ライフサイエンスコーパス: monocrotaline

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

2 bone marrow cells and were then treated with monocrotaline.

3 omized rats injected with the alkaloid toxin monocrotaline.

4 ypertension was induced by administration of monocrotaline.

5 ith loss of cell viability after exposure to monocrotaline.

6 SOS was induced in rats with monocrotaline.

7 enuated the protective effect of GSH against monocrotaline.

8 ial for explaining the pulmonary toxicity of monocrotaline.

9 transporter (SM22-5-HTT(+)), and rats given monocrotaline.

10 in male Sprague-Dawley rats by administering monocrotaline.

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

12 were treated with rifampicin, phenytoin, and monocrotaline.

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

14 days of hypoxia (sugen/hypoxia model), or by monocrotaline (60 mg/kg IP) injection (monocrotaline mod

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

16 r drug, rifampicin, plus phenobarbitone, and monocrotaline, a DNA adduct-forming alkaloid.

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

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

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

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

21 One week after monocrotaline administration, the percentage of muscular

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

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

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

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

26 In two experimental models of PAH (i.e., monocrotaline and Su5416/hypoxia treated rats) palbocicl

27 lar mechanisms responsible for RV failure in monocrotaline and Sugen with hypoxia models may identify

28 Transcriptomic signature of RV failure in monocrotaline and Sugen with hypoxia models showed simil

29 wo animal models with established PAH (i.e., monocrotaline and Sugen/hypoxia-treated rats), pharmacol

30 the murine pulmonary artery banding, and rat monocrotaline and Sugen5416/hypoxia models.

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

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

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

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

35 myocyte mitochondrial morphology in control, monocrotaline, and monocrotaline-SC-144 (GP130 antagonis

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

37 gle intraperitoneal injection of 60 mg/kg of monocrotaline, and rats were studied 21 days later when

38 d similar transcriptomic profiles of RV from monocrotaline- and Sugen with hypoxia-induced RV failure

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

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

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

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

43 Rifampicin and monocrotaline can cause liver failure in people.

44 Monocrotaline caused denudation of the hepatic sinusoida

45 Monocrotaline caused depolymerization of F-actin in sinu

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

47 Monocrotaline caused hepatic vein NO to decrease by 30%

48 Monocrotaline causes depolymerization of F-actin in sinu

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

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

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

52 Monocrotaline decreased GSH in sinusoidal endothelial ce

53 Monocrotaline enhanced transplanted cell engraftment wit

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

55 Nevertheless, monocrotaline exposure did not cause right ventricular h

56 ped more severe PH than wild-type rats after monocrotaline exposure or chronic hypoxia exposure.

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

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

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

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

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

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

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

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

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

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

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

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

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

70 is lung-PAs-PASMCs, the co-delivery reversed monocrotaline-induced PAH by reducing pulmonary artery p

71 is lung-PAs-PASMCs, the co-delivery reversed monocrotaline-induced PAH by reducing pulmonary artery p

72 mechanisms responsible for LV mass loss in a monocrotaline-induced PAH rat model.

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

74 left and right ventricle over the course of monocrotaline-induced PAH to delineate potential therape

75 eomic profile of rats at different stages of monocrotaline-induced PAH.

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

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

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

79 ated virus (AAV) expression of Adar improved monocrotaline-induced PH in rats.

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

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

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

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

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

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

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

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

88 cal cord blood (UCB)-derived MSCs in the rat monocrotaline-induced pulmonary hypertension (PH) model.

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

90 The severity of monocrotaline-induced pulmonary hypertension in rats was

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

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

93 n, they performed a preclinical trial in the monocrotaline-induced pulmonary hypertension rat model t

94 We found that monocrotaline-induced pulmonary hypertension was associa

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

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

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

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

99 Simvastatin attenuates monocrotaline-induced pulmonary vascular remodeling with

100 Two well-established PAH models, the monocrotaline-induced rat model and hypoxia/Su5416-induc

101 In the monocrotaline-induced rat model of sinusoidal obstructio

102 tion in both, pulmonary artery banding - and monocrotaline-induced RV overload.

103 Monocrotaline induces prolonged changes in the liver tha

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

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

106 Ten days after monocrotaline injection, echocardiography was performed

107 Two weeks following monocrotaline injection, rats were administered daily La

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

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

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

111 Glutathione infusion started after monocrotaline is partially protective.

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

113 , hypoxia-induced pulmonary hypertension and monocrotaline lung injury model).

