ライフサイエンスコーパス: bile duct ligation

1 hepatic deposition of collagen 2 weeks after bile duct ligation.

2 sed markedly in the livers of mice following bile duct ligation.

3 IP-2 or rendered neutrophil deficient before bile duct ligation.

4 mice compared with wild-type mice following bile duct ligation.

5 y reduces the extent of acute fibrosis after bile duct ligation.

6 growth and mucosal injury in ileum caused by bile duct ligation.

7 lmonary syndrome developed only after common bile duct ligation.

8 ic acid on cholangiocyte proliferation after bile duct ligation.

9 proliferation and ductal mass in vivo after bile duct ligation.

10 cyte marker DPPIV were seen at 30 days after bile duct ligation.

11 and protein significantly decrease following bile duct ligation.

12 as influenced by other factors present after bile duct ligation.

13 ) controls were subjected to sham surgery or bile duct ligation.

14 production have also been found after common bile duct ligation.

15 ent lymphoproliferation (lpr) mice underwent bile duct ligation.

16 mice in two separate murine models: CCl4 and bile duct ligation.

17 th chronic liver failure secondary to common bile duct ligation.

18 latively maintained 3 and even 14 days after bile duct ligation.

19 of bile salt excretion was determined after bile duct ligation.

20 vels, similar to that observed in rat common bile duct ligation.

21 lveolar vascular staining was enhanced after bile duct ligation.

22 butes to intrapulmonary vasodilatation after bile duct ligation.

23 n pulmonary artery rings were assessed after bile duct ligation.

24 rat model of cholestasis secondary to common bile duct ligation.

25 nd fibrosis compared to wide-type mice after bile duct ligation.

26 liver fibrosis induced by CCl4 treatment or bile duct ligation.

27 duced cholestasis in mouse livers via common bile duct ligation.

28 ntibody or control IgG and subjected them to bile duct ligation.

29 o duct injury induced by virus infection and bile duct ligation.

30 m mice following administration of CCl(4) or bile duct ligation.

31 ceptor I (TNFRI)-deficient mice subjected to bile duct ligation.

32 aneous injections of sivelestat or underwent bile-duct ligation.

33 on of mice increased significantly following bile-duct ligation.

34 d development of sickness behavior following bile-duct ligation.

35 sed mesenteric vascular beds from rats after bile-duct ligation.

36 lated in three mouse models of liver injury (bile duct ligation, 1% cholic acid [CA] fed, and the Mdr

37 ers with biliary damage (Mdr2(-/-) knockout, bile duct ligation, 3,5-diethoxycarbonyl-1,4-dihydrocoll

38 Following bile duct ligation, alphaSMA and collagen alpha1(I) tran

39 ry in mouse models of cholestasis induced by bile duct ligation and 1% cholic acid-feeding, evidenced

40 and liver-specific p38alpha knockout mice by bile duct ligation and animals were sacrificed at 12 and

41 Two mouse models of liver injury (bile duct ligation and carbon tetrachloride) also exhibi

42 s of hepatic and bile duct injury, including bile duct ligation and CCl(4), D-galactosamine, and meth

43 The switch from Mnt to Myc during bile duct ligation and in hepatocytes treated with LCA i

44 dramatically increased in SHP(-/-) mice with bile duct ligation and in human cirrhotic livers, which

45 sis, fibrosis, and portal hypertension after bile duct ligation and is regulated by osmotically sensi

46 either carbon tetrachloride intoxication or bile duct ligation and promote fibrosis regression.

47 s were studied 4-weeks after sham surgery or bile duct ligation and were injected with saline or LPS

48 ormed with mice before and 2 weeks following bile duct ligation and with Fah-/- and Fah/p21-/- mice b

49 In the bile duct-ligation and alpha-naphthylisothiocyanate mode

50 with INT-747 or vehicle during 10 days after bile-duct ligation and then were assessed for changes in

51 esistant to experimental models of complete (bile duct ligation) and chemical obstructive cholestasis

52 f PDGFRalpha in murine carbon tetrachloride, bile duct ligation, and 0.1% 3,5-diethoxycarbonyl-1,4-di

53 jury through carbon tetrachloride treatment, bile duct ligation, and 0.1% 3,5-diethoxycarbonyl-1,4-di

54 w, increase with bile acid administration or bile duct ligation, and account for only a small fractio

55 centration increased significantly following bile duct ligation, and both of these were prevented by

56 ) expression in this BEC injury model, after bile duct ligation, and in patients with chronic cholang

57 carbon tetrachloride intoxication, following bile duct ligation, and in tissue culture models.

