Title of article :
The Effect of Nerol on Biochemical and Histological Parameters in Nonalcoholic Fatty Liver Disease in NMRI Mice
Author/Authors :
Givian, M. Department of Biology - Science and Research Branch - Islamic Azad University, Tehran, Iran , Ghobeh, M. Department of Biology - Science and Research Branch - Islamic Azad University, Tehran, Iran , Yaghmaei, P. Department of Biology - Science and Research Branch - Islamic Azad University, Tehran, Iran
Pages :
13
From page :
33
To page :
45
Abstract :
Fatty liver contains a range of clinical symptoms, including the accumulation of fat in the liver cells and it varies from a simple steatosis to nonalcoholic steatohepatitis and cirrhosis. Using natural therapies has always been a great concern for such health-related diseases. Herein, nerol, as a natural monoterpene, was applied to treat nonalcoholic fatty liver-induced NMRI (Naval Medical Research Institute) mice. The assessment included histological studies of the liver along with measurement of biochemical parameters, including insulin, glucose, HDL-C (high-density lipoprotein cholesterol), LDL-C (low-density lipoprotein cholesterol), Aspartate transaminase (AST), Alanine aminotransferase (ALT), Alkaline phosphatase (ALP), SOD (superoxide dismutase) and catalase. The results demonstrated that treatment with nerol (90 mg kg-1) modified the fatty liver indices by significantly reducing the levels of triglyceride, cholesterol, LDLC, glucose, and insulin (p < 0.001) whereas this treatment notably increased the levels of liver antioxidant enzymes, and HDL-C (p < 0.001). Nerol administration also improved the status of the liver tissue of the fatty liver condition. Therefore, nerol, in a dosedependent mode, showed capability of improving nonalcoholic fatty liver and could offer a reliable remedy.
Farsi abstract :
فاقد چكيده فارسي
Keywords :
Nerol , Nonalcoholic fatty liver , Lipid profiles , Antioxidant and liver enzymes , Glucose
Journal title :
Biomacromolecular Journal
Serial Year :
2020
Record number :
2629298
Link To Document :
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