ライフサイエンスコーパス: gemfibrozil

1 red only 22% with cholystyramine, niacin and gemfibrozil.

2 partially explained the beneficial effect of gemfibrozil.

3 l as a glucuronidated hydroxyl-metabolite of gemfibrozil.

4 en fed diets supplemented with clofibrate or gemfibrozil.

5 ACO mRNA were strongly stimulated by WY and gemfibrozil.

6 2) for rosuvastatin to 2.16 (0.06, 75.0) for gemfibrozil.

7 st identified bacterium capable of degrading gemfibrozil.

8 ibrozil through food chow than those without gemfibrozil.

9 e mutants abrogated the inhibitory effect of gemfibrozil.

10 mol/liter (39.7 +/- 7.1 mg/dl), while taking gemfibrozil (1,200 mg/day); by 35%, to 1.20 +/- 0.21 mmo

11 l 2.9 mmol/L (111 mg/dL), were randomized to gemfibrozil 1200 mg/d or placebo and were followed up fo

12 We conducted a double-blind trial comparing gemfibrozil (1200 mg per day) with placebo in 2531 men w

13 rticipants were randomly assigned to receive gemfibrozil, 1200 mg/d (n = 1264), or matching placebo (

14 and in 219 of the 1264 patients assigned to gemfibrozil (17.3 percent).

15 astewater matrices, and to measure levels of gemfibrozil (254 +/- 20 ng/L), chlorogemfibrozil (166 +/

16 Gemfibrozil (30 mg/kg) for 7 days before and after strok

17 Pretreatment with gemfibrozil (30 mg/kg) for 7 days moderately but signifi

18 SOD levels were also elevated by gemfibrozil (30 mg/kg).

19 Treatment with gemfibrozil, a drug that specifically reduces triglyceri

20 Although therapy with gemfibrozil, a fibric acid derivative, showed reduced oc

21 Gemfibrozil, a Food and Drug Administration-approved lip

22 This study underlines the importance of gemfibrozil, a Food and Drug Administration-approved lip

23 e present study underlines the importance of gemfibrozil, a lipid-lowering drug and an activator of p

24 re, we delineate that oral administration of gemfibrozil, a lipid-lowering drug, decreases glial infl

25 Earlier studies have shown that gemfibrozil, a lipid-lowering drug, has anti-inflammator

26 Gemfibrozil, a lipid-lowering drug, inhibited cytokine-i

27 Here, we delineate that gemfibrozil, a lipid-lowering drug, stimulates GDNF in a

28 ssion of myelin genes via PPAR-beta and that gemfibrozil, a prescribed drug for humans, may find furt

29 n of NF-kappaB, AP-1, and C/EBPbeta and that gemfibrozil, a prescribed drug for humans, may further f

30 in mediating the anti-inflammatory effect of gemfibrozil, a prescribed lipid-lowering drug for humans

31 A selective CFTR channel blocker, gemfibrozil, abrogated the protective effect of IPC.

32 Gemfibrozil administration resulted in a similar inducti

33 ous to examine whether prophylactic usage of gemfibrozil against stroke is beneficial.

34 mfibrozil; p < 0.001 combination therapy vs. gemfibrozil alone; p = 0.088 combination therapy vs. NA

35 In non-stroke animals gemfibrozil also altered gene expression levels of PPARs

36 Gemfibrozil also did not up-regulate myelin genes in oli

37 Gemfibrozil also induced the recruitment of KLF4 to the

38 Similarly, gemfibrozil also inhibited fibrillar amyloid beta (Abeta

39 Gemfibrozil also inhibited the encephalitogenicity of MB

40 Accordingly, gemfibrozil also normalized striatal neurotransmitters a

41 Oral gemfibrozil also stimulated the recruitment of PPARalpha

42 Medications such as the fibrate gemfibrozil alter statin metabolism and increase statin

43 lines the possible therapeutic importance of gemfibrozil, an activator of peroxisome proliferator-act

44 This study demonstrates that gemfibrozil, an agonist of peroxisome proliferator-activ

45 Gemfibrozil, an agonist of PPARalpha, induced the recrui

46 Taken together, our results suggest gemfibrozil, an approved drug for hyperlipidemia in huma

47 sodium hypochlorite yielded a 4'-chlorinated gemfibrozil analog (chlorogemfibrozil).

48 ted on the use of the older fibrates such as gemfibrozil and clofibrate.

