Dietary curcumin supplementation attenuates inflammation, hepatic injury and oxidative damage in a rat model of intra-uterine growth retardation

Br J Nutr. 2018 Sep;120(5):537-548. doi: 10.1017/S0007114518001630. Epub 2018 Jul 25.

Abstract

Rats with a normal birth weight (NBW) or intra-uterine growth retardation (IUGR) were fed basic diets (NBW and IUGR groups) or basic diets supplemented with curcumin (NC and IC groups) from 6 to 12 weeks. The body weight of IUGR rats was lower (P<0·05) than that of the controls. Rats with IUGR showed higher (P<0·05) concentrations of TNF-α, IL-1β and IL-6; higher (P<0·05) activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in their serum; and increased (P<0·05) concentrations of malondialdehyde (MDA), protein carbonyl (PC) and 8-hydroxy-2'-deoxyguanosine (8-OHDG) in the liver compared with the NBW rats. The livers of IUGR rats exhibited a lower (P<0·05) superoxide dismutase activity and decreased (P<0·05) metabolic efficiency of the hepatic glutathione redox cycle compared with those of the NBW rats. In response to dietary curcumin supplementation, concentrations of inflammatory cytokines and activities of AST and ALT in the serum and MDA, PC and 8-OHDG in the liver were lower (P<0·05), and the hepatic glutathione redox cycle in the liver was improved (P<0·05) in the IC group than in the IUGR group. These results were associated with lower (P<0·05) phosphorylated levels of the NF-κB pathway and Janus kinase 2 (JAK2) and higher (P<0·05) mRNA expression of genes involved in the nuclear factor, erythroid 2-like 2 (Nfe2l2)/antioxidant response element (ARE) pathway in the liver of the IC rats than that of the IUGR rats. Maternal undernutrition decreased birth weight and led to inflammation, oxidative damage and injury in rats. Curcumin appeared to be beneficial in preventing IUGR-induced inflammation, oxidative damage and injury by activating the expression of the NF-κB, JAK/STAT and Nfe2l2/ARE pathways in the liver.

Keywords: Gst glutathione S transferase; Hmox1 haeme oxygenase 1; Nfe2l2 nuclear factor erythroid 2-like 2; 8-OHDG 8-hydroxy-2’-deoxyguanosine; ALT alanine aminotransferase; AST aspartate aminotransferase; GPX glutathione peroxidase; GR glutathione reductase; IC intra-uterine growth retardation with curcumin supplementation; IUGR intra-uterine growth retardation; JAK Janus kinase; MDA malondialdehyde; NBW normal birth weight; NC normal birth weight with curcumin supplementation; PC protein carbonyl; SOD superoxide dismutase; STAT3 signal transducer and activator of transcription 3; Curcumin; Inflammation; Intra-uterine growth retardation; Liver; Oxidative damage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 8-Hydroxy-2'-Deoxyguanosine
  • ATP-Binding Cassette Transporters / analysis
  • Alanine Transaminase / blood
  • Animals
  • Animals, Newborn
  • Aspartate Aminotransferases / blood
  • Birth Weight
  • Caenorhabditis elegans Proteins / analysis
  • Curcumin / administration & dosage*
  • Cytokines / blood
  • Cytokines / genetics
  • Deoxyguanosine / analogs & derivatives
  • Deoxyguanosine / analysis
  • Dietary Supplements
  • Disease Models, Animal
  • Female
  • Fetal Growth Retardation / physiopathology*
  • Gene Expression / drug effects
  • Inflammation / blood
  • Inflammation / etiology
  • Inflammation / prevention & control*
  • Liver / drug effects
  • Liver / metabolism
  • Liver / pathology
  • Liver Diseases / etiology
  • Liver Diseases / metabolism
  • Liver Diseases / prevention & control*
  • Oxidation-Reduction
  • Oxidative Stress / drug effects*
  • Pregnancy
  • Rats

Substances

  • ABTM-1 protein, C elegans
  • ATP-Binding Cassette Transporters
  • Caenorhabditis elegans Proteins
  • Cytokines
  • 8-Hydroxy-2'-Deoxyguanosine
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • Deoxyguanosine
  • Curcumin