58 ly impedes liver fibrosis induced by CCl(4), bile duct ligation, and more importantly NASH.

59 ary biliary cirrhosis was induced in rats by bile duct ligation, and portal hypertension was induced

60 ation; and 1-, 2-, 3-, 4-, and 5-week common bile duct ligation animals by Northern, Western and immu

61 ibition with tin protoporphyrin IX in common bile duct ligation animals was used to define effects on

62 cular monocytes/macrophages in 3-week common bile duct ligation animals, whereas pulmonary microvascu

63 ulation of hepatic endothelin 1 after common bile duct ligation are not fully characterized.

64 Using mouse bile duct ligation as an acute EHBD injury model, we use

65 l lamina propria of wild-type mice following bile duct ligation; bacterial translocation was facilita

66 eration and secretion in rats that underwent bile duct ligation (BDL rats).

67 osis in Alfp-Cre x Rosa26-YFP mice using the bile duct ligation (BDL) (2, 4, and 8 weeks), carbon tet

68 Bile duct ligation (BDL) and 1-naphthyl isothiocyanate (

69 o murine models of cholestatic liver injury, bile duct ligation (BDL) and alpha-naphthyl-isothiocyana

70 e found FOXM1/MAT2A/2B are upregulated after bile duct ligation (BDL) and carbon tetrachloride (CCl(4

71 The rat treated with bile duct ligation (BDL) and furan is a unique animal mo

72 In livers of mice subjected to bile duct ligation (BDL) and in cultured activated hepat

73 th factor (HGF) on liver fibrosis induced by bile duct ligation (BDL) and investigated potential mech

74 e 1 (ICAM-1) is induced in mouse liver after bile duct ligation (BDL) and plays a key role in neutrop

75 kout) mice (SIRT(hep-/-) ) were subjected to bile duct ligation (BDL) and were fed with a 0.1% DDC (3

76 study, we aimed to first validate rats with bile duct ligation (BDL) as a model for hepatic pruritus

77 unctions) and (2) proliferate in response to bile duct ligation (BDL) by activation of cyclic adenosi

78 Vdr(-/-) mice subjected to bile duct ligation (BDL) displayed increased liver damag

79 Our results show that the bile duct ligation (BDL) experimental model of cholestas

80 e control (IL-6(+/+)) mice were subjected to bile duct ligation (BDL) for 12 weeks.

81 s, male Sprague-Dawley rats underwent common bile duct ligation (BDL) for 14 days and were treated wi

82 Hepatic fibrosis was induced by bile duct ligation (BDL) for 21 days or by methionine-ch

83 before sham operation or induction of AC by bile duct ligation (BDL) for 3 days.

84 with secondary biliary cirrhosis induced by bile duct ligation (BDL) for 4 weeks (n = 5) and in pair

85 Cholestasis was induced by bile duct ligation (BDL) for 5 days or 3 weeks.

86 Bile duct ligation (BDL) impairs basolateral-to-apical t

87 changes in the GSH synthetic enzymes during bile duct ligation (BDL) in mice and how treatment with

88 We found that bile duct ligation (BDL) in mice expanded the myeloid su

89 Here we show that bile duct ligation (BDL) in mice leads to severe anemia

90 ic enzymes and GSH levels fell 2 weeks after bile duct ligation (BDL) in mice.

91 Mrp3(Abcc3) is markedly induced following bile duct ligation (BDL) in the rat and in some human ch

92 Cholestatic injury was induced by bile duct ligation (BDL) in wild-type and Sort1(-/-) mic

93 Bile duct ligation (BDL) induced liver injury characteri

94 Bile duct ligation (BDL) is a frequently used model of c

95 Common bile duct ligation (BDL) is a well-established murine mo

96 Bile duct ligation (BDL) is an established rodent model

97 Bile duct ligation (BDL) is an experimental procedure th

98 the cholestatic phenotype induced by common bile duct ligation (BDL) is reduced in mice genetically

99 We employed a bile duct ligation (BDL) model of cholestatic liver inju

100 Next, we used the murine bile duct ligation (BDL) model to induce cholestatic liv

101 Here, using the murine bile duct ligation (BDL) model, we showed that the abund

102 ol (AA) (periportal injury), as well as in a bile duct ligation (BDL) model.

