theanine and Reperfusion-Injury

This study was to use the partial differential mathematical model to analyze the magnetic resonance imaging (MRI) images of cerebral ischemia-reperfusion injury (CIRI) and to dynamically observe the role of L-theanine in CIRI based on this. 30 patients with cerebral ischemia in a hospital in a certain area were selected and divided into a cerebral ischemia group and a L-theanine treatment group. The two groups of patients were examined by MRI within 48 hours, and the relative apparent diffusion coefficient (rADC) of the cerebral ischemic part of the patients was determined. The partial differential mathematical model was used for data processing to obtain the function of cerebral ischemia time and infarct area, and the data of patients in the cerebral ischemia group and L-theanine treatment group were compared and analyzed. The results showed that the partial differential mathematical model could effectively analyze the linear relationship between the rADC value and time in the treatment of CIRI using L-theanine. The rADC values of the four points of interest in the L-theanine treatment group all increased with time, and there was a positive correlation between the variables

Topics: Adult; Aged; Brain Ischemia; Diffusion Magnetic Resonance Imaging; Glutamates; Humans; Magnetic Resonance Imaging; Middle Aged; Models, Theoretical; Reperfusion Injury

Theanine, as a naturally occurring component in tea, has been shown to deliver benefits against various diseases. However, the exact molecular mechanisms underlying theanine's protective actions against cerebral ischemia/reperfusion (IR) injury still remains largely unknown.. In this study, rat cerebral IR injury model was established and were randomly divided into the following five groups: Sham (SH), IR, IR + Theanine (TH), IR + TH+ heme oxygenase-1 (HO-1) inducer cobalt protoporphyrin (Copp), and IR + Copp groups.. We found that theanine significantly inhibited neuron damage and apoptosis in the hippocampus during the 48 h detection period, as detected by hematoxylin and eosin (HE) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. Meanwhile, reduced levels of malondialdehyde (MDA) and elevated activities of superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-PX) were observed in the theanine-treated group. Enzyme-linked immunosorbent (ELISA) assay also revealed that theanine markedly decreased the levels of inflammatory cytokines, such as IL-6, IL-1β, and TNF-α, in IR rats. The anti-apoptotic effect of theanine on IR injury was further verified by flow cytometry assay. Besides, theanine dramatically inhibited HO-1 expression and activity but increased extracellular signal-regulated kinase 1/2 (ERK1/2) activity in hippocampal tissue from rats with cerebral IR injury. However, co-treatment with Copp remarkably abolished the protective effects of theanine on cerebral IR injury.. These findings demonstrated that the neuroprotective role of theanine was associated with its anti-oxidative, anti-inflammatory, and anti-apoptotic properties, which might be through regulation of HO-1 activation in rats with cerebral IR injury.

Topics: Animals; Apoptosis; Brain Ischemia; Gene Expression Regulation; Glutamates; Heme Oxygenase (Decyclizing); Hippocampus; Inflammation; Male; MAP Kinase Signaling System; Neurons; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reperfusion Injury

Oral administration of cystine and theanine (CT) may modulate antioxidant glutathione (GSH) metabolism, thereby improving outcomes after gut ischemia reperfusion.. Experiment 1: Institute of Cancer Research mice (n = 35) were assigned to a Vehicle (n = 11), a CT140 (n = 14), or a CT280 (n = 10) group. The CT140 and 280 groups were given CT at respective dosages of 140 and 280 mg/kg (cystine: theanine = 5: 2) once daily via gavage for 5 days. All mice underwent 75-min occlusion of the superior mesenteric artery (SMA). Survival after reperfusion was observed. Experiment 2: Mice (n = 67) were pretreated for 5 days (Vehicle: n = 24, CT280: n = 20, vehicle/sham: n = 23). The Vehicle and CT280 groups underwent 60-min SMA occlusion. Levels of GSH, the oxidized form of GSH, Glutathione-S-S-Glutathione (GSSG), and GSH-related amino acids (cysteine and glutamic acid) in the small intestine, and plasma cytokine (IL-6, IL-1β, TNFα) levels, were evaluated before (0 h), 3, 6, or 9 h after reperfusion.. Experiment 1: The CT280 group showed significantly better survival than the Vehicle group. Experiment 2: Gut GSSG, cysteine, and glutamic acid levels were higher in the CT280 than in the Vehicle group after reperfusion. Plasma IL-6 and TNFα levels rose more rapidly in the CT280 than in the Vehicle group.. Oral administration of CT improves survival after gut I/R, possibly through the modulation of the GSH-redox cycle and cytokine responses.

