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L-theanine protects against D-galactose-induced aging in L6 skeletal muscle cells
[Display omitted] •L-theanine improved cell viability, antioxidant enzyme activities, and inhibited increases in proinflammatory factors in aged L6 cells.•L-theanine reduced senescence markers, decreased ROS and MDA, maintained mitochondrial membrane potential, and inhibited apoptosis.•L-theanine...
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Published in: | Journal of functional foods 2024-05, Vol.116, p.106135, Article 106135 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | [Display omitted]
•L-theanine improved cell viability, antioxidant enzyme activities, and inhibited increases in proinflammatory factors in aged L6 cells.•L-theanine reduced senescence markers, decreased ROS and MDA, maintained mitochondrial membrane potential, and inhibited apoptosis.•L-theanine's anti-aging effects may involve regulating cell cycle proteins to reduce arrest and promote proliferation and regulating apoptosis proteins via p53/Bax/Bcl-2.•L-theanine's protection against D-galactose-induced L6 cell aging may involve activating the p53/p21/CDK4 pathway.
L-theanine (LTA) is a key component in tea plants and is commonly used as a functional ingredient and dietary supplement. In a recent study, we investigated the potential antiaging properties of LTA using a D-galactose-induced L6 skeletal muscle aging cell model. The results showed that LTA treatment improved cell viability and antioxidant enzyme activities while reducing levels of proinflammatory factors and advanced glycation end products. Additionally, LTA demonstrated the ability to decrease senescence-associated beta-galactosidase-positive cells, lower reactive oxygen species and MDA levels, preserve mitochondrial function, inhibit apoptosis, and alleviate cell cycle arrest in the G2/M phase. These protective effects may be attributed to the activation of the p53/p21/CDK4 pathway, regulation of cell cycle-related protein expression, promotion of cell proliferation, and regulation of apoptosis-related protein expression through the p53/Bax/Bcl-2 pathway. |
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ISSN: | 1756-4646 2214-9414 |
DOI: | 10.1016/j.jff.2024.106135 |