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Metformins AMPK-dependent actions also extend to cardiopulmonary I/R models, where it reduces oxidative stress, suppresses inflammatory cytokines (TNF-, IL-1), and inhibits NF-B signaling, collectively preserving tissue integrity ( High-dose metformin treatment to inhibit complex I during early reperfusion protects the aged mouse heart via decreased mitochondrial permeability transition pore opening

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We also detected the expression of the microglial proinflammatory factors IL-1 and TNF- in the TNC during chronic NTG administration