Format

Send to

Choose Destination
Mol Med Rep. 2018 Jan;17(1):103-108. doi: 10.3892/mmr.2017.7911. Epub 2017 Oct 26.

Curcumin alleviates liver oxidative stress in type 1 diabetic rats.

Author information

1
Department of Agriculture and Biotechnology, Jinshan College of Fujian Agriculture and Forestry University, Fuzhou, Fujian 350002, P.R. China.

Abstract

The aim of the present study was to determine the effects of curcumin on antioxidants using a rat model of type 1 diabetes. Seven‑week‑old male Sprague‑Dawley rats were injected with Streptozotocin (STZ) intraperitoneally to induce this model, and then treated with 1.0% curcumin (weight ratio) mixed in their diet for 21 days. The present study included three groups: Control group (NC), diabetic rat model group (DC) and a curcumin treated group (Diab‑Cur). The results demonstrated that curcumin treatment markedly decreased the blood glucose levels, plasma malondialdehyde concentration and plasma activity of glutathione peroxidase (GSH‑Px) and catalase (CAT); however, it increased the plasma superoxide dismutase (SOD) and insulin levels. Curcumin treatment increased the expression of the CAT, GSH‑Px, HO‑1 and norvegicus NAD(P)H quinone dehydrogenase 1, and decreased the SOD1 expression, which, led to a diminished oxidative stress status. In addition, curcumin treatment significantly increased the protein expression of Keap1 in the Diab‑Cur group when compared with the DC group, decreased cytosolic concentrations of Nrf2 while increasing nuclear accumulation of Nrf2. The results provide evidence that oxidative stress in the STZ‑induced diabetic rat model may be attenuated by curcumin via the activation of the Keap1‑Nrf2‑ARE signaling pathway, as evidenced by a decrease in the blood glucose concentration and an increase in the transcription of several antioxidant genes.

PMID:
29115468
PMCID:
PMC5780069
DOI:
10.3892/mmr.2017.7911
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Spandidos Publications Icon for PubMed Central
Loading ...
Support Center