I'm sure no followup has occurred with NO stroke leadership.
Pros on using this:
Cons on using this:
Linjie Zhang
and
Li Yang *
Department of Neurology, Tianjin
Neurological Institute, Tianjin Medical University General Hospital,
154, Anshan Road, Heping District, Tianjin 300052, China
*
Author to whom correspondence should be addressed; Tel.: +86-22-6081-4536; Fax: +86-22-6081-7471.
Academic Editor:
Derek J. McPhee
Received: 24 October 2014 / Accepted: 19 December 2014 / Published: 26 December 2014
Abstract
:
Immune responses play an important role in the pathophysiology of
atherosclerosis and ischemic stroke. Atherosclerosis is a common
condition that increases the risk of stroke. Hyperlipidemia damages
endothelial cells, thus initiating chemokine pathways and the release of
inflammatory cytokines—this represents the first step in the
inflammatory response to atherosclerosis. Blocking blood flow in the
brain leads to ischemic stroke, and deprives neurons of oxygen and
energy. Damaged neurons release danger-associated molecular patterns,
which promote the activation of innate immune cells and the release of
inflammatory cytokines. The nuclear factor κ-light-chain-enhancer of
activated B cells κB (NF-κB) pathway plays a key role in the
pathogenesis of atherosclerosis and ischemic stroke. Vinpocetine is
believed to be a potent anti-inflammatory agent and has been used to
treat cerebrovascular disorders. Vinpocetine improves neuronal
plasticity and reduces the release of inflammatory cytokines and
chemokines from endothelial cells, vascular smooth muscle cells,
macrophages, and microglia, by inhibiting the inhibitor of the NF-κB
pathway. This review clarifies the anti-inflammatory role of vinpocetine
in atherosclerosis and ischemic stroke.
In mice or humans?
ReplyDeleteQuestions like that should be addressed to our stroke leaders in control of that stroke research database. I don't have the minions or money to get actual full text research.
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