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Specifically, EA treatment administered to rats for 60 min per day over 3 days significantly attenuated TBI-induced outcomes, including reduced infarct volume, grip strength loss, neuronal apoptosis (caspase-3 and TUNEL), microglia (Iba1), astrocyte (GFAP) activation, and TNF- expression

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These endogenous protective mechanisms provide potential intervention targets for heart failure-associated brain injury and neuroinflammation, revealing the central role of mitochondrial functional integrity in maintaining homeostasis along the heartbrain axis

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A rejection, delay, label limitation, or additional trial requirement would also matter