While the Camellia sinensis cultivar and processing method are key factors that affect tea flavor and aroma, the chemical changes in nonvolatile components associated with the tea processing method using a single cultivar of C. sinensis have not been reported. Fresh leaves from C. sinensis Longjing 43 were subjected to six tea processing methods and evaluated by targeted and untargeted chromatographic procedures. On the basis of targeted assessment of the total catechin content, three clusters were identified: yellow−green, oolong−white−dark, and black. However, principal component analysis of the total tea metabolome identified four chemical phenotypes: green−yellow, oolong, black−white, and dark. Differences in the noncatechin components included amino acids and γ-aminobutyric acid, which increased in white tea, and dihydroxyphenylalanine, valine, betaine, and theophylline, which increased in dark tea. Overall, this study identified a wide range of chemicals that are affected by commonly used tea processing methods and potentially affect the bioactivity of various tea types.

Large-leaf yellow tea (LYT) is made from mature tea leaves with stems and has unique sensory characteristics different from other teas. To study the chemical changes of LYT during processing, samples were collected from each step for quantitative and qualitative analyses by high-performance liquid chromatography and liquid chromatography−mass spectrometry (LC-MS). LC-MS-based nontargeted and targeted metabolomics analyses revealed that the tea sample after roasting was markedly different from samples before roasting, with the levels of epicatechins and free amino acids significantly decreased, but the epimerized catechins increased dramatically. After accounting for common compounds in tea, N-ethyl-2pyrrolidinone-substituted flavan-3-ols were found to be the marker compounds responsible for the classification of all samples, as they rapidly rose with increasing processing temperature. These findings suggested that the predominant changes in the tea constituents during large-leaf yellow tea roasting were the thermally induced degradation and epimerization of catechins and the formation of N-ethyl-2-pyrrolidinone-substituted flavan-3-ols from L-theanine.

Theanine, a unique bioactive constituent from tea ( Camellia sinensis) leaves, is widely used as a functional ingredient and dietary supplement. To evaluate the anti-inflammatory and hepatoprotective effects of theanine and its molecular mechanism, the lipopolysaccharide (LPS)-induced inflammation mouse model was employed in this study. The survival rate of mice in the theanine-treated group increased significantly compared with that of LPS-only group mice. Furthermore, ICR male mice were randomly divided into three or four groups: control, LPS (LPS treatment only), LPS + theanine (20 mg/kg/day), and theanine (theanine treatment only). The results showed that compared with the LPS group, the liver damage and oxidative stress of the theanine-treated group decreased significantly, based on plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) concentrations, hepatic total superoxide dismutase (T-SOD), and malondialdehyde (MDA) levels, and histological scores and apoptosis [terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) staining and caspase-3 activity] in the liver tissues. Furthermore, compared with no treatment, pretreatment with theanine significantly decreased the release of interleukin (IL)-1β and tumor necrosis factor (TNF)-α, inhibited the expression of several inflammatory factors (including IL-1β, TNF-α, and IL-6), and increased the IL-10/interferon (IFN)-γ ratio in the hepatic tissues. In the LPS-induced inflammation model, theanine inhibited the expression of proinflammatory mediators involved in the nuclear factor-kappa B (NF-κB) pathway, such as inducible nitric oxide synthase (iNOS) and matrix metalloproteinase-3 (MMP-3), and attenuated the phosphorylation of NF-κB in the hepatic tissues. Moreover, theanine suppressed the acute-phase response (elevated nitric oxide and C-reactive protein levels). Furthermore, theanine suppressed the LPS-induced inflammatory state by normalizing hypothalamic-pituitary-adrenal (HPA) axis hyperactivity. Taken together, the results suggest that theanine potentially ameliorates LPS-induced inflammation and acute liver injury; molecular mechanism of action may involve normalization of HPA axis hyperactivity and inactivation of the NF-κB signaling pathway.

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Scope The consumption of green tea is considered to be associated with a lower incidence of neurodegenerative diseases. In the present study, it is investigated the role of amyloid precursor protein cleavage, glial cell activation, neuroinflammation, and synaptic alterations in the protective effects of green tea against the amyloid β (Aβ) accumulation and cognitive impairment. Methods and Results 5XFAD mice are treated with green tea extract (GTE) for 8 or 16 weeks. Barnes maze and Y maze testing demonstrated that spatial learning and memory ability are markedly improved by GTE treatment. Immunofluorescence staining, ELISA, and western blot showed GTE significantly alleviate the formation of Aβ and reduce the levels of sAPPβ and C99, as well as sAPPα and C83. Meanwhile, GTE suppressed GFAP and Iba1 levels in the glial cells, increased PSD95 and synaptophysin levels in synaptic cells. Further, the IL‐1β level is decreased, RNA sequencing reveals the genes annotated in response to stimulus and immune response are regulated. Conclusion Our findings indicate GTE suppresses Aβ levels and alleviate cognitive impairment in 5XFAD mice. These beneficial effects are accompanied by inhibition of APP cleavage pathways, suppression of glial cell activation and pro‐inflammatory responses, and a reduction of synapse loss.