theanine and Liver-Diseases

For thousands of years, humans have consumed tea made from leaves of Camellia sinensis, first as a medicinal herb and then as a widely popular beverage. In the past 10 years, theanine, a tea-derived, unique, nonproteinic amino acid, has been extensively studied for its health benefits. Recently, multiple lines of evidence have proven its beneficial effects on hepatic and immune functions. One possible mechanism for its biological activity involves the downregulation of the inflammatory response through the induction of nitric oxide production and glutathione synthesis. In this review, we summarize published results describing the potential mechanisms for these beneficial health effects and provide new insight into how theanine can be therapeutic for liver injury and chronic liver disease.

Topics: Biological Availability; Camellia sinensis; Glutamates; Health Promotion; Humans; Immunologic Factors; Liver Diseases; Plant Extracts; Plant Leaves; Tea

Liver diseases induce a severe decrease in quality of life. Stem cell based therapy shows therapeutic potential in the treatment of liver injury. Theanine is a unique amino acid found in green tea and could confer beneficial effects on cell protection. This study investigates if protective effect on the liver by stem cells preincubated with theanine is better than that from stem cells without preincubated theanine.. We transplanted theanine preincubated adipose-derived stem cells (ADSC) to male Wistar rats with liver dysfunction induced by N-nitrosodiethylamine. The viability, migration and antioxidant capabilities were performed in the ADSC pre-incubated with theanine. Hepatic functional, structural and molecular assays were determined in the animals with or without theanine preincubated ADSC.. Cell model revealed that ADSC preincubated with green tea theanine (T-ADSC) increased cell capabilities including viability, migration and paracrine secretion. In vivo results indicated that several pathological conditions were observed in rats with liver injury induced by DEN including structural changes and expression of pyroptosis as well as autophagy markers. The above pathological conditions were improved when the rats received both ADSC and T-ADSC treatment. Furthermore, T-ADSC showed better therapeutic effect on rats with liver injury than ADSC due to significant suppression of pyroptosis markers caspase-1 and IL-1β as well as autophagy marker LC3-II accompanied with intensive paracrine VEGF from T-ADSC.. Increased paracrine VEGF secretion from T-ADSC plays a crucial role in liver regeneration. A future clinical study may be designed for further verification of these experimental in vivo findings.

Topics: Adipose Tissue; Animals; Antioxidants; Autophagy; Biomarkers; Caspases; Diethylnitrosamine; Glutamates; Liver Diseases; Liver Regeneration; Male; Pyroptosis; Quality of Life; Rats; Rats, Wistar; Reactive Oxygen Species; Stem Cells; Tea; Vascular Endothelial Growth Factor A

Redox and inflammation imbalances are associated with increased levels of advanced glycation end products (AGEs), leading to the degeneration of body function. l-Theanine, derived from tea, reportedly inhibits AGE formation in vitro. We investigated the effects on AGE content, oxidative stress, and inflammatory factors in d-galactose-induced aging rats for prevention and treatment of age-related liver dysfunction. l-Theanine increased activities of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase, thus enhancing total antioxidant capacity, and decreasing malondialdehyde and nitric oxide synthase levels in serum and liver. Levels of the pro-inflammatory factors, interleukin (IL)-1β, tumour necrosis factor-alpha, and IL-6 were decreased in serum and liver, whereas those of anti-inflammatory factors, IL-4 and IL-10, were increased in the serum. Further, l-theanine inhibited AGE production and decreased the levels of the liver function markers, alanine aminotransaminase and aspartate aminotransferase. It also significantly increased the mRNA expression levels of FoxO1 and downregulated NF-κB(p65) but suppressed the phosphorylation of both FOXO1 and NF-κB (p65). Moreover, l-theanine effectively attenuated d-galactose-induced oedema and vacuole formation, thus protecting the liver. Overall, l-theanine reversed the d-galactose-induced imbalance in oxidative stress and inflammatory responses, reduced AGEs content in aging rats, maintained homeostasis in the body, and ameliorated liver aging.

Topics: Aging; Animals; Antioxidants; Galactose; Glutamates; Glycation End Products, Advanced; Inflammation; Liver; Liver Diseases; Male; Oxidation-Reduction; Oxidative Stress; Rats; Rats, Sprague-Dawley

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.

Topics: Acute Disease; Alanine Transaminase; Animals; Aspartate Aminotransferases; Glutamates; Humans; Hypothalamo-Hypophyseal System; Lipopolysaccharides; Liver; Liver Diseases; Male; Malondialdehyde; Mice; Mice, Inbred ICR; NF-kappa B