Effects of L-Theanine on Hepatic Ischemia-Reperfusion Injury in Rats.

OBJECTIVES: The effects of L-theanine on hepatic microcirculation during hepatic ischemia-reperfusion injury have not yet been investigated. The aim of this study was to investigate the influence of L-theanine on hepatic ischemia-reperfusion injury in rats. MATERIALS AND METHODS: Thirty-two male Sprague Dawley rats weighing 250 to 300 g were used. Rats were divided into 4 groups: sham + saline, sham + L-theanine, hepatic ischemia-reperfusion injury + saline, and hepatic ischemia-reperfusion injury + L-theanine. Hepatic ischemia-reperfusion injury in rats was induced by 60 minutes of 70% ischemia and 4 hours of reperfusion. The extent of hepatic cell injury, functional capillary density, hepatic functions, and changes in some enzyme markers in hepatic tissue were investigated in the 4 groups. RESULTS: The induction of hepatic ischemia-reperfusion injury resulted in significant increases in hepatic necrosis; serum activity of alanine aminotransferase, lactate dehydrogenase, gamma-glutamyltransferase, and tumor necrosis factor alpha; tissue activity of inducible nitric oxide synthase, myeloperoxidase, and malondialdehyde, and oxide glutathione; and H score for hypoxia-inducible factor 1-alpha in the liver. In the liver, there were significant reductions in reduced glutathione, ratio of reduced glutathione-to-oxide glutathione, and functional capillary density. The use of L-theanine improved these changes. CONCLUSIONS: L-theanine demonstrated protective effects on hepatic injury after ischemia-reperfusion injury in rats. However, new studies are needed to confirm the preventive or reducing effects of L-theanine on hepatic ischemia-reperfusion injury.

l-theanine alleviates liver and kidney dysfunction in septic rats induced by cecal ligation and puncture.

AIMS: Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response against infection that triggers systemic inflammatory response syndrome. l-theanine (LT), a glutamate derivative, is a non-protein amino acid derived from tea (Camellia sinensis), and a valuable nutraceutical product used as an additive in the food industry. This study we aimed to investigate whether LT would exert any therapeutic effect on liver and kidney tissues in Sprague Dawley rats with sepsis induced with cecal ligation and puncture (CLP). MAIN METHODS: Rats were divided into four groups; sham, CLP, CLP+LT1 (2x250 mg/kg) and CLP+LT2 (2 × 750 mg/kg). Liver and kidney tissues were subjected to histopathological examination. Apoptotic index percentages (AI%) were examined using the TUNEL method. The oxidized glutathione to total glutathione (GSSG/TGSH) ratio (as a marker of oxidative stress, levels of caspase-3 (a marker of apoptosis), glutathione peroxidase (GPx) and glutathione S-transferase (GST) (as antioxidant enzymes), inducible nitric oxide synthase (iNOS) and the tumor necrosis factor-α to Interleukin-10 ratio (TNF-α/IL-10) (as markers of inflammation) were investigated using commercial kits. Levels of malondialdehyde (MDA) (a marker of oxidative stress) were determined spectrophotometrically. KEY FINDINGS: A high dose of LT exhibited more significant effects in reducing oxidative stress, inflammation and apoptosis than a low dose of LT in liver and kidney tissues with CLP-induced sepsis (p < 0.05). SIGNIFICANCE: Our results indicated that LT significantly and dose-dependently inhibited sepsis induced liver and kidney injury. This effect may be attributed to the antioxidant, anti-inflammatory, and anti-apoptotic activities of LT.