Protective effects of 16,16-dimethyl PGE2 on the liver and kidney

Ruwart, Mary J.; Rush, Bob D.; Friedle, N.M.; Piper, R. C.; Kolaja, Gerald J.

doi:10.1016/0090-6980(81)90124-6

Cited by 80 publications

(29 citation statements)

References 4 publications

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“…The results of experiment 1 indicated that the administration of 10 gg enprostil /kg BW decreased hepatic triacylglycerol concentration most effectively and this effect was confirmed in experiment 2. This dose used here was similar to that used in other experiments, in which enprostil or 16, 16-dimethyl prostaglandin E2 protected liver cell necrosis and fatty infiltration by CC14 [10,12,13]. Our findings suggest that enprostil also affects hepatic lipid metabolism in animals under normal condition.…”

Section: Discussionsupporting

confidence: 58%

Prostaglandin E2 derivative, enprostil, reduces hepatic triacylglycerol content in Japanese quail

et al. 1996

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Section: Discussionsupporting

confidence: 58%

Prostaglandin E2 derivative, enprostil, reduces hepatic triacylglycerol content in Japanese quail

et al. 1996

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“…The percentage of PCNA-positive cells tocellular necrosis caused by several hepatotoxins. [13][14][15][16][17][18][19][20][21][22] It has also been reported that HGF stimulated prostaglandin E 2 in WT mice was very low at 0 hours and 24 hours after treatment, but increased at 48 hours. To clarify the mecha-(PGE 2 ) production through increases in both cytosolic phospholipase A 2 and cyclooxyganase activity in human gastric nisms via which HGF acts, we measured hepatic HGF and prostaglandin E 2 (PGE 2 ) contents after D-GalN administration carcinoma TMK-1 cells 23 and primary cultured rat hepatocytes.…”

Section: Hepatocyte Growth Factor (Hgf) Has Been Reported To Bementioning

confidence: 99%

“…Serum levels of The protective effect of PGE 2 and PGE 1 on acute liver injury is well known. [13][14][15][16][17][18][19][20][21][22] Because biological activity of PGE 2 is almost identical to PGE 1 , 41 and PGE 2 is the main prostanoid secreted by cultured Kupffer cells, 42 we examined hepatic PGE 2 content. Cytoprotective action of PGE 2 was exerted in several kinds of liver injuries such as D-GalN, 13,19,22 carbon tetrachloride, 14,16,20 a-naphtylisothiocyanate, 15 lipopolysaccharide, 18 and immune reaction against liver antigen.…”

Section: Effect Of Anti-pge 2 Antibody On D-galn -Induced Livermentioning

confidence: 99%

Protective action of hepatocyte growth factor for acute liver injury caused by D-galactosamine in transgenic mice

1997

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Hepatocyte growth factor (HGF) has been reported to beHepatocyte growth factor (HGF) is a potent mitogen for mature hepatocytes and plays a pivotal role in liver regeneraa potent mitogen for hepatocytes in vivo and in vitro. Recent reports have shown that HGF has cytoprotective actions in tion after liver injury. HGF was identified from the serum of partially hepatectomized rats, 1 rat platelets, 2 rabbit serum, 3 acute liver injury models, but its mechanisms remain to be resolved. In the present study, we investigated whether HGF the human plasma of fulminant hepatic failure, 4 and human lung fibroblasts.5 Numerous investigations of HGF have recould work as an anti-hepatitis agent for acute liver injury caused by D-galactosamine (D-GalN) using transgenic (TG) vealed that HGF has pleiotropic functions such as a mitogen, a morphogen, a motogen, and a tumor suppressor. [6][7][8] Remice expressing HGF in hepatocytes, compared with wildtype (WT) mice of their siblings. After administration of 3 g/ cently, it has been reported that HGF works as an antihepatitis agent against acute liver injuries of in vivo and in kg body weight of D-GalN, elevated serum transaminase levels and severe liver damage that were observed in WT mice were vitro models, 9-12 but its exact mechanisms remain to be clarified. significantly improved in TG mice. In TG mice, the percentage of proliferating cell nuclear antigen (PCNA)-positive hepatoIt has been reported that prostaglandins, which are metabolites of arachidonic acid, act as a cytoprotector against hepacytes was high at 0 hours after D-GalN treatment, and increased at 24 hours. The percentage of PCNA-positive cells tocellular necrosis caused by several hepatotoxins. [13][14][15][16][17][18][19][20][21][22] It has also been reported that HGF stimulated prostaglandin E 2 in WT mice was very low at 0 hours and 24 hours after treatment, but increased at 48 hours. To clarify the mecha-(PGE 2 ) production through increases in both cytosolic phospholipase A 2 and cyclooxyganase activity in human gastric nisms via which HGF acts, we measured hepatic HGF and prostaglandin E 2 (PGE 2 ) contents after D-GalN administration carcinoma TMK-1 cells 23 and primary cultured rat hepatocytes. 24 These data are indicative of a close relationship beby an enzyme immunoassay. Total hepatic HGF contents, which were composed of murine (endogeneous) and human tween HGF and PGE 2 .In our previous reports, we examined the important role (derived from transgene) HGF, in TG mice were higher than those in WT mice at 0, 12, and 24 hours after administration of HGF in liver regeneration by using transgenic mice expressing HGF persistently in hepatocytes under the control of 3 g/kg body weight of D-GalN. Hepatic PGE 2 contents in TG mice were also significantly higher than those in WT of albumin regulatory sequences. 25,26 In those reports, we showed that the livers of HGF transgenic mice recovered mice. Hepatic PGE 2 contents had a positive correlation with total HGF contents at both 12 hours and 24 hours after the ...

