在怀孕和哺乳期摄入微生物源抗氧化剂可减轻高脂饮食诱导的母鼠及其后代的肝脏氧化应激、脂质紊乱和NLRP3炎性小体。
Inclusion of microbe-derived antioxidant during pregnancy and lactation attenuates high-fat diet-induced hepatic oxidative stress, lipid disorders, and NLRP3 inflammasome in mother rats and offspring.
作者信息
Luo Zhen, Xu Xue, Zhao Sen, Sho Takami, Luo Wenli, Zhang Jing, Xu Weina, Hon Kong, Xu Jianxiong
机构信息
Shanghai Key Laboratory of Veterinary Biotechnology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Vocational College of Agriculture and Forestry, Shanghai, China.
出版信息
Food Nutr Res. 2019 Aug 23;63. doi: 10.29219/fnr.v63.3504. eCollection 2019.
OBJECTIVE
This study aimed to evaluate the effects of microbe-derived antioxidant (MA) on high-fat diet (HFD)-induced hepatic lipid disorders in mother rats and offspring.
METHODS
A total of 36 female rats were randomly divided into three groups at the beginning of pregnancy: the control group (CG), HFD, and HFD with 2% MA. Mother rats were slaughtered at the first and 10th day of lactation (L1 and L10) and offspring were slaughtered at L10. The plasma and liver of mother rats, and liver of offspring were collected.
RESULTS
The results showed that MA reversed HFD-induced activities of inducible nitric oxide synthase (iNOS) and antioxidative enzymes in liver of mother rats and offspring. In addition, MA reduced HFD-induced lipid accumulation through decreasing the low-density lipoprotein cholesterol (LDLC) content in plasma of mother rats and improving hepatic fatty acid synthase (FAS) in mother rats and offspring. MA decreased HFD-induced hepatic alkaline phosphatase (AKP) activity in liver of mother rats and offspring. Furthermore, MA reduced HFD-activated nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome in liver of mother rats and offspring.
CONCLUSIONS
MA supplementation reversed HFD-induced hepatic oxidative stress, lipid accumulation, NLRP3 inflammasome, and function in mother rats and offspring, suggesting MA can be functional ingredients to improve maternal-fetal health.
目的
本研究旨在评估微生物源抗氧化剂（MA）对高脂饮食（HFD）诱导的母鼠及其后代肝脏脂质紊乱的影响。
方法
在妊娠初期，将36只雌性大鼠随机分为三组：对照组（CG）、高脂饮食组和添加2% MA的高脂饮食组。母鼠在哺乳期第1天和第10天（L1和L10）处死，后代在L10处死。收集母鼠的血浆和肝脏以及后代的肝脏。
结果
结果表明，MA可逆转HFD诱导的母鼠及其后代肝脏中诱导型一氧化氮合酶（iNOS）的活性和抗氧化酶的活性。此外，MA通过降低母鼠血浆中低密度脂蛋白胆固醇（LDLC）含量以及改善母鼠及其后代肝脏中的脂肪酸合酶（FAS），减少了HFD诱导的脂质积累。MA降低了HFD诱导的母鼠及其后代肝脏中碱性磷酸酶（AKP）的活性。此外，MA减少了HFD激活的母鼠及其后代肝脏中含吡咯结构域的NOD样受体蛋白3（NLRP3）炎性小体。
结论
补充MA可逆转HFD诱导的母鼠及其后代肝脏氧化应激、脂质积累、NLRP3炎性小体及功能异常，提示MA可作为改善母婴健康的功能性成分。
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