Fluvastatin reduced liver injury in rat model of extrahepatic cholestasis

Aim. To investigate the role of vitamin A in liver damage induced by bile duct ligation (BDL) in rats.Methods. Thirty male Wistar rats were randomly divided into three groups: SHAM group, BDL group, and BDL + VitA group . The concentrations of retinol and retinyl palmitate in the liver were analyzed using HPLC, and liver function was evaluated by the level of TBIL, ALT, AST, and ALP in serum. Hepatic oxidative status was estimated by measuring T-SOD, CAT, GSH, MDA, and AOPP. Nrf2 expression was assessed using immunohistochemistry and western blotting, and EMSA was performed to determine Nrf2 DNA-binding activity. The expression of the downstream factors such as Ho1 and Nqo1 was also examined using immunohistochemistry and western blotting assays.Results. Vitamin A treatment restored levels of retinoids in liver, improved liver function, alleviated oxidative stress, and facilitated the translocation of Nrf2 to the nucleus in the experimental obstructive jaundice. Vitamin A was also found to increase the expression of Nrf2 downstream proteins such as Ho1 and Nqo1.Conclusion. Vitamin A was here found to ameliorate cholestatic liver injury. This effect may be related to the activation of Nrf2/ARE pathway in bile duct ligation rats.

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Targeting HMGB1/TLR4 axis and miR-21 by rosuvastatin: role in alleviating cholestatic liver injury in a rat model of bile duct ligation

Naunyn-Schmiedeberg s Archives of Pharmacology ◽

10.1007/s00210-018-1560-y ◽

2018 ◽

Vol 392 (1) ◽

pp. 37-43 ◽

Cited By ~ 5

Author(s):

Enas S. Nabih ◽

Omnyah A. El-kharashi

Keyword(s):

Bile Duct ◽

Liver Injury ◽

Rat Model ◽

Bile Duct Ligation ◽

Duct Ligation ◽

Cholestatic Liver Injury

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Evaluation of antioxidant and antiapoptogenic effects of Sumach seed extract on liver injury induced by amethopterin in male rat model

Egyptian Pharmaceutical Journal ◽

10.4103/epj.epj_43_20 ◽

2020 ◽

Vol 19 (4) ◽

pp. 391

Keyword(s):

Liver Injury ◽

Rat Model ◽

Seed Extract ◽

Male Rat

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Bone marrow-derived mesenchymal stem cells ameliorate liver injury in a rat model of sepsis by activating Nrf2 signaling

Histochemistry and Cell Biology ◽

10.1007/s00418-018-1731-4 ◽

2018 ◽

Vol 151 (3) ◽

pp. 249-262 ◽

Cited By ~ 1

Author(s):

Sally A. Selim ◽

Samia A. Abd El-Baset ◽

Asmaa A. A. Kattaia ◽

Eman M. Askar ◽

Eman Abd Elkader

Keyword(s):

Stem Cells ◽

Bone Marrow ◽

Mesenchymal Stem Cells ◽

Liver Injury ◽

Rat Model

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Hepatoprotective effect ofAmomum xanthoidesagainst dimethylnitrosamine-induced sub-chronic liver injury in a rat model

Pharmaceutical Biology ◽

10.3109/13880209.2013.770040 ◽

2013 ◽

Vol 51 (7) ◽

pp. 930-935 ◽

Cited By ~ 14

Author(s):

Jing-Hua Wang ◽

Jian Wang ◽

Min-Kyung Choi ◽

Fang Gao ◽

Dong-Soo Lee ◽

...

Keyword(s):

Liver Injury ◽

Rat Model ◽

Chronic Liver ◽

Hepatoprotective Effect ◽

Chronic Liver Injury

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Danaparoid sodium reduces ischemia/reperfusion-induced liver injury in rats by attenuating inflammatory responses

Thrombosis and Haemostasis ◽

10.1160/th06-04-0226 ◽

2007 ◽

Vol 97 (01) ◽

pp. 81-87 ◽

Cited By ~ 11

Author(s):

Naoaki Harada ◽

Hidefumi Kohmura ◽

Mitsuhiro Uchiba ◽

Tsutomu Tomita ◽

Kenji Okajima

Keyword(s):

Liver Injury ◽

Rat Model ◽

Inflammatory Responses ◽

Ischemia Reperfusion ◽

Hepatic Tissue ◽

Therapeutic Effects ◽

Danaparoid Sodium ◽

Cgrp Release ◽

Neuron Activation

SummaryThis study was undertaken to examine the mechanism by which danaparoid sodium (DS), a heparinoid that contains mainly heparan sulfate, prevents reperfusion-induced hepatic damage in a rat model of ischemia/reperfusion (I/R)-induced liver injury. Administration of DS significantly reduced liver injury and inhibited the decrease in hepatic tissue blood flow in rats. DS attenuated hepatic I/R-induced increases in hepatic tissue levels of tumor necrosis factor (TNF) and myeloperoxidase (MPO) in vivo. In contrast, neither monocytic TNF production nor neutrophil activation was inhibited by DS in vitro. DS enhanced I/R-induced increases in levels of calcitonin-gene related peptide (CGRP), a neuropeptide released from sensory neurons, and of 6-ketoprostaglandin (PG) F1α, a stable metabolite of PGI2, in liver tissues. The therapeutic effects of DS were not seen in animals pretreated with capsazepine, an inhibitor of sensory neuron activation. The distribution of heparan sulfate in the perivascular area was significantly increased by DS administration in this rat model. DS significantly increased CGRP release from isolated rat dorsal root ganglion neurons (DRG) in vitro, while DX-9065a, a selective inhibitor of activated factor X, did not. DS enhanced anandamide-induced CGRP release from DRG in vitro. These observations strongly suggested that DS might reduce I/R-induced liver injury in rats by attenuating inflammatory responses. These therapeutic effects of DS might be at least partly explained by its enhancement of sensory neuron activation, leading to the increase the endothelial production of PGI2.

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