103 isposition toward infections, the effects of bile duct ligation (BDL) on bulk intrahepatic T cells ha

104 estasis and the PiZZ phenotype, we performed bile duct ligation (BDL) on C57BL/6 mice possessing a tr

105 The effects of bile duct ligation (BDL) on Oct1 protein, messenger RNA

106 icroscopy in fibrotic livers from mice after bile duct ligation (BDL) or CCl(4) administration and in

107 high-fat diet (HFD) were subjected to either bile duct ligation (BDL) or CCl4 treatment.

108 Common bile duct ligation (BDL) or feeding of a novel bile acid

109 late cells from rat livers injured by either bile duct ligation (BDL) or repeated carbon tetrachlorid

110 rague-Dawley rats were studied 4 weeks after bile duct ligation (BDL) or sham operation.

111 s studied in rats at 1, 2, and 4 weeks after bile duct ligation (BDL) or sham operation.

112 sis factor-receptor-deficient mice underwent bile duct ligation (BDL) or sham operations.

113 e obtained from serum and bile of rats after bile duct ligation (BDL) or sham surgery and applied to

114 Male Sprague-Dawley rats were subjected to bile duct ligation (BDL) or sham surgery, and liver and

115 was performed on liver tissue 24 hours after bile duct ligation (BDL) or sham surgery.

116 HSC isolated from rats after bile duct ligation (BDL) showed prominent increases in I

117 Bile duct ligation (BDL) surgery in rodents is often stu

118 Biliary hyperplasia was induced in rats via bile duct ligation (BDL) surgery, and galanin was increa

119 s study, Spraque-Dawley rats received common bile duct ligation (BDL) to induce cirrhosis.

120 te cotransporting polypeptide (Ntcp), common bile duct ligation (BDL) was performed in pregnant rats

121 e mapped in vivo during the first week after bile duct ligation (BDL) when peak BEC DNA synthesis is

122 egulated in mice with cholestasis induced by bile duct ligation (BDL), 5-diethoxycarbonyl-1,4-dihydro

123 Finally, cholestasis induced by bile duct ligation (BDL), a manipulation known to slow t

124 ocytes isolated from rats that had undergone bile duct ligation (BDL), an experimental model of bilia

125 ely functional hepatectomy (HepX), and 2-day bile duct ligation (BDL), as well as cultured human fibr

126 s were performed in wild-type (WT) mice with bile duct ligation (BDL), BDL SR(-/-) mice, or Mdr2(-/-)

127 Experimental fibrosis was induced by bile duct ligation (BDL), CCl4 intoxication, thioacetami

128 (HA) and MCs infiltrate the liver following bile duct ligation (BDL), increasing intrahepatic bile d

129 During bile duct ligation (BDL), the growth of large cholangioc

130 After bile duct ligation (BDL), the hepatic expression of Th17

131 After bile duct ligation (BDL), the vagus nerve was resected;

132 massive hepatic necrosis and mortality after bile duct ligation (BDL), whereas treatment of these mic

133 estasis, hepatocytes cultured from livers of bile duct ligation (BDL)- or ethinyl estradiol (EE)-inje

134 cholic acid (LCA)-induced hepatotoxicity and bile duct ligation (BDL)-induced cholestasis.

135 nduced liver injury and fibrosis, a model of bile duct ligation (BDL)-induced hepatic fibrosis in viv

136 erize the detailed hemodynamics of mice with bile duct ligation (BDL)-induced liver fibrosis, by moni

137 e (TAA)-, carbon tetrachloride (CCl(4))-, or bile duct ligation (BDL)-induced liver fibrosis.

138 HNF-6 messenger RNA (mRNA) and protein after bile duct ligation (BDL)-mediated liver injury.

139 and SOD1mu mice were treated with CCl(4) or bile duct ligation (BDL).

140 carbon tetrachloride (CCl(4) ) injection or bile duct ligation (BDL).

141 ockout (NGB KO) mice after sham operation or bile duct ligation (BDL).

142 messenger RNA expression was increased after bile duct ligation (BDL).

143 e by either carbon tetrachloride (CCl(4)) or bile duct ligation (BDL).

144 ole of SHP in liver damage induced by common bile duct ligation (BDL).

145 blocking tPA exacerbates liver injury after bile duct ligation (BDL).

146 CCl(4)-treated mice, and mice that underwent bile duct ligation (BDL).

147 and their lean littermates were subjected to bile duct ligation (BDL).

148 -operated mice and chronic injured liver via bile duct ligation (BDL).

149 cretion in a model of cholestasis induced by bile duct ligation (BDL).

