X-Message-Number: 27171
Date: Mon, 3 Oct 2005 11:54:49 -0700 (PDT)
From: Doug Skrecky <>
Subject: Ethyl pyruvate is neuroprotective against stroke 24 hrs later

[I'm wondering if perhaps ethyl pyruvate shouldn't be a standard part of
all cryonics protocols. I'm not aware of anything else being this
effective at inhibiting ischemic injury, after such a substantial delay.]

Stroke. 2005 Sep 1; [Epub ahead of print]
Inhibition of the Cerebral Ischemic Injury by Ethyl Pyruvate With a
Wide Therapeutic Window.
BACKGROUND AND PURPOSE: Ethyl pyruvate (EP) is a pyruvate derivative
that has been reported recently to prevent lethality in mice with
established lethal sepsis and systemic inflammation. In this study, we
examined the neuroprotective effect of EP in a rat cerebral ischemia
model of middle cerebral artery occlusion (MCAO). METHODS: Male
Sprague-Dawley rats were subjected to 1 hour of MCAO, and EP was
administered at various time points before or after MCAO. The changes in
the brain infarction, neurological deficits, microglia activation, and
proinflammatory cytokine expression were evaluated. BV2 microglial cells
were also used to access the anti-inflammatory effect of EP. RESULTS:
The administration of EP intraperitoneally at 30 minutes before or at 4
or 12 hours after MCAO reduced the infarct volume to 10.3+/-3.4% (n=6;
P<0.05), 21.5+/-2.7% (n=6; P<0.05), and 44.3+/-4.0% (n=6; P<0.05),
respectively, of that of the control group. The significant reduction in
infarct volume was accompanied by the suppression of the clinical
manifestations associated with cerebral ischemia, including motor
impairment and neurological deficits, microglial activation, and
proinflammatory cytokine expression. The neuroprotective effect of EP
was yet evident when it was administered as late as 24 hours after
MCAO/reperfusion (76.5+/-4.70%; n=6; P<0.05). EP suppressed
lipopolysaccharide induced activation of BV2 cells, as was evidenced by
a reduction in NO release and the accompanying induction of
proinflammatory cytokines. CONCLUSIONS: These results suggest that EP
affords the strong protection of the delayed cerebral ischemic injury
with a wide therapeutic window.

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