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“…[20][21][22][23][24] Preliminary trials in humans also suggest that prostaglandins are useful in the treatment of FHF. [25][26][27] In an open-label pilot study conducted by Sinclair et al, 70% of patients with FHF treated with prostaglandins survived without the need for hepatic transplantation.…”

confidence: 99%

Treatment of fulminant hepatic failure with intravenous prostaglandin E1

et al. 1998

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Fulminant hepatic failure (FHF) is a severe, lifethreatening disorder. Previous studies have suggested that intravenous prostaglandin treatment may improve survival in FHF. The present study was performed to further investigate the possible benefit of intravenous prostaglandin E 1 (PGE 1 ) for patients with FHF. A total of 18 patients, all excluded as candidates for hepatic transplantation, were studied. Thirteen of 18 participated in a randomized, double-blind, placebo-controlled trial. PGE 1 was administered by continuous infusion at a dose of 10 to 40 g/h as tolerated. After 48 hours of blinded treatment, 3 of 7 patients randomized to placebo were converted to open-label PGE 1 for lack of biochemical and/or clinical improvement. Mean values for alanine transaminase, aspartate transaminase, total bilirubin, prothrombin time, factor V percent, factor VII percent, hepatic encephalopathy score, days from onset of symptoms to initiation of treatment, and cause of FHF were similar between treatment groups. Ten of 18 patients (55%) enrolled in this trial survived. However, survival was not different between PGE 1 -(60%) and placebo (50%) treated patients. The greatest predictor of survival was the number of days from onset of symptoms to hospitalization, which was significantly (P ‫؍‬ .002) shorter for survivors (3.3 v 12.4 days), regardless of PGE 1 treatment. Six of 8 patients (75%) who began PGE 1 therapy and 4 of 5 placebo-treated patients (80%) hospitalized within 10 days of onset of symptoms survived. By contrast, all 5 patients who were hospitalized and subsequently began PGE 1 treatment 10 days or longer after the onset of symptoms died. We conclude that early recognition and hospitalization is the most important factor in reduction of mortality from FHF. It is unclear whether PGE 1 treatment is beneficial when administered during this period. However, it is apparent that PGE 1 was not effective for treatment of FHF if treatment started more than 10 days after onset of this clinical syndrome.

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Protective effects of 16,16-dimethyl PGE2 on the liver and kidney

Cited by 80 publications

References 4 publications

Prostaglandin E2 derivative, enprostil, reduces hepatic triacylglycerol content in Japanese quail

Prostaglandin E2 derivative, enprostil, reduces hepatic triacylglycerol content in Japanese quail

Protective action of hepatocyte growth factor for acute liver injury caused by D-galactosamine in transgenic mice

Treatment of fulminant hepatic failure with intravenous prostaglandin E1

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