150 ils aggravate cholestatic liver injury after bile duct ligation (BDL).

151 injury, inflammation, and fibrogenesis after bile duct ligation (BDL).

152 C from cholestatic liver fibrosis induced by bile duct ligation (BDL).

153 ating cholangiocyte proliferation induced by bile duct ligation (BDL).

154 he pathogenesis of liver fibrosis induced by bile duct ligation (BDL).

155 Cs activated in rats in vivo after 1 week of bile duct ligation (BDL).

156 injected with 600 mg/kg of APAP or underwent bile duct ligation (BDL).

157 eding (a model of sclerosing cholangitis) or bile duct ligation (BDL).

158 chloride (CCl4 ), and a rat model induced by bile duct ligation (BDL).

159 ioration of cholestasis in a murine model of bile duct ligation (BDL).

160 hosis due to carbon tetrachloride (CCl4 ) or bile duct ligation (BDL).

161 cholestatic liver injury and fibrosis after bile duct ligation (BDL).

162 loride (CCl(4) ) administration and surgical bile duct ligation (BDL).

163 Adult Sprague-Dawley rats 4 weeks after bile duct ligation (BDL)/Sham-operation, or naive rats f

164 1/MT2 double KO (DKO) mice underwent sham or bile duct ligation (BDL); these mice were also treated w

165 onyl-1, 4-dihydrocollidine (DDC) feeding and bile-duct ligation (BDL) in mice.

166 the cerebral cortex using rat models of HE (bile duct ligation [BDL] and induced hyperammonemia) and

167 s, rats and mice with liver fibrosis (due to bile duct ligation [BDL] or administration of carbon tet

168 Cirrhotic (bile duct ligation/BDL; CCl4 intoxication) and non-cirrh

169 ld-type controls to compensate for long-term bile duct ligation because of significantly greater hepa

170 Because inducible NOS is induced after bile duct ligation but not after CCl4-induced cirrhosis,

171 ein levels increased severalfold with common bile duct ligation but were unchanged with either endoto

172 ent of hepatopulmonary syndrome after common bile duct ligation, but not in thioacetamide-induced cir

173 nd S-adenosylmethionine are anti-fibrotic in bile duct ligation, but this effect was nearly lost if G

174 n response to secretin and proliferate after bile duct ligation by activation of cyclic adenosine 3',

175 rvival of immunodeficient rats who underwent bile duct ligation by ameliorating the hyperammonaemia a

176 mental hepatopulmonary syndrome after common bile duct ligation by stimulating pulmonary endothelial

177 Bile duct ligation caused liver fibrosis in wild-type bu

178 Bile duct ligation caused neutrophilic infiltration of t

179 ion were assessed in rat livers after common bile duct ligation (CBDL) from 1-7 days, and taurocholat

180 Three-day common bile duct ligation (CBDL) induced renal tubular epitheli

181 In the common bile duct ligation (CBDL) model, endothelin-1 (ET-1) rel

182 s of endotoxin, ethinylestradiol, and common bile duct ligation (CBDL) on Mrp2 protein, messenger RNA

183 To address this issue, common bile duct ligation (CBDL) was performed in wild-type and

184 Cirrhosis was induced in rats by common bile duct ligation (CBDL), and they were compared with s

185 In a rat model of HPS induced by common bile duct ligation (CBDL), but not thioacetamide (TAA)-i

186 A (miRNA) screen of mouse liver after common bile duct ligation (CBDL), we found that miR-199a-5p was

187 hepatopulmonary syndrome (HPS) after common bile duct ligation (CBDL).

188 from rats with cirrhosis secondary to common bile duct ligation (CBDL).

189 hepatopulmonary syndrome (HPS) after common bile duct ligation (CBDL).

190 s study examined rats 1 to 3 wk after common bile-duct ligation (CBDL), at which time they had hyperb

191 Bile duct ligation, CCl(4), and thioacetamide each incre

192 Following bile duct ligation, cholangiocyte proliferation, peribil

193 d mitochondrial glutathione levels following bile duct ligation compared to Stard1f/f mice.

194 totoxin (carbon tetrachloride) injection and bile duct ligation, constitutive FGFR1 signalling in liv

195 Concentrations increased 7-8-fold with bile duct ligation; deoxycholate and hyodeoxycholate dis

196 t mice fed bile acids or subjected to common bile duct ligation develop hypercortisolemia.

