Among these drugs was SNC80, a small molecule drug originally developed as a nonaddictive pain reliever that acts independently of the mu-opioid pathway.12 This drug caught our attention because it has been shown to induce hypothermia and protect against the effects of spinal cord ischemia in rodents.
Specifically, reduced functionality of the mitochondrial electron transport chain system without the endogenous antioxidant and anti-inflammatory molecules released by hibernators can result in the release of reactive oxygen species and cause tissue damage.8
Several molecular strategies have been proposed to achieve metabolic suppression for organ preservation, including modulating H2S, AMPK, opioid receptors, microRNAs, HO-1, and Nrf2.8 H2S exposure has been reported to induce a hypometabolic state (reduced metabolism and body temperature) in a rodent model
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