RenaissanceMan
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- Jun 30, 2021
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Protective Effect and Mechanism of Theanine on Lipopolysaccharide-Induced Inflammation and Acute Liver Injury in Mice - PubMed
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...
pubmed.ncbi.nlm.nih.gov
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.
A Focus on the Effect of L-Theanine on Improving Depression and Cognition in C57BL/J Male Mice Subjected for Chronic Stress Induced Neuroinflammation
Introduction One of the serious burden of society is stress which may be psychological, physiological or environmental stressors resulting in neuropsychological dysfunction like Major depressive disorder (MDD) with cognitive impairment.1,2 According to world health organization, 350 million peopl
biomedpharmajournal.org
A long term stressful event in life altering immune system is a major factor for the development of psychopathological conditions. By now it’s clear that stress induced neuroinflammatory cytokines are the key role in mediating neurochemical and neuroendocrine systems causing the behavioral disorders and cognitive impairment. Current anti depressants are unable to correct neurotransmitters levels directly or indirectly by inhibiting cytokines expression. Present study was conducted to elucidate the effect and mechanism of L-theanine on chronic restrainer stress (CRS) induced neuroinflammation, anxiety-like, depression, learning and memory impairment in C57BL/J male mice. Chronic restrain stress was induced by well ventilated 50ml conical tube for 6 hours/day 21 consecutive days. After stressor cessation behavioral and recognition tests were conducted, at the end of study mice were sacrificed, brain and blood was collected. Cytokines (TNF-α and IL-6), neurotransmitters were quantified in prefrontal cortex and estimated corticosterone levels in plasma. Histopathological examination of the hippocampus was performed. The results was implicated that L-theanine significantly (p<0.05) reversed the effect of CRS induced behavioral changes and memory impairment, reduced cytokines expression and restored neurotransmitter levels in prefrontal cortex. It also alleviated neuronal apoptosis and lowered the corticosterone levels in plasma of CRS mice. These results indicate that L-theanine exerted protective effect on chronic stress induced neuroinflammation, anxiety, depression and cognitive dysfunction. The mechanism of protective effect is by reducing cytokine expression in frontal cortex and preventing hippocampal apoptosis.