197 O mice treated with carbon tetrachloride and bile duct ligation developed reduced fibrosis versus wil

198 In the rat model, 5 days after bile duct ligation during increased TGF-beta expression,

199 The effects of common bile duct ligation, endotoxin, and ethinylestradiol on b

200 ce that were injected with iNKT cells before bile duct ligation exhibited significant decreases in ne

201 Following bile duct ligation, FAAH(-/-) mice displayed increased h

202 +/+) and IL-6(-/-) mice subjected to chronic bile duct ligation for 12 weeks.

203 ce showed increased liver fibrosis following bile duct ligation for 21 days or chronic carbon tetrach

204 Rats underwent bile duct ligation for 3 hours to 8 days.

205 After bile duct ligation for 3 weeks, FoxO1(+/-) mice are more

206 asis-induced liver injury and fibrosis using bile duct ligation for 3 wk.

207 Bile duct ligation for 5 days of Fl/Fl and LKO mice was

208 d hyperplastic cholangiocytes isolated after bile duct ligation from either syngeneic Wistar or allog

209 -alpha (TGF-alpha) was observed 7 days after bile duct ligation in adult rats, the expression of all

210 e established by thioacetamide injection and bile duct ligation in Balb/C mice and treated with soraf

211 h SCF and c-kit were clearly increased after bile duct ligation in both control and mutant mice.

212 procedure to reconstruct biliary flow after bile duct ligation in C57BL/6 mice to generate a model o

213 n-transposase complex was coupled with lobar bile duct ligation in C57BL/6 mice, followed by administ

214 ion of fibrosis with either thioacetamide or bile duct ligation in EIIIA(-/-) mice.

215 y expressed in small bile ducts 7 days after bile duct ligation in immature rats up to 5 weeks of age

216 Cholestasis was obtained by common bile duct ligation in mice.

217 d from liver and kidney 14 days after common bile duct ligation in rats and assessed by RNA protectio

218 ic acid on cholangiocyte proliferation after bile duct ligation in rats.

219 th portal hypertension was established using bile duct ligation in rats.

220 hepatic endothelin 1 production after common bile duct ligation in relation to thioacetamide cirrhosi

221 Common bile duct ligation in the rat is a model of the hepatopu

222 vo by carbon tetrachloride i.p. injection or bile duct ligation in wild-type and SEMA7A knockout (KO)

223 from the TGFbeta receptor is increased after bile duct ligation in wild-type mice but not in beta6(-/

224 Cholestatic liver injury was induced by bile duct ligation in Wistar rats.

225 opolysaccharide-resistant C3H/HeJ mice after bile duct ligation, indicating that Toll-like receptor 4

226 nse to both chronic carbon tetrachloride and bile duct ligation induced injury was also impaired and

227 Here we show that bile duct ligation induced profound resistance against F

228 Spraque-Dawley rats with common bile duct ligation-induced cirrhosis or sham operation r

229 ic ornithine transcarbamylase deficiency and bile duct ligation-induced cirrhosis), TLR4 inhibition r

230 ncreases ceramide(d18:1/18:1) and attenuates bile duct ligation-induced CLI in female mice with reduc

231 ocyte-selective knockout of EZH2 exacerbates bile duct ligation-induced fibrosis whereas MDR2(-/-) mi

232 motile hepatic stellate cells, but not from bile duct ligation-induced fibrosis, in which portal fib

233 alizing PDGF-C antibodies are protected from bile duct ligation-induced liver fibrosis, and we compar

234 tive regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.

235 In vivo, knockdown of GCLC exacerbated bile duct ligation-induced liver injury and fibrosis.

236 cular compartments that occur in response to bile duct ligation-induced liver injury in rats.

237 creased serum levels of Ang II and augmented bile duct ligation-induced liver injury, as assessed by

238 In conclusion, our results support that bile duct ligation induces changes in the microbiome tha

239 in livers of wild-type and Fmod(-/-) mice by bile duct ligation, injection of CCl(4), or administrati

240 In beta-Arr2-deficient mice, bile duct ligation injury (BDL) led to significantly red

241 Chronic bile duct ligation is associated with the development of

242 ing the profile seen in Stard1f/f mice after bile duct ligation leading to increased inflammatory res

243 ter, some mice also received left and median bile duct ligation (LMBDL) and, then 1 week later, were

244 expression increased in activated HSCs from bile duct ligation mice and during HSC activation in vit

245 spite the same insult of long-term (12-week) bile duct ligation, mice prone to decompensation showed

