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In summary, GSH enables antibiotic inactivation by serving as a substrate for detoxifying enzymes, such as FosA, and by modulating the expression or stability of antibiotic-degrading enzymes, including the downregulation of NDM-1
Cell Journal, 16 (2), 187194
It promotes cell migration, angiogenesis, anti-inflammatory regulation, and anti-apoptotic signaling, all critical for wound repair
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