Get your researcher to propose a stroke therapy protocol based on this research.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0045118
Abstract Top
Activation
of the sigma-1 receptor (Sig-1R) improves functional recovery in models
of experimental stroke and is known to modulate microglia function. The
present study was conducted to investigate if Sig-1R activation after
experimental stroke affects mediators of the inflammatory response in
the ischemic hemisphere. Male Wistar rats were subjected to transient
occlusion of the middle cerebral artery (MCAO) and injected with the
specific Sig-1R agonist
1-(3,4-dimethoxyphenethyl)-4-(3-phenylpropyl)piperazinedihydrochloride
(SA4503) or saline for 5 days starting on day 2 after MCAO. Treatment
did not affect the increased levels of the pro-inflammatory cytokines
interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNF-α),
interferon gamma (IFN-γ), interleukin 4 (IL-4), interleukin 5 (IL-5),
and interleukin 13 (IL-13) in the infarct core and peri-infarct area
after MCAO. In addition, treatment with SA4503 did not affect elevated
levels of nitrite, TNF-α and IL-1β observed in primary cultures of
microglia exposed to combined Hypoxia/Aglycemia, while the unspecific
sigma receptor ligand 1,3-di-o-tolylguanidine (DTG) significantly
decreased the production of nitrite and levels of TNF-α. Analysis of the
ischemic hemisphere also revealed increased levels of ionized calcium
binding adaptor molecule 1 (Iba1) levels in the infarct core of SA4503
treated animals. However, no difference in Iba1 immunoreactivity was
detected in the infarct core. Also, levels of the proliferation marker
proliferating cell nuclear antigen (PCNA) and OX-42 were not increased
in the infarct core in rats treated with SA4503. Together, our results
suggest that sigma-1 receptor activation affects Iba1 expression in
microglia/macrophages of the ischemic hemisphere after experimental
stroke but does not affect post-stroke inflammatory mediators.
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