49 on perpetrators with CYP2C8, glucuronides of gemfibrozil and clopidogrel showed marked clinical drug-

50 ferent treatment times and concentrations of gemfibrozil and di-n-butyl phthalate were almost identic

51 Because gemfibrozil and fenofibrate are known to activate peroxi

52 Oral administration of gemfibrozil and fenofibrate inhibited clinical signs of

53 Both gemfibrozil and fenofibrate up-regulated mRNA, protein,

54 This study reveals a novel use of gemfibrozil and fenofibrate, Food and Drug Administratio

55 lts suggest that PPAR alpha agonists such as gemfibrozil and fenofibrate, may be attractive candidate

56 l of the anionic micropollutants diclofenac, gemfibrozil and ibuprofen from EfOM.

57 These studies highlight a new property of gemfibrozil and indicate its possible therapeutic use in

58 cally relevant drug compounds (indomethacin, gemfibrozil and probenecid), with high efficiency (s >10

59 These studies highlight a new property of gemfibrozil and suggest its possible therapeutic use in

60 rent compounds ranged from <10 to 3830 ng/L (gemfibrozil), and those of chloro/bromo byproducts range

61 on the uptake of cimetidine, fluoxetine, and gemfibrozil, and other ionizable PPCPs, to confirm the u

62 -alpha (PPARalpha), the role of PPARalpha in gemfibrozil- and fenofibrate-mediated up-regulation of T

63 l percentage of cerivastatin users also took gemfibrozil, approximately half of the case reports of r

64 tin with nicotinic acid and pravastatin with gemfibrozil are well-tolerated combinations that can mai

65 The drugs diclofenac, fluoxetine, and gemfibrozil belong to different pharmaceutical classes w

66 Events were reduced even further with gemfibrozil beyond that explained by increases in HDL-C

67 rhabdomyolysis, of which 25% were related to gemfibrozil-cerivastatin combination therapy, has focuse

68 The PPAR alpha agonists, gemfibrozil, ciprofibrate, and fenofibrate, have an exce

69 Similar to gemfibrozil, clofibrate, another fibrate drug, also inhi

70 Gemfibrozil consistently inhibited the expression and DN

71 , between serum triglyceride (TG) levels and gemfibrozil consumption with periodontal parameters.

72 e of several enzymes potentially involved in gemfibrozil degradation as well as resulted in the produ

73 Gemfibrozil degradation by Bacillus sp. GeD10 was here s

74 Bacillus sp. GeD10, a gemfibrozil-degrader, was previously isolated from activ

75 study represents the first omics study on a gemfibrozil-degrading bacterium.

76 genes may allow for monitoring of potential gemfibrozil-degrading organisms in situ and increase the

77 ts with hypertriglyceridemia who were taking gemfibrozil did not show significant differences in CAL

78 0 mg/day, n=53), 2) simvastatin placebo plus gemfibrozil (dose adjusted for renal function, n=36), an

79 queous exposure to halogenated degradates of gemfibrozil enhanced the antiandrogenicity of the parent

80 Overall, gemfibrozil exposure in Bacillus sp. GeD10 increased the

81 32, fold change (log2) >/= 1) in response to gemfibrozil exposure.

82 ce that had been treated with fenofibrate or gemfibrozil for 7 days.

83 wed that CHD events were reduced by 11% with gemfibrozil for every 5-mg/dL (0.13-mmol/L) increase in

84 sent study underlines a novel application of gemfibrozil (gem), a Food and Drug Administration-approv

85 viously found that a combination of low-dose gemfibrozil (GFB; a drug approved to treat high choleste

86 We report here that gemfibrozil (GFZ) inhibits axenic and intracellular grow

87 in the placebo group (9 fatal) and 58 in the gemfibrozil group (3 fatal), for a relative risk reducti

88 cholesterol level was 4 percent lower in the gemfibrozil group than in the placebo group.

89 was 72% in the simvastatin group, 72% in the gemfibrozil group, and 77% in the placebo control group

90 iving NNRTI-based antiretroviral therapy and gemfibrozil had triglyceride responses similar to those

91 icillin, tetracycline, erythromycin-H2O, and gemfibrozil have significant pollution risk quotients (R

92 n of the derivatives of ibuprofen, naproxen, gemfibrozil, helional, and amino acids.

93 ol, bezafibrate, clofibric acid, diclofenac, gemfibrozil, ibuprofen, ketoprofen, naproxen, sulfametho

94 , beclomethasone, carbamazepine, diclofenac, gemfibrozil, ibuprofen, ketoprofen, norethindrone, propr

95 thesized that prophylactic administration of gemfibrozil improves outcome after ischemic stroke.