Topics: Animals; Cystine; Cytokines; Glutamates; Glutathione; Male; Mice, Inbred ICR; Random Allocation; Reperfusion Injury

Theanine and caffeine, 2 naturally occurring components in tea, have repeatedly been shown to deliver unique cognitive benefits when consumed in combination. In this study, we assessed the beneficial synergistic effects of concurrent treatment with theanine and caffeine against cerebral damage in rats. Theanine and caffeine had no effect on physiological variables, including pH, partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2), mean arterial blood pressure, plasma glucose, or regional cerebral blood flow. Treatment with theanine (1 mg/kg body mass, intraperitoneal injection) alone significantly reduced cerebral infarction induced by cerebral ischemia-reperfusion, but caffeine (10 mg/kg, intravenous administration) alone only had a marginal effect. However, the combination of theanine plus caffeine resulted in a significant reduction of cerebral infarction and brain edema compared with theanine monotherapy. Meanwhile, increased malondialdehyde levels as well as decreased superoxide dismutase activity, glutathione peroxidase activity, and glutathione levels observed in the cerebral cortex after cerebral ischemia-reperfusion were significantly ameliorated by the combination therapy. Furthermore, the elevated inflammatory response levels observed in the cortex after cerebral ischemia-reperfusion were markedly attenuated by the combined treatment. Thus, it is suggested that the neuroprotective potential of a combination therapy with theanine and caffeine against cerebral ischemia-reperfusion is partly ascribed to their antioxidant and anti-inflammatory properties.

Topics: Animals; Antioxidants; Brain Edema; Brain Ischemia; Caffeine; Cerebral Cortex; Cerebral Infarction; Drug Synergism; Glutamates; Glutathione; Glutathione Peroxidase; Inflammation; Male; Malondialdehyde; Neuroprotective Agents; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Superoxide Dismutase

While the neuroprotective effect of green tea (Camellia sinensis) might be explained by the presence of amino acid L-theanine in the tea leaves, it is not known whether postischemic administration of L-theanine could also provide neuroprotection. In the present study, we investigated the neuroprotective effect of L-theanine (1 and 4 mg/kg) administered at 3, 12, and 24 h after reperfusion in the rat model of stroke. We also studied the effect of L-theanine on brain injury caused by exogenous administration of N-methyl-D-aspartate and α-amino-3-hydroxy-5-methyl-isoxazole-4-propionate/kainate receptor agonists during reperfusion. Rats were subjected to 30-min middle cerebral artery occlusion followed by 48-h reperfusion. Neurological deficit and infarct size were determined at the end of reperfusion. At 3 and 12 h, but not at 24 h of reperfusion, L-theanine substantially reduced the size of brain infarct. Neurological status was improved when L-theanine was administered 3, 12, and 24 h after reperfusion. Repeated intrastriatal injections of L-theanine at a total dose of 800 µg/kg during reperfusion prevented brain injury caused by glutamate receptor agonists. In conclusion, L-theanine at reperfusion exerts neuroprotective effect in the in vivo rat model of stroke. Local treatment with L-theanine at reperfusion prevents glutamate receptor agonist-mediated brain injury.

Topics: Animals; Brain; Camellia sinensis; Excitatory Amino Acid Agonists; Glutamates; Infarction, Middle Cerebral Artery; Male; N-Methylaspartate; Neuroprotective Agents; Rats; Rats, Wistar; Receptors, Glutamate; Reperfusion Injury; Tea

To study the effects of theanine on dopamine (DA), 5-hydroxy tryptamine (5-TH) and glutamate receptor 2 (GluR2) mRNA, phospholipase-γ1 (PLC-γ1) mRNA in cerebral ischemia-reperfusion injury rats and explore the mechanism of protective effects of theanine on the induced brain injury by ischemia-reperfusion in rats.. According to random number table, a total of 56 sprague-dawley rats in SPF grade about six-week old and 100 - 120 grams weighting were divided into five groups according to the body weight levels: model group (n = 12), sham-operation group (n = 8), low theanine group (10 mg/kg), middle theanine group (30 mg/kg) and high theanine group (90 mg/kg). There were 12 rats in each of the theanine group. The rats in model group and sham-operation groups were given distilled water, and the rats in theanine groups were given corresponding theanine solution intragastrically for fifteen days. Then the cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion (MCAO). The score of neurological behavior was evaluated at the 3rd and 24th hours after reperfusion. Rats were sacrificed at 24 hours after reperfusion, the concentrations of DA, 5-HT and theanine in rats brain following ischemia-reperfusion were determined. At the same time, we determined the levels of reactive oxygen species (ROS) and activities of catalase (CAT) in mitochondria of brain. The expressions of GluR2 mRNA and PLC-γ1 mRNA in rat brain were examined by reverse transcription polymerase chain reaction (RT-PCR) technique.. The score of neurological behavior of rats in model group, theanine-low, middle, high dose groups at the 3rd hour was 6.000 ± 0.926, 4.100 ± 0.738, 3.444 ± 0.726 and 2.250 ± 0.886 respectively (F = 29.70, P < 0.01), and the score at the 24th hour in these groups was 6.625 ± 0.916, 5.000 ± 0.817, 3.667 ± 0.707 and 2.625 ± 0.916 respectively(F = 34.68, P < 0.01). The concentration of DA in model group, theanine-low, middle, high dose groups and sham-operation group was (10.26 ± 1.12), (12.48 ± 1.09), (14.55 ± 0.94), (15.97 ± 0.92) and (11.98 ± 0.63) µg/g respectively (F = 43.76, P < 0.01). The concentration of 5-HT in these groups was (1.091 ± 0.160), (0.818 ± 0.101), (0.571 ± 0.050), (0.453 ± 0.111) and (0.863 ± 0.063) µg/g respectively (F = 48.68, P < 0.01). The level of ROS was (3.072 ± 0.503), (1.331 ± 0.268), (1.295 ± 0.061), (0.804 ± 0.200) and (2.158 ± 0.218) U×min⁻¹×mg⁻¹ (F = 80.82, P < 0.01) respectively and the activities of CAT in these groups were (4.880 ± 1.121), (8.405 ± 1.356), (9.535 ± 2.511), (15.090 ± 4.054) and (21.260 ± 6.054) U/g respectively (F = 28.58, P < 0.01). The expressions of GluR2 mRNA were 0.842 ± 0.020, 1.063 ± 0.100, 1.170 ± 0.152, 1.254 ± 0.131 and 1.012 ± 0.056 respectively (F = 9.23, P < 0.01). The expressions of PLC-γ1 mRNA in these groups were 0.737 ± 0.090, 0.887 ± 0.045, 0.963 ± 0.025, 0.991 ± 0.049 and 0.867 ± 0.079 respectively(F = 10.24, P < 0.01).. Theanine has a protective effect on the induced brain injury by ischemia-reperfusion in rats, which might be associated with its interaction with monoamine neurotransmitters and up-regulating the expressions of GluR2 mRNA and PLC-γ1 mRNA.

