Anti-Inflammatory Mechanism Of Rice Protein Via Methionine Metabolism

Inflammation can induce many diseases,so the effectively inhibition of inflammatory response is an important way for disease prevention and health care.Oxidative stress is the main cause of inflammation,of which the occurrence and development are regulated by NF-κB signaling pathway.Therefore,activating endogenous antioxidant response and inhibiting NF-κB activation are the main antiinflammatory mechanisms of the body to effectively prevent diseases.Rice protein,which is rich in methionine,is a plant protein with many functional properties such as anti-oxidation and reducing lipid levels in the body.However,so far,it has not been fully analyzed whether rice protein has anti-inflammatory effect in vivo,especially there is still lacking in in-depth research on how rice protein activates endogenous anti-inflammatory mechanism and whether methionine metabolism regulates the anti-inflammatory response of rice protein.Therefore,this paper took rice protein as the research object with different dietary conditions such as normal diet,cholesterol-enriched diet and oil-enriched diet,etc.,as well as experimental animals with different ages(growing and adult rats)were adopted.After free feeding and oral gastric feeding,the study method that combining dietary protein and amino acids was adopted,and then from the perspective of methionine metabolism,a series of in vivo experiments on the anti-inflammatory effect of rice protein,the activation of NF-κB signaling pathway inhibited by rice protein,the mechanism of methionine regulating inflammatory response,and the endogenous antiinflammatory mechanism of rice protein induced by methionine metabolism were carried out.The main findings were as follows:Under normal diet,cholesterol-enriched diet and oil-enriched diet,after 2 weeks of free feeding,the experimental results showed that rice protein had anti-inflammatory effects in vivo through effectively reducing the plasma activities of ALT/AST and promoting the hepatic gene levels and protein expressions of IL-10 in growing and adult rats.The main endogenous anti-inflammatory mechanisms of rice protein were to inhibiting PI3K/Akt expressions,promote IκBα expressions,inhibite the activation of NF-κB signal pathway and effectively reduce hepatic gene levels and protein expressions of inflammatory factors such as IL-1β,IL-6,TNF-α,i NOS,COX-2 and MCP-1.were,and the effect was not affected by the age of experimental animals,dietary cholesterol,and dietary oils.Meanwhile,rice protein could increase the hepatic gene levels and protein expressions of Msr A,Msr B2,Msr B3 in growing and adult rats,and increase hepatic molecular expressions of MAT1 A,SAHH,CBS and CTH.The regulation effects of rice protein on inhibiting the activation of NF-κB signal pathway,activating the endogenous antioxidant system of MSR and promoting the transsulfur metabolism of methionine were not affected by animal age,dietary cholesterol and dietary oil.After oral gavage of different doses of methionine for 2 weeks,the experimental results showed that methionine could increase the molecule expressions of transsulfuration metabolizing enzymes,promote GSH synthesis,activate the MSR antioxidant system,activate the endogenous Nrf2-ARE antioxidant pathway,inhibit the activation of NF-κB regulated by PI3K/Akt,which effectively reducing the expressions of inflammatory factors.Inhibiting the activation of the NF-κB signaling pathway and initiating the endogenous antioxidant response were the main anti-inflammatory mechanisms of methionine.The results showed that the anti-inflammatory effect of methionine was positively correlated with the intake of methionine.Using oral gavage with methionine and free intake of rice protein,the comparative analysis of the anti-inflammatory effects between rice protein and methionine showed that methionine metabolism had vital regulation effects on endogenous antiinflammatory mechanisms of rice protein by inhibiting NF-κB activation regulated by PI3K/Akt,effectively reducing inflammatory factors,activating the Nrf2-ARE antioxidant pathway,initiating the MSR endogenous antioxidant system,promoting GSH synthesis and metabolism regulated by methionine transsulfur metabolism,and enhancing the molecular expressions of endogenous antioxidant enzymes,which showed that methionine metabolism could initiate the endogenous anti-inflammation effect of rice protein.Under different dietary conditions such as normal diet,cholesterol-enriched diet and oil-enriched diet,and adopting the rice protein and rice protein added with methionine as the main dietary protein sources,after feeding growing rats and adult rats for 2 weeks,the experimental results showed that the methionine supplement could enhance the anti-inflammatory effect of rice protein by cooperating with rice protein to inhibit molecular expressions of PI3K/Akt,increase molecular expressions of IκBα,prevent the expressions of p50 and p65 into the nucleus,inhibit activation of NF-κB,reduce the molecular expressions of inflammatory factors,enhance the methionine transsulfur metabolism of rice protein,increase the molecular expressions of Msr A,Msr B2,and Msr B3,reduce ROS accumulation and enhance the antioxidant capacity of rice protein.The supplement of methionine had a synergistic regulatory effect on the anti-inflammatory mechanism of rice protein based on the regulation of methionine metabolism.This paper clarified that inhibiting the activation of NF-κB signaling pathway and activating the endogenous antioxidant system were the main endogenous antiinflammatory mechanism of rice protein from the overall levels and molecular levels,and the paper also revealed the synergistic regulation effect of methionine metabolism on initiating the endogenous anti-inflammatory mechanism of rice protein,which providing a theoretical basis for opening up a new way for the application of rice protein to effectively prevent inflammatory diseases,and providing a new research idea for comprehensively analyzing disease prevention and health functions of rice protein.