Bule QI1, Dandan Wu1, Xiaoyun Wu1, Naqin1, Shiqi Hao1, Rimutu Ji1,2 and Liang Ming1,2
1Key Laboratory of Dairy Biotechnology and Bioengineering, Ministry of Education, College of Food Science and
Engineering, Inner Mongolia Agricultural University, 010018, Hohhot, China
2Camel Research Institute of Inner Mongolia, 737300, Alashan, China
ABSTRACT
This study aims to explore the protective effect of camel milk (CM) on oxidative stress in mice and analyse its mechanism of action. The experimental animals were randomly divided into four groups: NC (normal diet), ET (normal diet, then ethanol), CM (normal diet and CM ) and ET+CM (normal diet and CM, then ethanol). Then by measuring serum and liver tissue superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activity, glutathione (GSH), malondialdehyde (MDA) and other indicators to explore its antioxidant capacity. The results showed that CM attenuated ethanol-induced hepatotoxicity by reducing elevated liver enzyme, decreasing ethanol-induced reactive oxygen species (ROS) generation, inhibiting malonaldehyde (MDA) levels and reversing depletion of antioxidative defense system in mice liver. Furthermore, CM ameliorated ethanol-induced oxidative stress by down-regulating the expression of cytochrome P4502 E1 (CYP2E1) enzyme. These data suggest that CM, a health-promoting antioxidant food, exhibits hepatoprotective effects. The hepatoprotective mechanisms of CM were associated with alleviation of ethanol-induced oxidative stress through inhibiting CYP2E1 enzyme.
Key words: Alcoholic liver injury, Camel milk, CYP2E1, Oxidative damage
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