Assessment of Hepatic Function in Rabbits with Steroid-Induced Cholestatic Liver Injury

1981 ◽  
Vol 1 (4) ◽  
pp. 329-333
Author(s):  
B.C. TENNANT ◽  
T. BALAZS ◽  
B.H. BALDWIN ◽  
W.E. HORNBUCKLE ◽  
W.L. CASTLEMAN ◽  
...  
Keyword(s):  
Liver Injury ◽  
Hepatic Function ◽  
Cholestatic Liver Injury

Abstract #1005: Oral Iodine for Treatment of Decompensated Hyperthyroidism in Methimazole Induced Cholestatic Liver Injury

2017 ◽  
Vol 23 ◽  
pp. 211-212
Author(s):  
Abhijana Karunakaran ◽  
Kristin Criner ◽  
Jonathan Anolik
Keyword(s):  
Liver Injury ◽  
Cholestatic Liver Injury

Bid-mediated apoptosis does not contribute to cholestatic liver injury following bile duct ligation

2009 ◽  
Vol 47 (01) ◽  
Author(s):  
P Nalapareddy ◽  
S Schüngel ◽  
MP Manns ◽  
H Jaeschke ◽  
A Vogel
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Bile Duct Ligation ◽  
Duct Ligation ◽  
Cholestatic Liver Injury

Combined function of c-Jun N-terminal kinases in hepatocytes protects mice from fibrosis development during cholestatic liver injury

2019 ◽  
Author(s):  
MR Mohamed ◽  
FJ Cubero ◽  
G Zhao ◽  
YA Nevzorova ◽  
N Gassler ◽  
...  
Keyword(s):  
Liver Injury ◽  
Cholestatic Liver Injury

scholarly journals Comprehensive Review of Molecular Mechanisms during Cholestatic Liver Injury and Cholangiocarcinoma

2018 ◽  
Vol 07 (03) ◽  
Author(s):  
Shohaib Virani ◽  
Austin Akers ◽  
Kristen Stephenson ◽  
Steven Smith ◽  
Lindsey Kennedy ◽  
...  
Keyword(s):  
Liver Injury ◽  
Molecular Mechanisms ◽  
Comprehensive Review ◽  
Cholestatic Liver Injury

scholarly journals PPARα activation protects against cholestatic liver injury

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Qi Zhao ◽  
Rui Yang ◽  
Jing Wang ◽  
Dan-Dan Hu ◽  
Fei Li
Keyword(s):  
Liver Injury ◽  
Cholestatic Liver Injury

Beneficial effect of docosahexaenoic acid on cholestatic liver injury in rats

2012 ◽  
Vol 23 (3) ◽  
pp. 252-264 ◽  
Author(s):  
Wen-Ying Chen ◽  
Shih-Yi Lin ◽  
Hung-Chuan Pan ◽  
Su-Lan Liao ◽  
Yu-Han Chuang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Docosahexaenoic Acid ◽  
Beneficial Effect ◽  
Cholestatic Liver Injury

scholarly journals Hydroethanolic Extract of Defatted Buchholzia coriacea Seeds Alleviates Tamoxifen-Induced Hepatic Triglyceride Accumulation, Inflammation and Oxidative Distress in Rat

Medicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 1
Author(s):  
Ayokanmi Ore ◽  
Abideen Idowu Adeogun ◽  
Oluseyi Adeboye Akinloye
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Liver Injury ◽  
Hepatic Function ◽  
Protein Carbonyls ◽  
Control Group ◽  
Hepatic Triglyceride ◽  
Triglyceride Accumulation ◽  
Group I ◽  
Hydroethanolic Extract

Background: Tamoxifen (TMX) has proven to be effective in the prevention and treatment of breast cancer. However, long-term use of TMX is associated with hepatic steatosis, oxidative liver injury and hepatocarcinoma. Buchholzia coriacea seeds (BCS) have been widely applied in traditional medicine due to their nutritional and therapeutic potentials. This study investigates the protective effect of hydroethanolic extract of (defatted) B. coriacea seeds (HEBCS) against TMX–induced hepatotoxicity in rats. Methods: Thirty-six (36) male albino rats were divided into six groups (n = 6/group). Group I served as control. Group II received 50 mg/kg/day TMX orally (p.o.) (TMX) for 21 days, group III received TMX plus 125 mg/kg/d HEBCS p.o. (HEBCS 125) for 21 days, group IV received TMX plus 250 mg/kg/d HEBCS p.o. (HEBCS 250) for 21 days and rats in group V and VI received HEBCS 125 and HEBCS 250 respectively for 21 days. Results: Compared with the control, TMX caused a significant increase (p < 0.05) in serum hepatic function biomarkers: alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase by 57%, 60% and 68% respectively. TMX also caused a significant increase in hepatic triglycerides level by 166% when compared with control and a significant decrease in serum HDL-cholesterol level by 37%. Compared with control, hepatic marker of inflammation, tumour necrosis factor alpha (TNF-α) increased significantly by 220%, coupled with significant increase in expression of interleukin 6 and cyclooxygenase 2. There was also significant increase in levels of Biomarkers of oxidative stress, nitric oxide, malondialdehyde and protein carbonyls in the TMX group by 89%, 175% and 114% respectively when compared with the control. Hepatic antioxidants, reduced glutathione (GSH) level and activities of superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) decreased significantly in the TMX group by 35%, 67%, 41%, 59% and 53% respectively when compared with the control. However, HEBCS at 250 mg/kg significantly protected against TMX–induced hepatotoxicity by decreasing hepatic triglyceride content, serum hepatic function biomarkers, hepatic inflammation and oxidative stress with significant improvement in hepatic antioxidant system. Histopathological findings show that HEBCS alleviate TMX–induced hepatocyte ballooning. Conclusions: Current data suggest that HEBCS protected against TMX–induced hepatotoxicity in rats. HEBCS may be useful in managing TMX–induced toxicities in breast cancer patients. It may also be helpful against other forms of liver injury involving steatosis, inflammation, free radicals, and oxidative damage.

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