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1- Department of Physiology, Faculty of Basic Medical Sciences, College of Medical Sciences, University of Calabar, Calabar, Nigeria. , odupeterori@unical.edu.ng
2- Department of Physiology, Faculty of Basic Medical Sciences, College of Medical Sciences, University of Calabar, Calabar, Nigeria.
3- Department of Anatomy, Faculty of Basic Medical Sciences, College of Medical Sciences, University of Calabar, Calabar, Nigeria.
2- Department of Physiology, Faculty of Basic Medical Sciences, College of Medical Sciences, University of Calabar, Calabar, Nigeria.
3- Department of Anatomy, Faculty of Basic Medical Sciences, College of Medical Sciences, University of Calabar, Calabar, Nigeria.
Abstract: (16 Views)
Background: Aging is a gradual decline in physiological functions that affect various organs of the body, including the liver. D-galactose is a reducing sugar used to mimic aging in animal models when administered in high doses. The study investigated the ameliorative potential of luteolin against D-galactose-induced hepatotoxicity and metabolic alterations in aging mice.
Materials and Methods: Twenty-five male mice were randomly divided into five groups (n=5). D-galactose (200 mg/kg) was administered subcutaneously for 56 days to induce aging, while luteolin (10 or 20 mg/kg) was administered orally to the intervention groups from day 29 to day 56. After administration, fasting blood glucose was assessed via the tail vein. Blood samples were collected to evaluate serum glycated hemoglobin, lipid profile - total cholesterol (Tcho), low-density lipoprotein (LDL-c), triglyceride (TG) and high-density lipoprotein (HDL-c) levels, and liver enzymes, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). The livers were harvested for histological examination.
Results: D-galactose did not cause significant changes in glycemic indices in the treatment groups when compared to the control. Luteolin significantly (p<0.05) reversed D-galactose-induced lipid alterations with decreases in Tcho, LDL-c and TG levels, and an increase in HDL-c level.
The ALT, AST, and ALP levels significantly decreased (p<0.05) in the luteolin intervention groups compared to the untreated D-galactose group. Liver histology showed that luteolin treatment preserved hepatic architecture and protected the liver against injuries.
Conclusion: These findings suggest that luteolin exhibits natural ameliorative potential capable of reversing dyslipidemia, hepatic dysfunction, and metabolic alterations associated with aging.
Materials and Methods: Twenty-five male mice were randomly divided into five groups (n=5). D-galactose (200 mg/kg) was administered subcutaneously for 56 days to induce aging, while luteolin (10 or 20 mg/kg) was administered orally to the intervention groups from day 29 to day 56. After administration, fasting blood glucose was assessed via the tail vein. Blood samples were collected to evaluate serum glycated hemoglobin, lipid profile - total cholesterol (Tcho), low-density lipoprotein (LDL-c), triglyceride (TG) and high-density lipoprotein (HDL-c) levels, and liver enzymes, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). The livers were harvested for histological examination.
Results: D-galactose did not cause significant changes in glycemic indices in the treatment groups when compared to the control. Luteolin significantly (p<0.05) reversed D-galactose-induced lipid alterations with decreases in Tcho, LDL-c and TG levels, and an increase in HDL-c level.
The ALT, AST, and ALP levels significantly decreased (p<0.05) in the luteolin intervention groups compared to the untreated D-galactose group. Liver histology showed that luteolin treatment preserved hepatic architecture and protected the liver against injuries.
Conclusion: These findings suggest that luteolin exhibits natural ameliorative potential capable of reversing dyslipidemia, hepatic dysfunction, and metabolic alterations associated with aging.
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The Iranian Journal of Toxicology
Arak University of Medical Sciences in collaboration with the Iranian Society of Toxicology
Website: http://ijt.arakmu.ac.ir
Email: tox.journal@gmail.com
