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 ompounds, namely cryptospirolepine (505 Da), retrorsine (351 Da), and estrone (270 Da), to demonstrat

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

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

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

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

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

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

10 e, senecionine, echimidine, intermedine, and retrorsine being the most studied.

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

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

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

14 Pretreatment with retrorsine crosslinks host hepatocyte DNA and prevents p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 Despite the retrorsine-induced blockade of hepatocyte proliferation,

35 In retrorsine-induced hepatocellular injury the capacity of

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

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

38 Retrorsine is a member of the pyrrolizidine alkaloid fam

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

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

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

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

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

44 The retrorsine-partial hepatectomy model was used for liver

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

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

47 ubstantially increased liver repopulation in retrorsine/partial hepatectomy model.

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

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

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

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

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

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

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

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

56 Retrorsine (RTS), a retronecine-based PA, is highly toxi

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

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

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

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

61 In retrorsine-treated liver, transplanted cells formed larg

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

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

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

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

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