes.

44 Bezafibrate treatment prevented conversion of type I oxi

45 Bezafibrate treatment restored the impaired PPARgamma, P

46 Bezafibrate treatment significantly decreased tau hyperp

47 Since bezafibrate was given to the mice before tau pathology h

48 Despite lowering plasma TAG, bezafibrate was not effective in preventing an increased

49 acologic treatment with the pan-PPAR agonist bezafibrate would correct a deficiency of PGC-1alpha and