ライフサイエンスコーパス: monocrotaline

1 2 experimental rat models (Sugen/hypoxia and monocrotaline).

2 omized rats injected with the alkaloid toxin monocrotaline.

3 ypertension was induced by administration of monocrotaline.

4 ith loss of cell viability after exposure to monocrotaline.

5 SOS was induced in rats with monocrotaline.

6 enuated the protective effect of GSH against monocrotaline.

7 ial for explaining the pulmonary toxicity of monocrotaline.

8 in male Sprague-Dawley rats by administering monocrotaline.

9 lpha activator, cobalt, chronic hypoxia, and monocrotaline.

10 were treated with rifampicin, phenytoin, and monocrotaline.

11 bone marrow cells and were then treated with monocrotaline.

12 HVOD was induced in rats with monocrotaline 160 mg/kg i.g. on day 0.

13 was induced in rats by a single injection of monocrotaline (60 mg/kg).

14 ed simultaneously, we studied the effects of monocrotaline, a pyrollizidine alkaloid, with reported t

15 in vivo studies examined changes induced by monocrotaline, a pyrrolizidine alkaloid that induces sin

16 ontinuation of the GSH infusion 5 days after monocrotaline administration led to severe hepatic veno-

17 olized AAV1.SERCA2a delivered at the time of monocrotaline administration limited adverse hemodynamic

18 One week after monocrotaline administration, the percentage of muscular

19 ted with NOX-A12 from Day 21 to Day 35 after monocrotaline administration.

20 levels were more than 70% to 80% depleted by monocrotaline and azathioprine, respectively, before cel

21 xperimental PH induced by chronic hypoxia or monocrotaline and in human PH (idiopathic or associated

22 AH in rats with medial hypertrophy following monocrotaline and in rats with neointima formation follo

23 hed animal models of pulmonary hypertension (monocrotaline and SuHx).

24 We then induced PAH in rats by injection of monocrotaline and, at day 21, began a 2-week treatment w

25 Compared with animals that received monocrotaline and/or underwent pneumonectomy but did not

26 Previous in vitro studies with azathioprine, monocrotaline, and dacarbazine suggested that toxins tha

27 hypertrophy, and vascular remodelling after monocrotaline, and prevented progression of established

28 human and rat tissues from PAH patients and monocrotaline- and Sugen/hypoxia-exposed rats were used

29 Azathioprine and monocrotaline are selectively toxic to SEC; the mechanis

30 Pneumonectomized rats injected with monocrotaline at 4 weeks demonstrated severe PAH at 11 w

31 Pneumonectomized rats injected with monocrotaline at 7 days develop severe hypertensive pulm

32 Monocrotaline caused denudation of the hepatic sinusoida

33 Monocrotaline caused depolymerization of F-actin in sinu

34 Together, phenytoin, rifampicin, and monocrotaline caused further endothelial damage, reflect

35 Monocrotaline caused hepatic vein NO to decrease by 30%

36 Monocrotaline causes depolymerization of F-actin in sinu

37 ry arteriolar muscularization in response to monocrotaline challenge compared with immunocompetent co

38 and pulmonary arteriolar muscularization in monocrotaline-challenged animals versus saline-treated c

39 enitor cells derived from the bone marrow of monocrotaline-challenged rats were dysfunctional and wer

40 Monocrotaline decreased GSH in sinusoidal endothelial ce

41 Monocrotaline enhanced transplanted cell engraftment wit

42 rtrophy and pulmonary vascular remodeling in monocrotaline-exposed rats.

43 Nevertheless, monocrotaline exposure did not cause right ventricular h

44 cell numbers in pulmonary arteries caused by monocrotaline exposure was prevented by NO inhalation.

45 roups A and B received the mitotic inhibitor monocrotaline, followed by male F344 (DPPIV(+)) bone mar

46 n of GSH, which suggests that selectivity of monocrotaline for SEC may be attributable to differences

47 GSH infusion starting 24 hours after monocrotaline ("glutathione rescue") offered substantial

48 H was induced in male Sprague Dawley rats by monocrotaline, hypoxia, or bleomycin challenge.

49 The effects of monocrotaline in Fischer 344 rats were examined by tissu

50 ed in intense accumulation of the peptide in monocrotaline-induced and SU5416/hypoxia-induced hyperte

51 Infusion of V-PYRRO-NO prevented the monocrotaline-induced increase in MMP-9.

52 rs in bone marrow cells developed hypoxia or monocrotaline-induced increase in pulmonary pressure and

53 Through this and other possible mechanisms, monocrotaline-induced injury in the endothelial compartm

54 -neointimal pattern of remodeling after mild monocrotaline-induced injury was converted into a neoint

55 cells are the major source of both basal and monocrotaline-induced matrix metalloproteinase-9/matrix

56 ved cardiac vascular density and function of monocrotaline-induced PAH animals.

57 In both hypoxia and monocrotaline-induced PAH rat models, which display redu

58 zed anti-miRs were administered to rats with monocrotaline-induced PAH.

