Journal of Tea Science Research, 2025, Vol.15, No.1, 30-37 http://hortherbpublisher.com/index.php/jtsr 31 The study provides an overview of the anti-inflammatory activity of tea, highlighting the bioactive molecules responsible for the activity and the mechanisms at the molecular level. The effectiveness of tea in regulating inflammation is appraised by discussing current experimental and clinical studies. It also discusses the future application of tea products in therapeutic and preventive medicine, including considerations of bioavailability, safety, and dosage. By consolidating current research, this study illuminates tea's prospects in inflammation management and directs further research along these lines. 2 Major Anti-inflammatory Active Compounds in Tea 2.1 Tea polyphenols Catechins, and especially epigallocatechin gallate (EGCG), are the primary polyphenols of green tea. EGCG is reported to suppress the gene and protein expression of inflammatory cytokines and inflammation-related enzymes, for instance, TNF-α, IL-6, and COX-2, thereby reducing inflammation. Anti-inflammatory activity of green tea is primarily because of these catechins, which act through suppression of central inflammatory pathways (Preeja et al., 2021; Varshini et al., 2023). 2.2 Theaflavins, thearubigins, and other polyphenol derivatives Theaflavins and thearubigins are black tea fermented polyphenol derivatives. They have been identified to possess anti-inflammatory activity by inhibiting pro-inflammatory mediators and enzymes. Synergistic interaction via blending teas, such as peppermint with white tea, also enhances these effects by leading to increased inhibition of pro-inflammatory cytokines and pathways involved (Xia et al., 2020; Malongane et al., 2022). 2.3 Theanine and amino acid compounds L-theanine, a unique amino acid found in tea, has been found to possess anti-inflammatory effects, particularly when combined with other bioactive molecules. For example, L-theanine-chlorogenic acid blend has shown a more pronounced anti-inflammatory effect than either of the molecules by itself, reflecting synergism (Varshini et al., 2023). 2.4 Caffeine and its synergistic effects Caffeine, a well-known tea stimulant, can also be involved in anti-inflammatory activities, especially in combination with polyphenols and other tea constituents. While its anti-inflammatory action against inflammation is less potent than that of catechins, caffeine is capable of modulating and defining inflammatory responses, in addition to enhancing the activity of other bioactive substances (Varshini et al., 2023). 2.5 Other potential anti-inflammatory molecules in tea Tea also contains polysaccharides and volatile oils, which have been reported to be involved in anti-inflammatory action. The polysaccharides can inhibit inflammatory mediators, while volatile oils can endow with both anti-inflammatory as well as antioxidant activity. The total combined anti-inflammatory effect of tea is hence a result of the combined action of these diverse compounds (Kartika et al., 2022; Malongane et al., 2022). 3 Molecular Mechanisms of the Anti-inflammatory Effects of Tea 3.1 Regulation of oxidative stress and ROS levels Tea polyphenols, such as catechins, are effective antioxidants, reducing intracellular reactive oxygen species (ROS) and cell-protective against oxidative damage. For example, Jing-Si tea reduced the levels of ROS dramatically and protected synoviocytes from oxidative stress by H2O2-induced, inhibiting inflammation and apoptosis of cells (Kao et al., 2024). Green tea polyphenols also reduce lipid peroxidation and oxidative stress, which are responsible for their anti-inflammatory activity (Rhee et al., 2018). 3.2 Inhibition of inflammatory signaling pathways Tea and its compounds suppress major inflammatory signaling cascades. White tea and peppermint suppress phosphorylation of IκB-α and MAPK, leading to downregulation of NF-κB and MAPK pathways, central to the transcription of inflammatory genes (Ni et al., 2024). Jing Si Herbal Tea has been shown to decrease nuclear
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