Hepatoprotective and anti-hyperglycemic effects of ferulic acid in arsenic-exposed mice

被引:7
|
作者
Daryagasht, Mahdi [1 ,2 ]
Moosavi, Mehrnoosh [1 ,2 ]
Khorsandi, Layasadat [3 ]
Azadnasab, Reza [1 ]
Khodayar, Mohammad Javad [1 ,2 ]
机构
[1] Ahvaz Jundishapur Univ Med Sci, Med Basic Sci Res Inst, Toxicol Res Ctr, Ahvaz, Iran
[2] Ahvaz Jundishapur Univ Med Sci, Fac Pharm, Dept Toxicol, Ahvaz, Iran
[3] Ahvaz Jundishapur Univ Med Sci, Med Basic Sci Res Inst, Cellular & Mol Res Ctr, Ahvaz, Iran
关键词
ACTIVATED RECEPTOR-GAMMA; NF-KAPPA-B; OXIDATIVE STRESS; PEROXISOME PROLIFERATOR; PPAR-GAMMA; LIVER; BETA; PATHWAYS; WATER;
D O I
10.1016/j.fct.2023.113924
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Arsenic is a toxic metalloid that increases the risk of hepatotoxicity and hyperglycemia. The objective of the present study was to assess the effect of ferulic acid (FA) in mitigating glucose intolerance and hepatotoxicity caused by sodium arsenite (SA). A total of six groups including control, FA 100 mg/kg, SA 10 mg/kg, and groups that received different doses of FA (10, 30, and 100 mg/kg), respectively just before SA (10 mg/kg) for 28 days were examined. Fasting blood sugar (FBS) and glucose tolerance tests were conducted on the 29th day. On day 30, mice were sacrificed and blood and tissues (liver and pancreas) were collected for further investigations. FA reduced FBS and improved glucose intolerance. Liver function and histopathological studies confirmed that FA preserved the structure of the liver in groups received SA. Furthermore, FA increased antioxidant defense and decreased lipid peroxidation and tumor necrosis factor-alpha level in SA-treated mice. FA, at the doses of 30 and 100 mg/kg, prevented the decrease in the expression of PPAR-& gamma; and GLUT2 proteins in the liver of mice exposed to SA. In conclusion, FA prevented SA-induced glucose intolerance and hepatotoxicity by reducing oxidative stress, inflammation, and hepatic overexpression of PPAR-& gamma; and GLUT2 proteins.
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页数:9
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