59 ased progressively during the development of monocrotaline-induced PH and correlated with plasma-memb

60 hibitor, caused selective MPAP reductions in monocrotaline-induced PH and in spontaneous PH in fawn-h

61 nd function were reduced in human PAH and in monocrotaline-induced PH in rats.

62 l activation of KCNK3 significantly reversed monocrotaline-induced PH in rats.

63 helial IDO in hypoxia-induced PH in mice and monocrotaline-induced PH in rats.

64 ronic hypoxia-induced PH in mice and A-17 in monocrotaline-induced PH in rats.

65 In the monocrotaline-induced PH rat model, A-17 treatment signi

66 armacological activation of KCNK3 alleviated monocrotaline-induced PH, thus demonstrating that loss o

67 dministered both in rat chronic hypoxia- and monocrotaline-induced PH.

68 AND We exposed mice and rats with hypoxia or monocrotaline-induced pulmonary arterial hypertension to

69 or Ep3 deletion attenuated both hypoxia and monocrotaline-induced pulmonary hypertension and restrai

70 an aortocaval fistula, on the development of monocrotaline-induced pulmonary hypertension in rats.

71 tes, rather than worsens, the development of monocrotaline-induced pulmonary hypertension in rats.

72 We found that monocrotaline-induced pulmonary hypertension was associa

73 udy the effects of blocking SDF-1, rats with monocrotaline-induced pulmonary hypertension were treate

74 ar remodeling, and inflammation of rats with monocrotaline-induced pulmonary hypertension.

75 vitro and in vivo and on the progression of monocrotaline-induced pulmonary hypertension.

76 lmonary arterioles in models of hypoxia- and monocrotaline-induced pulmonary hypertension.

77 Simvastatin attenuates monocrotaline-induced pulmonary vascular remodeling with

78 In the monocrotaline-induced rat model of sinusoidal obstructio

79 Monocrotaline induces prolonged changes in the liver tha

80 so found in the chronically hypoxic mice and monocrotaline-injected rats as models of human PAH.

81 matinib started 2 weeks after a subcutaneous monocrotaline injection substantially attenuated the abn

82 Ten days after monocrotaline injection, echocardiography was performed

83 W1(+) cells was also increased in rats after monocrotaline injection.

84 mal lesions develop between 3 and 5 wk after monocrotaline injury is coupled with increased pulmonary

85 In order to produce these lesions, monocrotaline is oxidized to monocrotaline pyrrole in th

86 Glutathione infusion started after monocrotaline is partially protective.

87 In conclusion, development of drugs with monocrotaline-like effects will help advance liver cell

88 ary vascular neointimal formation 4 wk after monocrotaline (MCT) administration.

89 tion and their pharmacological efficacy in a monocrotaline (MCT) induced rat model of PAH.

90 pattern of remodeling in response to injury, monocrotaline (MCT) injury in Sprague-Dawley rats was fo

91 ptor-deficient rats to the endothelial toxin monocrotaline (MCT) leads to the development of neointim

92 ir and remodeling of lung and heart in a rat monocrotaline (MCT) model of pulmonary hypertension.

93 tissue from normal chronic hypoxia (CH) and monocrotaline (MCT) models of pulmonary hypertension (PH

94 Monocrotaline (MCT) was administered to 2 groups of Spra

95 Two days after transposon delivery, monocrotaline (MCT) was administered to induce PH.

96 synthase and nuRFP) were tested in rats with monocrotaline (MCT)-induced PAH.

97 Cav-1 mimetic peptide on the development of monocrotaline (MCT)-induced PH.

98 iterpenoid triepoxide) on the development of monocrotaline (MCT)-induced pulmonary hypertension in pn

99 In the monocrotaline (MCT)-treated rat, there is marked stimula

100 n (IPAH) patients, hypoxia-exposed mice, and monocrotaline (MCT)-treated rats.

101 ingestion of pyrrolizidine alkaloids such as monocrotaline (Mct).

102 eceived either a single subcutaneous dose of monocrotaline (MCT, 60 mg/kg) to induce PH-associated RV

103 of the LV in rats with pressure-induced RVF (monocrotaline [MCT] injection, n = 25; controls with sal

104 A model of PH induced by drug (monocrotaline, MCT) has been extensively used in mice to

105 arteries from patients with PAH and the rat monocrotaline model of PAH in comparison with controls.

106 gonists that showed oral efficacy in the rat monocrotaline model of pulmonary arterial hypertension (

107 Lung perfusion was evaluated in the monocrotaline model of pulmonary arterial hypertension i

108 In the monocrotaline model, the NOX-A12-induced reduction of ma

109 feration, and regress established PAH in the monocrotaline model.

110 t group C was used to analyze the effects of monocrotaline on transplanted bone marrow cells.

111 conditions: no accompanying injury, or after monocrotaline or balloon endarterectomy injury.