246 In the bile duct ligation model of obstructive cholestasis in m

247 A 4-week bile duct ligation model was used to develop cirrhosis w

248 However, in the bile duct ligation model, there was no effect of tpl2 de

249 Three and 7 days after bile duct ligation Mrp3 expression was significantly inc

250 Different animal models (bile duct ligation: n = 31, carbon tetrachloride: n = 12

251 n compared with control mice after pIVCL and bile-duct ligation; neutrophil recruitment into sinusoid

252 er models of chronic liver injury, including bile duct ligation, nonalcoholic steatohepatitis, and ob

253 Bile duct ligation of the Pkd1l1 -deficient mouse model

254 m obstructive extrahepatic cholestasis after bile duct ligation or administration of alpha-naphthylis

255 Liver injury and/or cirrhosis was induced by bile duct ligation or administration of CCl4.

256 Liver fibrosis was induced in mice by bile duct ligation or administration of thioacetamide.

257 Cholestasis was induced by bile duct ligation or by a 3,5-diethoxycarbonyl-1,4-dihy

258 as well as against liver fibrosis induced by bile duct ligation or carbon tetrachloride.

259 sis and fibrosis or were subjected to either bile duct ligation or CCl(4) injury.

260 Mice were subjected to bile duct ligation or CCl(4)-liver injury, and livers we

261 electively lost from biliary epithelia after bile duct ligation or endotoxin treatment.

262 Following common bile duct ligation or left hepatic bile duct ligation, t

263 levels varied after liver injury induced by bile duct ligation or repeated CCl4 administration, incl

264 othelin 1 levels were evaluated after common bile duct ligation or thioacetamide administration.

265 mined in rat cholangiocytes before and after bile duct ligation or treatment with endotoxin.

266 After bile duct ligation or upon a cholic acid-enriched diet,

267 Mice underwent bile duct ligation or were fed 3,5-diethoxycarbonyl-1,4-

268 ed in the livers of mice that have undergone bile duct ligation or were fed a 3,5-diethoxycarbonyl-1,

269 We performed bile-duct ligations or sham surgeries on C57BL/6 or toll

270 rkedly inhibited the fibrogenic phenotype in bile duct ligation- or thioacetamide-treated mice.

271 After bile duct ligation, p47phox-/- mice showed attenuated li

272 l of acute cholestatic liver injury, partial bile duct ligation (pBDL), with a novel longitudinal bio

273 iary fibrosis and early cirrhosis induced by bile duct ligation, preproET-1 mRNA and immunoreactive E

274 Bile duct ligation rats were treated with GABA for one w

275 progressively from 3 to 5 weeks after common bile duct ligation relative to controls (5-week protein

276 nd portal hypertension due to chronic common bile duct ligation reproduce the features of human hepat

277 genes in hepatocytes and in the liver after bile duct ligation required early growth response factor

278 Administering Ad-SMAdnPI3K to mice following bile duct ligation resulted in reduced HSC activation an

279 In rats with selective bile duct ligation (SBDL), ntcp mRNA levels were down-re

280 After common bile duct ligation, serum bile salts initially rose and

281 In the experimental model of bile duct ligation, silencing of PHB1 induced liver fibr

282 oreover, both Sl and W mice responded to the bile duct ligation, similar to the control mice, by deve

283 Upon carbon tetrachloride injection or bile duct ligation surgery-mediated liver injury, mesode

284 ng common bile duct ligation or left hepatic bile duct ligation, the expression of p53, c-Myc, and cy

285 Eight days after bile duct ligation, the relative increase in preproET-1

286 Following bile duct ligation, TLR2-deficient mice had less liver f

287 Sprague-Dawley rats underwent common bile duct ligation to establish an OJ model. Organ damag

288 Bile duct ligation was performed to induce the prolifera

289 Bile duct ligation was used to induce the proliferation

290 due to either carbon tetrachloride injury or bile duct ligation, we demonstrate de novo expression of

291 Following bile duct ligation, we demonstrated that diminished HNF-

292 ls isolated from adult rats with and without bile duct ligation were incubated with Hh ligand-enriche

293 Male Sprague-dawley rats with common bile duct ligation were killed after 48 and 72 hours.

294 Lastly, HSC isolated from rats after bile duct ligation were more susceptible to NO-induced a

295 After bile duct ligation, wild-type mice overexpress AQP1 that

296 of portal hypertension were employed: common bile duct ligation with cirrhosis and long-term partial

297 stablished chimeric livers were subjected to bile duct ligation, with or without pretreatment with th