4.5 Article

Effect of maternal curcumin supplementation on intestinal damage and the gut microbiota in male mice offspring with intra-uterine growth retardation

期刊

EUROPEAN JOURNAL OF NUTRITION
卷 61, 期 4, 页码 1875-1892

出版社

SPRINGER HEIDELBERG
DOI: 10.1007/s00394-021-02783-x

关键词

Curcumin; IUGR intestine; Antioxidant; Microbiota

资金

  1. National Natural Science Foundation of China [31772634]

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The study aimed to explore the effects of maternal curcumin supplementation on intestinal damage and gut microbiota in offspring with IUGR. The results showed that maternal curcumin supplementation improved intestinal integrity, oxidative status, and gut microbiota in male offspring.
Purpose The present study investigated whether maternal curcumin supplementation might protect against intra-uterine growth retardation (IUGR) induced intestinal damage and modulate gut microbiota in male mice offspring. Methods In total, 36 C57BL/6 mice (24 females and 12 males, 6-8 weeks old) were randomly divided into three groups based on the diet before and throughout pregnancy and lactation: (1) normal protein (19%), (2) low protein (8%), and (3) low protein (8%) + 600 mg kg(-1) curcumin. Offspring were administered a control diet until postnatal day 35. Results Maternal curcumin supplementation could normalize the maternal protein deficiency-induced decrease in jejunal SOD activity (NP = 200.40 +/- 10.58 U/mg protein; LP = 153.30 +/- 5.51 U/mg protein; LPC = 185.40 +/- 9.52 U/mg protein; P < 0.05) and T-AOC content (NP = 138.90 +/- 17.51 U/mg protein; LP = 84.53 +/- 5.42 U/mg protein; LPC = 99.73 +/- 12.88 U/mg protein; P < 0.05) in the mice offspring. Maternal curcumin supplementation increased the maternal low protein diet-induced decline in the ratio of villus height-to-crypt depth (NP = 2.23 +/- 0.19; LP = 1.90 +/- 0.06; LPC = 2.56 +/- 0.20; P < 0.05), the number of goblet cells (NP = 12.72 +/- 1.16; LP = 7.04 +/- 0.53; LPC = 13.10 +/- 1.17; P < 0.05), and the ratio of PCNA-positive cells (NP = 13.59 +/- 1.13%; LP = 2.42 +/- 0.74%; LPC = 6.90 +/- 0.96%; P < 0.05). It also reversed the maternal protein deficiency-induced increase of the body weight (NP = 13.00 +/- 0.48 g; LP = 16.49 +/- 0.75 g; LPC = 10.65 +/- 1.12 g; P < 0.05), the serum glucose levels (NP = 5.32 +/- 0.28 mmol/L; LP = 6.82 +/- 0.33 mmol/L; LPC = 4.69 +/- 0.35 mmol/L; P < 0.05), and the jejunal apoptotic index (NP = 6.50 +/- 1.58%; LP = 10.65 +/- 0.75%; LPC = 5.24 +/- 0.71%; P < 0.05). Additionally, maternal curcumin supplementation enhanced the gene expression level of Nrf2 (NP = 1.00 +/- 0.12; LP = 0.73 +/- 0.10; LPC = 1.34 +/- 0.12; P < 0.05), Sod2 (NP = 1.00 +/- 0.04; LP = 0.85 +/- 0.04; LPC = 1.04 +/- 0.04; P < 0.05) and Ocln (NP = 1.00 +/- 0.09; LP = 0.94 +/- 0.10; LPC = 1.47 +/- 0.09; P < 0.05) in the jejunum. Furthermore, maternal curcumin supplementation normalized the relative abundance of Lactobacillus (NP = 31.56 +/- 6.19%; LP = 7.60 +/- 2.33%; LPC = 17.79 +/- 2.41%; P < 0.05) and Desulfovibrio (NP = 3.63 +/- 0.93%; LP = 20.73 +/- 3.96%; LPC = 13.96 +/- 4.23%; P < 0.05), and the ratio of Firmicutes/Bacteroidota (NP = 2.84 +/- 0.64; LP = 1.21 +/- 0.30; LPC = 1.79 +/- 0.15; P < 0.05). Moreover, Lactobacillus was positively correlated with the SOD activity, and it was negatively correlated with Il - 1 beta expression (P < 0.05). Desulfovibrio was negatively correlated with the SOD activity and the jejunal expression of Sod1, Bcl - 2, Card11, and Zo - 1 (P < 0.05). Conclusions Maternal curcumin supplementation could improve intestinal integrity, oxidative status, and gut microbiota in male mice offspring with IUGR.

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