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This research aims to explore the neuroprotective potential of hepatic cooling in ischemic stroke through modulation of liver-derived FGF21.

February 2, 2026Stroke

Abstract DP077: Neuroprotective Potential of Remote Hepatic Cooling in Ischemic Stroke via Modulation of Liver-derived FGF21

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This research aims to explore the neuroprotective potential of hepatic cooling in ischemic stroke through modulation of liver-derived FGF21.
Performed middle cerebral artery occlusion (MCAO) in male Sprague-Dawley rats
Applied hepatic cooling (HC) before reperfusion at 34°C
Measured infarct volume and neurological outcomes using various motor and cognitive tests
Analyzed mRNA and protein levels of TNF-α and FGF21 in various tissues
Evaluated hepatic oxidative stress through SOD and MDA levels
Hepatic cooling significantly reduced infarct volume and improved neurological outcomes
Stroke caused increased hepatic oxidative stress and TNF-α levels, which HC effectively reversed
Cerebral TNF-α knockdown prevented stroke-induced FGF21 elevation
Hepatic cooling suppressed both hepatic and neuronal FGF21 expression, limiting brain injury

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Demonstrates hepatic cooling enhances neurological outcomes in ischemic stroke, suggesting it as a neuroprotective strategy.

Wang et al. (2026) studied this question.

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