96 However, it remains unknown whether gemfibrozil improves outcome after stroke.

97 First, we tested gemfibrozil in a filamentous MCAO model.

98 iNOS promoter-driven luciferase activity by gemfibrozil in cytokine-stimulated U373MG astroglial cel

99 follow the in situ halogenation reaction of gemfibrozil in deionized water and wastewater matrices,

100 and suggest the possible therapeutic use of gemfibrozil in PD patients.SIGNIFICANCE STATEMENT Increa

101 This study underlines the importance of gemfibrozil in protecting dopaminergic neurons in an ani

102 t study identified another novel property of gemfibrozil in stimulating the expression of myelin-spec

103 red by laser speckle imaging was improved by gemfibrozil in the ischemic hemisphere.

104 In this study, we measured the impact of gemfibrozil in two permanent middle cerebral artery occl

105 This study delineates a novel property of gemfibrozil in up-regulating SOCS3 in glial cells via PI

106 hould investigate whether discontinuation of gemfibrozil in warfarin users results in serious underan

107 ted or untreated human oligodendrocytes, and gemfibrozil increased the expression of myelin genes in

108 Gemfibrozil increased the expression of Socs3 mRNA and p

109 We demonstrated that treatment with gemfibrozil increases expression of the Th2 transcriptio

110 Gemfibrozil induced peroxisome proliferator-responsive e

111 Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like facto

112 Interestingly, gemfibrozil induced the activation of p85alpha-associate

113 Interestingly, gemfibrozil induced the activation of type IA phosphatid

114 tin immunoprecipitation analysis showed that gemfibrozil induced the recruitment of PPAR-beta to the

115 the mechanism by which the PPARalpha agonist gemfibrozil induces immune deviation and protects mice f

116 Gemfibrozil inhibited LPS-induced expression of inducibl

117 -mediated inhibition of iNOS suggesting that gemfibrozil inhibits iNOS independent of PPAR-alpha.

118 PAR-alpha-/- mice, we have demonstrated that gemfibrozil inhibits the activation of microglia indepen

119 mfibrozil via the PI3K pathway suggests that gemfibrozil inhibits the activation of NF-kappaB and the

120 These results suggest that gemfibrozil inhibits the induction of iNOS probably by i

121 this combination therapy, and a cerivastatin-gemfibrozil interaction was supported by the results of

122 Although gemfibrozil is a known activator of peroxisome prolifera

123 The cholesterol-lowering pharmaceutical gemfibrozil is a relevant environmental contaminant beca

124 Gemfibrozil is a widely used hypolipidemic and triglycer

125 Since gemfibrozil is known to activate peroxisome proliferator

126 On the other hand, gemfibrozil markedly increased the expression of PPAR-be

127 Furthermore, gemfibrozil may be of therapeutic value in the treatment

128 PARalpha may be beneficial for JNCL and that gemfibrozil may be repurposed for the treatment of this

129 ediated activation of KLF4 and suggests that gemfibrozil may find therapeutic application in neuroinf

130 ver, DeltahPPAR-alpha was unable to abrogate gemfibrozil-mediated inhibition of iNOS suggesting that

131 ), we investigated the role of PPAR-alpha in gemfibrozil-mediated inhibition of iNOS.

132 e PPARa-dependent astroglial GDNF pathway in gemfibrozil-mediated protection of dopaminergic neurons

133 Gemfibrozil-mediated protection of the nigrostriatal and

134 y and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.

135 ase and AKT by chemical inhibitors abrogated gemfibrozil-mediated up-regulation of SOCS3.

136 t not PPARbeta and PPARgamma, is involved in gemfibrozil-mediated up-regulation of TFEB.

137 ell as resulted in the production of several gemfibrozil metabolites.

138 mia were prospectively randomized to receive gemfibrozil, NA or combination therapy in an open-label,

139 n byproducts of salicylic acid, bisphenol A, gemfibrozil, naproxen, diclofenac, technical 4-nonylphen

140 -) mice from MPTP intoxication suggests that gemfibrozil needs the involvement of peroxisome prolifer

141 Gemfibrozil, niacin, and cholestyramine or corresponding

142 sitivity across a suite of analytes studied (gemfibrozil, nonylphenol, triclosan, 2,4,6-trichlorophen

143 PI3K also abolished the inhibitory effect of gemfibrozil on Abeta-, PrP-, poly IC-, Tat-, and MPP+-in

144 etected, and a 2.5% chance that an effect of gemfibrozil on acute rejection (versus placebo) was not

145 nt of p110 enhanced the inhibitory effect of gemfibrozil on LPS-induced expression of proinflammatory

146 R-gamma, abrogated the stimulatory effect of gemfibrozil on myelin genes in human oligodendrocytes.

147 The effects of gemfibrozil on NMR-measured LDL and HDL particle subclas

148 a); therefore, we investigated the effect of gemfibrozil on the activation of these transcription fac

149 demonstrate that the differential effect of gemfibrozil on the expression of T-bet and GATA3 was due

150 es also demonstrate the inhibitory effect of gemfibrozil on the invasion of T-bet-positive T cells in

151 e we describe that after Th2 polarization by gemfibrozil or other drugs, MBP-primed T cells induced t

152 aseline and after 7 months of treatment with gemfibrozil or placebo.

