Rice protein suppresses 4-hydroxy-2-nonenal-induced inflammation owing to methionine availability.

Abstract

4-Hydroxy-2-nonenal (HNE) is one of the most important products of lipid peroxidation, which induces inflammation. To investigate the effects of rice protein (RP) on suppressing HNE-induced inflammation and the role of methionine in regulating the anti-inflammatory function of RP, Wistar rats (male, weighing 180-200 g) were either ad libitum fed a pellet diet with oral administration of methionine or ad libitum fed RP for 2 weeks. RP and methionine significantly reduced HNE levels and effectively suppressed the expressions of cyclooxygenase-2, tumor necrosis factor alpha, interleukin-1β (IL-1β) and IL-6, and inducible nitric oxide synthase. The anti-inflammatory action of RP was evident from the upregulation of IL-10 and glutathione S-transferase (GST), which played a role in the detoxification of HNE. The results show that the molecular mechanism responsible for the anti-inflammatory function of RP is the inhibition of nuclear factor kappa B (NF-κB) activation by the downregulation of protein kinase B/phosphoinositide 3 kinase. Further, this study demonstrates that Met availability contributes to the suppression of HNE-induced inflammation through upregulating IL-10 and GST in rats fed RP. Novelty: RP suppresses HNE-induced inflammation. Methionine plays a role in upregulating IL-10 and GST. Methionine availability regulates the inhibition of NF-κB by RP.