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early life stress or chronic drug exposure [15,16,17], may lead to redox dysfunction and chronic oxidative stress, strongly linked to the pathophysiology of schizophrenia [18,19,20,21,22]

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Our recent metabolomic analysis has shown that the ocular anti-inflammation caused by GTE was indirect through induced systemic phosphorylcholine lipids to suppress the inflammatory responses and alleviate the hepatic damage and mitochondrial stress [66]

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