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By integrating findings from experimental and limited clinical studies, it aims to provide a rational scientific framework to inform future investigation and development of ginsenoside-based strategies for depression, while emphasizing the need for further rigorous clinical validation.

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These abnormalities were previously regarded as secondary epiphenomena of metabolic dysfunction, but accumulating evidence now indicates that they arise from hyperglycaemia-driven OCTN2 impairment, insulin resistance, and oxidative stress, together forming a distinct carnitine-related metabolic signature

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