scholarly journals Simvastatin Improves the Jaw Bone Microstructural Defect Induced by High Cholesterol Diet in Rats by Regulating Autophagic Flux

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Jianhua Zhou ◽  
Xiaoli Gao ◽  
Shengyun Huang ◽  
Li Ma ◽  
Yanjun Cui ◽  
...  
Keyword(s):  
High Cholesterol Diet ◽  
Autophagic Flux ◽  
Cholesterol Diet ◽  
Sprague Dawley ◽  
High Cholesterol ◽  
Trabecular Thickness ◽  
Simvastatin Treatment ◽  
Jaw Bone ◽  
Microstructural Defect ◽  
Sprague Dawley Rats

Objective. The objective of this study is to evaluate the effect of simvastatin on the jaw bone microstructural defect and autophagy in rats with high cholesterol diet (HCD). Methods. Male Sprague-Dawley rats were fed a standard rodent chow (NC group) or a high cholesterol diet for 32 weeks and the HCD-fed rats were treated with vehicle (HC group) or simvastatin (5 mg/kg orally daily for 8 weeks, HC + SIM group, and n=10/group). The static histomorphometric changes in the jaw bone tissues in individual rats were evaluated. The relative levels of OPG, RANKL, NF-κB, LC3, and p62 in the jaw bone tissues were determined by quantitative RT-PCR and/or immunohistochemistry. Results. Compared with the NC group, the HC groups had lower trabecular bone volume, trabecular thickness and trabecular number, and increased ratios of RANKL/OPG in the jaw bone, accompanied by enhanced NF-κB activation and autophagy. Simvastatin treatment inhabited these changes, including the decreased levels of serum proinflammatory cytokines and increased autophagy. Conclusion. Simvastatin treatment could inhibit the hyperlipidemia-induced jaw bone microstructural defect in rats by increasing autophagic flux.

High-fat and high-cholesterol diet rapidly induces non-alcoholic steatohepatitis with advanced fibrosis in Sprague-Dawley rats

2014 ◽  
Vol 45 (4) ◽  
pp. 458-469 ◽  
Author(s):  
Mayuko Ichimura ◽  
Miku Kawase ◽  
Miki Masuzumi ◽  
Mika Sakaki ◽  
Yasuo Nagata ◽  
...  
Keyword(s):  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
Advanced Fibrosis ◽  
Sprague Dawley ◽  
High Cholesterol ◽  
High Fat ◽  
Alcoholic Steatohepatitis ◽  
Sprague Dawley Rats

scholarly journals Effect of Introducing the Jordanian Common Rue (Ruta chalepensis L.) on Liver Enzymes and Lipid Peroxidation in Adult Male Sprague Dawley Rats Toxified With Paracetamol

2020 ◽  
Vol 12 (4) ◽  
pp. 298
Author(s):  
Dana N. Abdelrahim ◽  
Hamed R. Takruri ◽  
Khalid M. Al-Ismail
Keyword(s):  
Lipid Peroxidation ◽  
Hepatic Injury ◽  
Liver Enzymes ◽  
Liver Weight ◽  
Normal Diet ◽  
High Cholesterol Diet ◽  
Sprague Dawley ◽  
High Cholesterol ◽  
Ruta Chalepensis ◽  
Sprague Dawley Rats

This study aimed to determine the effect of Ruta chalepensis L. plant on liver enzymes, liver weight and lipid peroxidation using rats toxified with paracetamol. An animal experiment was conducted using five groups of Sprague Dawley rats, 9 rats each. The groups were fed: Normal diet, high cholesterol diet, with or without the plant or the liver toxicant paracetamol (PCM). The experiment lasted six weeks; at the end of the sixth week; a single dose of 3 g paracetamol/kg body weight was given for rats of two groups, then blood and liver samples were collected. The hepatoprotective effect of the plant was evaluated using aspartate aminotransferase (AST), alanine aminotransferase (ALT) and total bilirubin (TBL) levels as indicators. This study finds that the groups to which plant and PCM were given had significantly lower MDA levels in comparison with other groups that didn’t receive plant before PCM toxification. Tested liver enzymes levels were significantly (P < 0.05) lowered by the introduction of plant to the diet. Introducing PCM without ingestion of plant in the diet significantly (P < 0.05) increased the rats absolute liver weight. It is concluded that the use of Ruta chalepensis L. plant significantly lowered hepatic toxicity as indicated by the liver enzymes levels. Also, the plant lowered the MDA level and liver weight. The ingestion of the plant can be significantly protective against hepatic injury.

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