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This was achieved by reducing colony formation and invasion, or by activating the cascade of Bax/Bcl-2/Caspase-3 (58)

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This selectivity makes it ideal for modeling growth hormone (GH) release mechanisms while avoiding off-target effects such as ACTH, prolactin, FSH, LH, TSH, or cortisol modulation

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Oxidative stress also activates the Kelch-like ECH-associated protein 1 (Keap1)-Nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) redox regulator pathway, releasing Nrf2 to regulate the expression of genes that control antioxidant, inflammatory and immune system responses, facilitating GSH activity