Mechanisms of Curcumin in Metabolic Syndrome via Oxidative Stress Regulation: A Review

Abstract

Metabolic syndrome (MetS) is a group of related problems in our body, centering on insulin resistance. This is a great challenge to the health of the whole world. Oxidative stress, which occurs when there are too many reactive oxygen species (ROS) and our antioxidant defense can’t work normally, is a very important point to promote MetS. Curcumin (Cur), a lipophilic polyphenol from the root stem of long ginger, is very interesting because of its properties, which act on several targets. This review explains how curcumin regulates oxidative stress to improve MetS. This paper mainly discusses the signal pathway of antioxidant axis Keap1/Nrf2/ARE, SIRT1, and the communication between antioxidant and anti-inflammatory networks. Curcumin activates Nrf2 by changing the important cysteine residue on Keap1. This leads to more phase II detoxification enzymes, such as superoxide dismutase (SOD), catalase (CAT) and heme oxygenase -1(HO-1). Together, these enzymes help restore the redox balance in cells. In addition, other mechanisms have been found, such as SIRT1 signal axis, post-transcriptional regulation of microRNAs (miRNAs) and mitochondrial bioenergy. These findings indicate that curcumin has many therapeutic potentials. This review accurately explains how curcumin regulates oxidative stress. This provides a solid theoretical basis for developing curcumin as a dietary intervention strategy and a supplementary therapeutic agent for MetS.