Curcumin intake during lactation suppresses oxidative stress through upregulation of nuclear factor erythroid 2-related factor 2 in the kidneys of fructose-loaded female rat offspring exposed to maternal protein restriction.

BACKGROUND: A high-fructose diet causes the progression of chronic kidney disease. Maternal malnutrition during pregnancy and lactation increases oxidative stress, leading to chronic renal diseases later in life. We investigated whether curcumin intake during lactation could suppress oxidative stress and regulate NF-E2-related factor 2 (Nrf2) expression in the kidneys of fructose-loaded female rat offspring exposed to maternal protein restriction. METHODS: Pregnant Wistar rats received diets containing 20% (NP) or 8% (LP) casein and 0 or 2.5 g "highly absorptive curcumin" /kg diet containing-LP diets (LP/LP or LP/Cur) during lactation. At weaning, female offspring received either distilled water (W) or 10% fructose solution (Fr) and were divided into four groups: NP/NP/W, LP/LP/W, LP/LP/Fr, and LP/Cur/Fr. At week 13, glucose (Glc), triacylglycerol (Tg), and malondialdehyde (MDA) levels in the plasma, macrophages number, fibrotic area, glutathione (GSH) levels, glutathione peroxidase (GPx) activity, protein expression levels of Nrf2, heme oxygenase-1 (HO-1), and superoxide dismutase 1 (SOD1) in the kidneys were examined. RESULTS: The plasma levels of Glc, TG, and MDA, the number of macrophages, and the percentage of fibrotic area in the kidneys of the LP/Cur/Fr group were significantly lower than those of the LP/LP/Fr group. The expression of Nrf2 and its downstream molecules HO-1 and SOD1, GSH levels, and GPx activity in the kidneys of the LP/Cur/Fr group were significantly higher than those of the LP/LP/Fr group. CONCLUSIONS: Maternal curcumin intake during lactation may suppress oxidative stress by upregulating Nrf2 expression in the kidneys of fructose-loaded female offspring exposed to maternal protein restriction.

Lignin-derived low-molecular-weight oxidized lignophenol stimulates AMP-activated protein kinase and suppresses renal inflammation and interstitial fibrosis in high fat diet-fed mice.

Excess weight and obesity increase the risk of developing major risk factors for chronic kidney disease. Lignin comprises 20%-30% of the global plant biomass; however, it is not well utilized because of its resistance to chemical and biological degradation. We investigated whether low-molecular-weight oxidized lignophenol (LOLP), a lignin derivative, could alter inflammation and fibrosis in the kidneys of a high-fat diet (HFD)-fed mice. Male mice were divided into three treatment groups: HFD; HFD +0.3% LOLP; and HFD +0.6% LOLP. The control mice (Cont) were fed a low-fat diet. Macrophage kinetics, the degree of fibrosis, the extent of phosphorylation of AMP-activated protein kinase (AMPK), and mRNA expression of proinflammatory mediators in the kidneys were examined. The number of macrophages, the percentage of fibrotic area, and the mRNA expression of proinflammatory markers, TNF-α and Ccl2, and a marker of fibrosis, TGF-ß, were significantly higher in the kidneys of mice in the HFD group than those in the Cont group. Conversely, treatment with 0.6% LOLP for 8 weeks significantly suppressed the degree of macrophage infiltration, interstitial fibrotic area, and the increased mRNA expression of proinflammatory and fibrosis markers induced by HFD. In conclusion, LOLP suppressed macrophage infiltration and the increase in fibrotic area, and upregulated AMPK phosphorylation in the kidneys of HFD-fed mice; thus, it may ameliorate HFD-induced kidney injury.