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

115 niques were used to assess RV remodelling in monocrotaline (MCT) and Sugen hypoxia (SuHx) PH rats.

116 female C57BL/6 mice by weekly injections of monocrotaline (MCT) for 8 weeks.

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

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

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

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

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

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

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

124 RNA sequencing was performed on the lungs of monocrotaline (MCT), Sugen-hypoxia (SuHx), and control r

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

126 d weekly and underwent RNA-sequencing in the monocrotaline (MCT)-induced PH rat model to explore gene

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

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

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

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

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

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

133 Male Sprague-Dawley rats received monocrotaline (MCT; 60 mg/kg) or saline.

134 ods: Rats with decompensated RV hypertrophy (monocrotaline [MCT] and Sugen-5416 hypoxia [SuHx]) were

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

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

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

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

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

140 or by monocrotaline (60 mg/kg IP) injection (monocrotaline model).

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

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

143 of which are salient characteristics of the monocrotaline model.

144 In both sugen/hypoxia and monocrotaline models, sFUS treatment reduces right ventr

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

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

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

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

149 RNA sequencing on RV from rats treated with monocrotaline or Sugen with hypoxia/normoxia.

150 /BMP10 ligand trap ALK1(ECD) administered in monocrotaline or Sugen/hypoxia (SuHx) rats substantially

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

152 rat models of PH evoked by chronic hypoxia, monocrotaline, or Sugen/hypoxia, administration of Orai1

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

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

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

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

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

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

159 E2 or ER-a agonist rescued monocrotaline pulmonary hypertension and restored RV ape

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

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

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

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

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

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

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

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

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

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

170 In the monocrotaline rat model of PH, pharmacologic modulation

171 the first application of (129)Xe MRI to the monocrotaline rat model of pulmonary hypertension.

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

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

174 These results were replicated in the monocrotaline rat model.

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

176 erload (pulmonary artery banding-induced and monocrotaline rat models).

177 The monocrotaline rat PAH model also showed increased lung (

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

179 of SC-144 on RV-pulmonary artery coupling in monocrotaline rats (8-16 rats per group).

180 PASMCs from monocrotaline rats are hyperproliferative and display no

181 Sugen/hypoxia mice and monocrotaline rats showed elevated expression of CLIC4,

182 Monocrotaline rats were treated with oral dichloroacetat

183 In monocrotaline rats with established PAH, gene transfer o

184 odent models of pulmonary hypertension (PH): monocrotaline rats, Sugen5416-hypoxia rats, and Treg-dep

185 optosis inhibitor, mitigated PAH severity in monocrotaline rats.

186 derangements in the RV, and improves RVD in monocrotaline rats.

187 cated increased mitochondrial fission in the monocrotaline RV, which SC-144 mitigated.

188 ein expression and t-tubule structure in the monocrotaline RV.

189 al morphology in control, monocrotaline, and monocrotaline-SC-144 (GP130 antagonist) rats.

190 In conclusion, monocrotaline selectively depletes sinusoidal endothelia

191 PAs including monocrotaline, senkirkine, senecionine, seneciphylline a

192 Monocrotaline sensitized the liver to carbon tetrachlori

193 with PAH, rats with Sugen5416 + hypoxia- or monocrotaline + shunt-induced PAH, and rats with RV pres

194 ent trials in Sugen5416 + hypoxia-PAH and in monocrotaline + shunt-PAH.

195 prague-Dawley rats were injected (i.p.) with monocrotaline to induce PH (n = 16), or a vehicle contro

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

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

198 In contrast, monocrotaline toxicity in hepatocytes was largely unaffe

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

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

201 ssue pathology caused by chronic hypoxia and monocrotaline toxicity.

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

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

204 Monocrotaline-treated rats developed increased right ven

205 rtrophy, inflammation, and fibrosis in RA of monocrotaline-treated rats versus control.

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

207 In monocrotaline-treated rats, transplanted cells integrate

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

209 wing or rotor activity occurred in the LA of monocrotaline-treated rats.

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

211 he Fabaceae family contained senecionine and monocrotaline type PAs.

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

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

214 Monocrotaline was administered 1 wk after the creation o

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

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

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

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

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

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

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