Topics: Animals; Biogenic Monoamines; Brain; Brain Ischemia; Glutamates; Male; Neurotransmitter Agents; Phospholipase C gamma; Rats; Rats, Sprague-Dawley; Receptors, AMPA; Reperfusion Injury; RNA, Messenger

To study the protective effect of theanine on cerebral ischemia-reperfusion injury induced by focal cerebral ischemia in rats.. Sprague-Dawley rats were randomly assigned into five groups: model group, shame (SH) control group and 3 theanine groups (Th-L,Th-M and Th-H). The rats in model and SH groups were given distilled water, and the rats in Th groups were given theanine solution (10, 30 and 90 mg/kg respectively) intragastrically for 15 days. Then the cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion (MCAO) in the model and Th groups, and SH group was used as a fake surgery control. The score of neurological behavior was evaluated at the 3rd and 24th hours after reperfusion. Rats were sacrificed at 24h after reperfusion, and the brain index was measured. The concentrations of aspartic acid (Asp), glutamic acid (Glu), glycine (Gly), gamma-aminobutyricacid (GABA) and theanine (The) in rat brain following ischemia-reperfusion were determined. The expressions of BDNF mRNA and Bcl-2 mRNA in hippocampi were examined by reverse transcription polymerase chain reaction (RT-PCR) technique.. Compared with model control group, the neurological deficits of theanine treated groups were milder; and the symptoms were more gently. The concentration of neurotransmitter Asp was lower while the Gly and GABA were higher, and a trend of dose-effect relation was existed. The expressions of BDNF mRNA and Bcl-2 mRNA in hippocampi were up-regulated in the theanine treated groups compared with model group (P < 0.05).. Theanine has a protective effect on cerebral ischemia-reperfusion injury in rats, which may be associated with its interaction with amino acid neurotransmitters and up-regulating the expression of BDNF mRNA and Bcl-2 mRNA.

Topics: Animals; Aspartic Acid; Brain Ischemia; Brain-Derived Neurotrophic Factor; Glutamates; Male; Neuroprotective Agents; Proto-Oncogene Proteins c-bcl-2; Rats; Rats, Sprague-Dawley; Reperfusion Injury; RNA, Messenger

We examined the protective effect of gamma-glutamylethylamide (theanine) on ischemic delayed neuronal death in field CA1 of the gerbil hippocampus. One microliter of theanine from each three concentrations (50, 125 and 500 microM) was administered through the lateral ventricle 30 min before ischemia. Transient forebrain ischemia was induced by bilateral occlusion of the common carotid arteries for 3 min under careful control of brain temperature at approximately 37 degrees C. Seven days after ischemia, the number of intact CA1 neurons in the hippocampus was assessed. Ischemia-induced neuronal death in hippocampal CA1 region was significantly prevented in a dose-dependent manner in the theanine-pretreated groups. These findings indicate that theanine might be useful clinically for preventing ischemic neuronal damage.

Topics: Animals; Brain Ischemia; Cell Count; Cell Death; Excitatory Amino Acid Antagonists; Gerbillinae; Glutamates; Glutamic Acid; Hippocampus; Nerve Degeneration; Neurons; Neuroprotective Agents; Reperfusion Injury