ライフサイエンスコーパス: retrorsine

1 re length of protocol and carcinogenicity of retrorsine.

2 gative (DPPIV-) Fischer host rats exposed to retrorsine.

3 Treatment of rats with retrorsine, a pyrrolizidine alkaloid, blocks endogenous

4 patocyte transplantation in rats primed with retrorsine and partial hepatectomy showed accelerated ki

5 By contrast, in animals preconditioned with retrorsine and partial hepatectomy, cell transplantation

6 ration was analyzed in rats conditioned with retrorsine and partial hepatectomy.

7 ion, recipient animals were conditioned with retrorsine and two-thirds partial hepatectomy (PH), whic

8 treated with 2 doses (30 mg/kg body weight) retrorsine (at 6 and 8 weeks of age) followed by PH 5 we

9 presence of 2-acetylaminofluorene (2AAF) or retrorsine, both of which are injury models that favor s

10 rats treated with the pyrrolizidine alkaloid retrorsine can be accomplished through the activation, e

11 ulation was induced in the host by injecting retrorsine, creating a portacaval shunt, and performing

12 Pretreatment with retrorsine crosslinks host hepatocyte DNA and prevents p

13 To study the mechanism by which retrorsine-damaged hepatocytes are removed after PH, we

14 ls in the organoid cultures, we utilized the retrorsine/DPPIV system of hepatocyte transplantation to

15 tic indices for hepatocytes in the livers of retrorsine-exposed and control rats up to 14 days post-P

16 protein are localized to the mitochondria of retrorsine-exposed rat livers after PH during the same t

17 SHPCs obtained from retrorsine-exposed rats 6-8 days and 13-15 days after PH

18 ation of primary liver cell dispersions from retrorsine-exposed rats 6-8 days and 13-15 days after PH

19 was indistinguishable from that observed in retrorsine-exposed rats after PH.

20 ere never seen in the livers of DAPM-treated retrorsine-exposed rats after PH.

21 riched SHPC populations can be isolated from retrorsine-exposed rats and established in short-term cu

22 nduced blockade of hepatocyte proliferation, retrorsine-exposed rats are able to reconstitute complet

23 ighest (approximately 6.0%) in the livers of retrorsine-exposed rats at 1 day post-PH, gradually decl

24 Nevertheless, retrorsine-exposed rats can replace their entire liver m

25 tration of 4,4'-methylenedianiline (DAPM) to retrorsine-exposed rats impaired the emergence of SHPC c

26 n after surgical partial hepatectomy (PH) in retrorsine-exposed rats is accomplished through the outg

27 tic protein Bax are increased in livers from retrorsine-exposed rats relative to the levels observed

28 ration secondary to bile duct destruction in retrorsine-exposed rats treated with 4,4'-diaminodipheny

29 ted period of liver regeneration after PH in retrorsine-exposed rats.

30 epatocytes as the origin of SHPC clusters in retrorsine-exposed rats.

31 eins known to be induced in rat livers after retrorsine exposure.

32 Despite the retrorsine-induced blockade of hepatocyte proliferation,

33 In retrorsine-induced hepatocellular injury the capacity of

34 These observations combine to suggest that retrorsine-injured hepatocytes are removed after PH via

35 The extensive proliferation of SHPCs in retrorsine-injured livers is accompanied by the progress

36 Retrorsine is a member of the pyrrolizidine alkaloid fam

37 rats treated with the pyrrolizidine alkaloid retrorsine is accomplished through the activation, expan

38 ce of SHPCs to the mitoinhibitory effects of retrorsine may be directly related to a lack of CYP enzy

39 tocyte-like progenitor cells observed in the retrorsine model reflect a novel mechanism of complete l

40 ogen, to stimulate liver repopulation in the retrorsine model.

41 ibitory effect of the pyrrolizidine alkaloid retrorsine on hepatocytes in the resident liver while tr

42 The retrorsine-partial hepatectomy model was used for liver

43 Moreover, studies in the retrorsine-partial hepatectomy rat model showed that int

44 rategy for hepatocyte transplantation, using retrorsine/partial hepatectomy (PH) in a DPPIV- mutant F

45 ly 10 cell doublings) under the influence of retrorsine/partial hepatectomy, and both repopulation an

46 as augmented in bile ducts and oval cells in retrorsine/partial hepatectomy-treated liver, and this c

47 Tissues from DPPIV chimeric livers after retrorsine/PH treatment showed large numbers of SHPC clu

48 en transplanted into rats that had undergone retrorsine pretreatment and partial hepatectomy.

49 ial hepatectomy into the liver of normal and retrorsine (Rs) treated syngeneic dipeptidyl peptidase I

50 rat liver by transplanted hepatocytes using retrorsine (RS), a pyrrolizidine alkaloid that alkylates

51 In the retrorsine (RS)-based model of massive liver repopulatio

52 After transplantation into the liver of retrorsine (RS)-treated SCID/beige mice, naive hAECs dif

53 a lack of CYP enzymes required to metabolize retrorsine to its toxic derivatives.

54 portally (2 x 10(6) cells) into the liver of retrorsine-treated Dipeptidyl peptidase IV- mutant Fisch

55 yl peptidase IV (DPPIV)-positive donors into retrorsine-treated DPPIV-negative recipients subjected t

56 her (F)344 rats to repopulate the normal and retrorsine-treated liver was studied throughout a 6-mont

57 In retrorsine-treated liver, transplanted cells formed larg

58 In retrorsine-treated liver, transplanted Thy-1(+) fetal li

59 d normal adult liver and totally repopulated retrorsine-treated liver.

60 h severe-combined immunodeficiency underwent retrorsine treatment and either partial hepatectomy befo

61 PPIV-positive hepatocytes, were subjected to retrorsine treatment followed by partial hepatectomy (PH

62 senkirkine, senecionine, seneciphylline and retrorsine were determined by ultra-performance liquid c