153 atients with hypertriglyceridemia and taking gemfibrozil over a 3-month period (group M).

154 ared with baseline/washout; p < 0.005 NA vs. gemfibrozil; p < 0.001 combination therapy vs. gemfibroz

155 mg/dl), while taking combination therapy of gemfibrozil plus NA (p < 0.001 for all interventions as

156 Fenofibrate and gemfibrozil, previously reported to induce TPP1 activity

157 eaction produced an additional 4'-brominated gemfibrozil product (bromogemfibrozil).

158 Moreover, gemfibrozil protected nigral neurons, normalized striata

159 (GDNF) gene in astrocytes via PPARa and that gemfibrozil protected nigral neurons, normalized striata

160 ministration of the human equivalent dose of gemfibrozil protected tyrosine hydroxylase (TH)-positive

161 Simvastatin, but not gemfibrozil, reduced total and low density lipoprotein c

162 Its activation by the drug gemfibrozil reduces clinical events in humans with estab

163 cal study has shown that one type of fibrate gemfibrozil reduces stroke incidence in men.

164 ow HDL cholesterol, and low LDL cholesterol, gemfibrozil reduces stroke incidence.

165 PARalpha (Cln3DeltaJNCL(DeltaPPARalpha)) and gemfibrozil remained unable to decrease SCMAS accumulati

166 gs, such as pravastatin, sodium benzoate, or gemfibrozil, restored the expression of Foxp3 in MBP-pri

167 The treatment of gemfibrozil solutions with sodium hypochlorite yielded a

168 estigating further mechanisms, we found that gemfibrozil stimulated the transcription of glial-derive

169 These results suggest that gemfibrozil stimulates the expression of myelin genes vi

170 Interestingly, gemfibrozil strongly inhibited the activation of NF-kapp

171 Patients with HIV infection beginning gemfibrozil therapy had substantially smaller reductions

172 Gemfibrozil therapy resulted in a significant reduction

173 icantly lower in SJL/J female mice receiving gemfibrozil through food chow than those without gemfibr

174 3DeltaJNCL(DeltaPPARalpha)) and inability of gemfibrozil to decrease SCMAS accumulation, reduce glial

175 bout the concomitant use of cerivastatin and gemfibrozil to the package insert for more than 18 month

176 astatin, nicotinic acid, cholestyramine, and gemfibrozil) to decrease total cholesterol levels to les

177 With gemfibrozil, total cholesterol level was unchanged; the

178 e were unable to detect PPAR-alpha in either gemfibrozil-treated or untreated human oligodendrocytes,

179 Accordingly, gemfibrozil treatment also improved locomotor activities

180 Furthermore, gemfibrozil treatment also led to the recruitment of PPA

181 Gemfibrozil treatment decreased the number of T-bet-posi

182 Gemfibrozil treatment increased LDL size and lowered num

183 ial (LOCAT), a trial examining the effect of gemfibrozil treatment on progression of atherosclerosis

184 nges in conventional lipid risk factors with gemfibrozil treatment only partially explain the reducti

185 Concentrations of HDL-C achieved with gemfibrozil treatment predicted a significant reduction

186 Oral gemfibrozil treatment reduced microglial and astroglial

187 ncreased transcription of Tfeb in the CNS by gemfibrozil treatment via PPARalpha.

188 e and averaged during the first 18 months of gemfibrozil treatment with the combined incidence of non

189 During gemfibrozil treatment, only the increase in HDL-C signif

190 of Cln3DeltaJNCL mice, which increased after gemfibrozil treatment.

191 -trans-retinoic acid, alone or together with gemfibrozil, up-regulated TPP1.

192 % vs. 59.3%; P < 0.001), and reductions with gemfibrozil varied by antiretroviral therapy class (44.0

193 on and inhibition of NF-kappaB activation by gemfibrozil via the PI3K pathway suggests that gemfibroz

194 tment with fat restriction, weight loss, and gemfibrozil was continued after hospitalization.

195 More importantly, gemfibrozil was shown to shift the cytokine secretion of

196 of these LDL and HDL particles achieved with gemfibrozil were significant, independent predictors of

197 ing patients with the fibric acid derivative gemfibrozil when the predominant lipid abnormality was l