L-Theanine mediates the p38MAPK signaling pathway to alleviate heat-induced oxidative stress and inflammation in mice

• Published in: Food & function 2022-02, Vol.13 (4), p.2120-2130
• Main Authors: Liu, Kehong, Liu, Enshuo, Lin, Ling, Hu, Yuan, Yuan, Yong, Xiao, Wenjun
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants; Antioxidants - pharmacology; Antioxidants - therapeutic use; Camellia sinensis; Diet; Dietary Supplements; Disease Models, Animal; Enzymatic activity; Enzyme activity; Glutamates - pharmacology; Glutamates - therapeutic use; Heat; Heat stress; Heat tolerance; Hot Temperature; Hsp27 protein; IL-1β; Inactivation; Inflammation; Inflammation - drug therapy; Interleukin 6; Jejunum; Jejunum - drug effects; Liver - drug effects; Male; MAP Kinase Signaling System; Mice; Mice, Inbred BALB C; Oxidative stress; Oxidative Stress - drug effects; Phytotherapy; Signal transduction; Signal Transduction - drug effects; Signaling; Specific Pathogen-Free Organisms; Tea; Theanine; Tumor necrosis factor-α
• ISSN: 2042-6496; 2042-650X
• DOI: 10.1039/d1fo03077a

L-Theanine, an active ingredient in the tea plant ( ) associated with calming, is widely used as a functional ingredient and dietary supplement. In this study, a heat stress mouse model was used to evaluate the anti-heat stress effect of L-theanine and its possible mechanism of action. Mice subjected to heat stress (40 °C) that were administered L-theanine at various doses (100, 200, and 400 mg kg d ) had reduced oxidative stress and inflammatory factors when L-theanine was administered both long-term and as a preventative treatment. Our L-theanine intervention countered the reduction in growth and feed intake of mice under heat stress and reversed liver and jejunum tissue damage. Moreover, L-theanine countered the increase in inflammatory factors TNF-α, IL-6, and IL-1β and antioxidant enzymes SOD and CAT; it also counteracted GSH-Px inactivation, the upregulation of AST and ALT enzyme activity, and MDA production. The mechanism of action may involve mediation of the P38 signaling pathway, inhibition of MK2 overexpression, and downregulation of p-P65/P65 caused by the overexpression of downstream HSP27. This would inhibit the heat stress-induced imbalance in oxidative stress and inflammatory responses.