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Effect of caffeic acid derivatives on polychlorinated biphenyls induced hepatotoxicity in male mice

机译:咖啡酸衍生物对多氯联苯诱导的雄性小鼠肝毒性的影响

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摘要

Chronic exposure to coplanar polychlorinated biphenyls (PCBs), a potent inducer of toxic reactive oxygen species (ROS), in the environment and food can cause liver diseases. It remains unknown whether caffeic acid derivatives (CADs) exerted protective effect on PCB-induced hepatotoxicity. We sought to evaluate the activities of 3 CADs on PCB169-induced oxidative stress and DNA damage in the liver. Male ICR mice were administered with 1 μmol/mL PCB169 at 5 mL/kg body weight for 2 weeks. The mice were given CADs by gastric gavage for 3 weeks. We found that PCB169 decreased the growth rate and reduced the levels of superoxide dismutase (SOD), glutathione (GSH) and GSH peroxidase (GPx). It increased the liver weight, malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels and CYP1A1 activity in the liver tissues and plasma of mice (P<0.05). Pretreatment of mice with CADs restored the above parameters to normal levels. There was a synergistic protective effect between CADs in preventing MDA and 8-OHdG formation and inducing CYP1A1 and phase II metabolism enzyme (SOD, GPx) activities (P<0.05). In conclusion, PCB169 induced hepatotoxicity and pretreatment with CADs had synergistic protective effects on liver damage.
机译:长期暴露于环境和食物中的共平面多氯联苯(PCBs)是有毒的活性氧(ROS)的有效诱因,会引起肝脏疾病。咖啡酸衍生物(CAD)是否对PCB诱导的肝毒性发挥保护作用仍是未知的。我们试图评估3种CAD对PCB169诱导的肝脏氧化应激和DNA损伤的活性。雄性ICR小鼠以5μmL/ kg体重的1μμmol/ mL PCB169给药2周。通过胃管灌胃给予小鼠CAD 3周。我们发现PCB169降低了生长速率并降低了超氧化物歧化酶(SOD),谷胱甘肽(GSH)和GSH过氧化物酶(GPx)的水平。它增加了小鼠肝脏和血浆中肝脏的重量,丙二醛(MDA)和8-羟基-2'-脱氧鸟苷(8-OHdG)水平和CYP1A1活性(P <0.05)。用CAD预处理小鼠可将上述参数恢复到正常水平。 CADs在预防MDA和8-OHdG形成以及诱导CYP1A1和II期代谢酶(SOD,GPx)活性方面具有协同保护作用(P <0.05)。总之,PCB169诱导的肝毒性和CAD预处理对肝脏损伤具有协同保护作用。

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