ScienceDaily (Dec. 18, 2007) — Stroke is the term used to describe deteriorating brain function due to either the leaking of blood vessels (hemorrhage) or oxygen deprivation (ischemia) in the brain.

Secretoneurin (SN) is a neural protein with various roles in the normal functioning of the brain and nervous system.

For example, SN increases blood vessel formation in mouse corneas, and its production is increased following transient brain ischemia in gerbils. In a new study, a team of researchers from the Academia Sinica, Republic of China, and the China Medical University, Republic of China, have revealed a neuroprotective role for SN in a rat model of stroke.

SN production by rats was found to be increased in neuronal and endothelial brain cells following the induction of ischemia in the brain. In vitro, SN treatment improved the survival of primary brain cell cultures subjected to oxygen/glucose deprivation.

Cell rescue was dependent on SN-induced expression of proteins that prevent a form of cell death called apoptosis.

Furthermore, when rats with ischemia-induced stroke were injected with SN, they exhibited reduced cerebral tissue death, improved motor performance, and enhanced brain function. In addition, stem cell targeting to the brain and subsequent blood vessel formation were also incited by SN injection in these animals.

From these results, the authors suggest that SN holds promise as a powerful small-molecule drug in the treatment of stroke.

Article title: Secretoneurin promotes neuroprotection and neuronal plasticity via the Jak2/Stat3 pathway in murine models of stroke

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