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. 2019 Aug 23:63.
doi: 10.29219/fnr.v63.3504. eCollection 2019.

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

Affiliations

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

Zhen Luo et al. Food Nutr Res. .

Abstract

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.

Keywords: NLRP3 inflammasome; high-fat diet; liver; microbe-derived antioxidant; rats.

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Conflict of interest statement

The authors declare that there is no conflict of interest in relation to this work.

Figures

Fig. 1
Fig. 1
Lipid profiles TG (A), FAS (B) in liver of mother rats at L1 and L10. Gene expression of lipid metabolism in the liver of mother rats at L1 (C), L10 (D), and offspring (E). Values with different letters differ significantly (p < 0.05). TG, triglyceride; FAS, fatty acid synthase; ACC, acetyl-CoA carboxylase; PPARα, peroxisome proliferator-activated receptor alpha; PPARγ, peroxisome proliferator-activated receptor gamma; PGC1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; CPT1α, carnitine palmitoyltransferase-1α; MACD, medium-chain acyl-CoA dehydrogenase; CG, control group; HFD, high-fat diet; HFDA, HFD +2% microbe-derived antioxidant (n = 6).
Fig. 2
Fig. 2
The activities of ALT (A), AST (B), and AKP (C) in plasma of mother rats at L1 and L10. The activities of ALT (D), AST (E), and AKP (F) in the liver of mother rats at L1, L10, and offspring. Values with different letters differ significantly (p < 0.05). AST, aspartate aminotransferase; ALT, alanine aminotransferase; AKP, alkaline phosphatase; CG, control group; HFD, high-fat diet; HFDA, HFD +2% microbe-derived antioxidant (n = 6).
Fig. 3
Fig. 3
The activities of caspase-3 (A), caspase-8 (B), and caspase-9 (C) in liver of mother rats at L1 and L10. Gene expression of caspase-3, caspase-8, and caspase-9 in offspring (D). Values with different letters differ significantly (p < 0.05). CG, control group; HFD, high-fat diet; HFDA, HFD +2% microbe-derived antioxidant (n = 6).
Fig. 4
Fig. 4
The activities of IL-1β (A), IL-18 (B), and caspase-1 (C) in plasma of mother rats at L1 and L10. Gene expression of NLRP3 inflammasome pathway in liver of mother rats at L1 (D), L10 (E), and offspring (F). Values with different letters differ significantly (p < 0.05). CG, control group; HFD, high-fat diet; HFDA, HFD +2% microbe-derived antioxidant (n = 6).

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