But did they account for the fact that
rodent inflammation does not correlate to human inflammation?
At least for those following up this research in humans.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0071056
Abstract
Following
traumatic brain injury (TBI) neuroinflammatory processes promote
neuronal cell loss. Alpha-melanocyte-stimulating hormone (α-MSH) is a
neuropeptide with immunomodulatory properties, which may offer
neuroprotection. Due to short half-life and pigmentary side-effects of
α-MSH, the C-terminal tripeptide α-MSH(11–13) may be an
anti-inflammatory alternative. The present study investigated the mRNA
concentrations of the precursor hormone proopiomelanocortin (POMC) and
of melanocortin receptors 1 and 4 (MC1R/MC4R) in naive mice and 15 min,
6, 12, 24, and 48 h after controlled cortical impact (CCI). Regulation
of POMC and MC4R expression did not change after trauma, while MC1R
levels increased over time with a 3-fold maximum at 12 h compared to
naive brain tissue. The effect of α-MSH(11–13) on secondary lesion
volume determined in cresyl violet stained sections (intraperitoneal
injection 30 min after insult of 1 mg/kg α-MSH(11–13) or 0.9% NaCl)
showed a considerable smaller trauma in α-MSH(11–13) injected mice. The
expression of the inflammatory markers TNF-α and IL-1β as well as the
total amount of Iba-1 positive cells were not reduced. However, cell
branch counting of Iba-1 positive cells revealed a reduced activation of
microglia. Furthermore, tripeptide injection reduced neuronal apoptosis
analyzed by cleaved caspase-3 and NeuN staining. Based on the results
single α-MSH(11–13) administration offers a promising neuroprotective
property by modulation of inflammation and prevention of apoptosis after
traumatic brain injury.
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