112 PAH was induced in Sprague-Dawley rats by monocrotaline or chronic hypoxia (10% oxygen) in combina

113 from patients with PAH and female rats with monocrotaline or chronic hypoxia+Sugen-5416 (CH+SU) PAH.

114 in which PAH develops in response to either monocrotaline or VEGF receptor inhibition combined with

115 AT(1) receptor antagonist (losartan) in the monocrotaline PAH rat model (60 mg/kg).

116 reas miR-126 up-regulation increased them in monocrotaline PAH rats.

117 hypertrophy, and fibrosis in comparison with monocrotaline-PAH rats treated with a control AAV1 carry

118 arterioles from SU-5416/hypoxia-PAH rats and monocrotaline-PAH rats with hyperaldosteronism expressed

119 Phenytoin, rifampicin, and monocrotaline produced injury in hepatocytes that was no

120 ation of multiple liver cell compartments by monocrotaline promoted transplanted cell engraftment and

121 d RV hypertrophy by use of a canine model of monocrotaline pyrrole (MCTP)-induced CPH.

122 of bicaval cardiac transplantation (TX) and monocrotaline pyrrole (MCTP)-induced CPH.

123 eks after a right atrial injection of either monocrotaline pyrrole (MCTP, n=8) or placebo (CTL, n=8).

124 these lesions, monocrotaline is oxidized to monocrotaline pyrrole in the liver followed by hematogen

125 mined specific endothelial targets for (14)C-monocrotaline pyrrole using two-dimensional gel electrop

126 function using a newly established model of monocrotaline pyrrole-induced chronic pulmonary hyperten

127 entricular hydraulic power in the setting of monocrotaline pyrrole-induced chronic pulmonary hyperten

128 cytotoxicity were similarly decreased in the monocrotaline rat and chronic hypoxia mouse models of PA

129 ent models of pulmonary hypertension (PH): a monocrotaline rat model and a hypoxia mouse model.

130 In the monocrotaline rat model of PAH, associated with reduced

131 In the monocrotaline rat model of PH, pharmacologic modulation

132 ry remodeling in PAH was investigated in the monocrotaline rat model.

133 rtal infusion of GSH can prevent HVOD in the monocrotaline rat model.

134 These results were replicated in the monocrotaline rat model.

135 sicles and blood cells; and (3) lungs from a monocrotaline rat model.

136 The monocrotaline rat PAH model also showed increased lung (

137 from patients with PAH and the lungs of the monocrotaline rat.

138 PASMCs from monocrotaline rats are hyperproliferative and display no

139 Monocrotaline rats were treated with oral dichloroacetat

140 In monocrotaline rats with established PAH, gene transfer o

141 In conclusion, monocrotaline selectively depletes sinusoidal endothelia

142 PAs including monocrotaline, senkirkine, senecionine, seneciphylline a

143 Monocrotaline sensitized the liver to carbon tetrachlori

144 A single administration of monocrotaline to rats results in pathologic alterations

145 of cytochrome P450 3A4 isoform that converts monocrotaline to toxic intermediates.

146 In contrast, monocrotaline toxicity in hepatocytes was largely unaffe

147 Intraportal infusion of GSH protects against monocrotaline toxicity, at least partially by maintainin

148 E), an inhibitor of NO synthase, exacerbated monocrotaline toxicity, whereas V-PYRRO/NO, a liver-sele

149 ssue pathology caused by chronic hypoxia and monocrotaline toxicity.

150 itrypsin were transplanted into the liver of monocrotaline-treated and partial-hepatectomized C57BL/6

151 Administration of TGFBRII-Fc to monocrotaline-treated or SU5416/hypoxia-treated rats wit

152 ated PH and pulmonary vascular remodeling in monocrotaline-treated rats, SU5416/hypoxia-treated rats,

153 In monocrotaline-treated rats, transplanted cells integrate

154 without Kupffer cell or hepatocyte damage in monocrotaline-treated rats.

155 PH was studied in monocrotaline-treated Sprague-Dawley rats, SU5416/hypoxi

156 he Fabaceae family contained senecionine and monocrotaline type PAs.

157 lmonary arteriole muscularization induced by monocrotaline (used experimentally to induce PAH) after

158 rtension (PAH-RVH; SU5416+chronic-hypoxia or Monocrotaline) versus pulmonary artery banding-induced R

159 Monocrotaline was administered 1 wk after the creation o

160 ytoin and rifampicin for 3 days, after which monocrotaline was given followed 1 day later by intraspl

161 In a rat pulmonary hypertension model (monocrotaline), we studied RV free wall tissues from rat

162 hepatocytes suffered inapparent damage after monocrotaline, we introduced further liver injury with c

163 Azathioprine and monocrotaline were found to be selectively more toxic to

164 Azathioprine and monocrotaline were studied as part of a series of studie

165 Lung FDG increases 1-2 weeks after monocrotaline (when PAH is mild) and is normalized by di

166 terial hypertension and in rats treated with monocrotaline, whereas it was upregulated in carotid art