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L-theanine (LTA) is a key component in tea plants and is commonly used as a functional ingredient and dietary supplement. In a recent study, we investigated the potential antiaging properties of LTA using a D-galactose-induced L6 skeletal muscle aging cell model. The results showed that LTA treatment improved cell viability and antioxidant enzyme activities while reducing levels of proinflammatory factors and advanced glycation end products. Additionally, LTA demonstrated the ability to decrease senescence-associated beta-galactosidase-positive cells, lower reactive oxygen species and MDA levels, preserve mitochondrial function, inhibit apoptosis, and alleviate cell cycle arrest in the G2/M phase. These protective effects may be attributed to the activation of the p53/p21/CDK4 pathway, regulation of cell cycle-related protein expression, promotion of cell proliferation, and regulation of apoptosis-related protein expression through the p53/Bax/Bcl-2 pathway.

Epigallocatechin-3-gallate (EGCG) and L-theanine (LTA), which are active ingredients in green tea, can inhibit fat accumulation; however, EGCG bioavailability is

l-Theanine (LTA), a non-protein-derived amino acid, is widely used as a functional ingredient. Here, we established an immune-stressed mouse model by infecting mice with enterotoxigenic Escherichia coli (ETEC) to study the immunomodulatory effects of LTA with respect to nucleotide-binding oligomerization domain (NOD)-like receptor signaling in vivo. Compared to ETEC control group, LTA alleviated ileal tissue lesions, significantly attenuated interleukin-1 beta (IL-1β) and tumor necrosis alpha (TNFα) overexpression, which was consistent with their protein levels. Additionally, LTA inhibited the ETEC-induced overexpression of NOD2 and receptor-interacting protein 2 (RIP2) proteins and mRNAs, TGE-beta-activated kinase 1 (TAK1) and proteasome subunit alpha type-7 (PSMA7) mRNAs, and partially decreased nuclear factor-κB (NF-κB) p65 protein levels. Furthermore, it suppressed c-Jun NH2-terminal kinase 1/2 (JNK1/2), extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 mitogen-activated protein kinase (p38) phosphorylation. Thus, we demonstrated that LTA regulates the innate immunity of ETEC-induced immune-stressed mice via NOD1/2-NF-κB and NOD1/2-MAPK pathways.

l-theanine, a non-protein-derived amino acid, is widely used as a functional ingredient in foods. Here, we evaluated the in vivo effects of l-theanine on glutamine metabolism in healthy rats and in a stressed rat model, which was established by infecting rats with enterotoxigenic Escherichia coli (E44813). The results showed that l-theanine significantly enhanced the synthesis of glutamine and stabilized the intestinal tract in healthy rats. In E44813-stressed rats, l-theanine could replace l-glutamine, thereby alleviating intestinal stress by reducing the expression of inflammatory factors, enhancing the activities of antioxidant enzymes, and regulating glutamine metabolism by modulating its synthesis. Treatment with a combination of l-theanine and l-glutamine was superior to treatment with l-glutamine alone in enhancing the activity of antioxidant enzymes, reducing the expression of inflammatory factors, and increasing the intestinal villi height and crypt depth.

l-Theanine (LTA), a non-protein-derived amino acid, is isolated from tea and is used as dietary supplement or beverage ingredient. This study established an enterotoxigenic Escherichia coli (ETEC)-infected mouse model of oxidative stress to examine the antioxidative mechanisms of LTA in vivo. LTA regulated non-enzymatic antioxidative activity and increased catalase (CAT) mRNA expression in non-ETEC-infected mice. In addition, LTA decreased oxidative parameters and the activity and mRNA levels of CAT in ETEC-infected mice. LTA increased superoxide dismutase (SOD) activity and mRNA expression of CuZn-SOD, ECSOD and glutathione peroxidase 1 (Gpx1); it restored MnSOD mRNA levels as well. Our results demonstrate that LTA has antioxidative properties via regulation of non-enzymatic pathways. In addition, LTA protects against superoxide and hydrogen peroxide via SOD or Gpx1 as the first and second defence line. Thus, LTA differentially regulates antioxidative enzymes depending on the dose and pathophysiological conditions through transcription, post-transcriptional and post-translational mechanisms in mice.