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Neuroprotective effect of Scutellaria baicalensis on spinal cord injury in rats
Author(s) -
Yune Tae Y.,
Lee Jee Y.,
Cui Chun M.,
Kim Ho C.,
Oh Tae H.
Publication year - 2009
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2009.06214.x
Subject(s) - neuroprotection , scutellaria baicalensis , proinflammatory cytokine , nitric oxide , pharmacology , spinal cord injury , microglia , nitric oxide synthase , oxidative stress , inflammation , reactive oxygen species , tumor necrosis factor alpha , apoptosis , medicine , chemistry , spinal cord , immunology , biochemistry , endocrinology , pathology , alternative medicine , traditional chinese medicine , psychiatry
Inflammation has been known to play an important role in the pathogenesis after spinal cord injury (SCI). Microglia are activated after injury and produce a variety of proinflammatory factors such as tumor necrosis factor‐α, interleukin‐1β, cyclooxygenase‐2, and reactive oxygen species leading to apoptosis of neurons and oligodendrocytes. In this study, we examined the neuroprotective effects of total ethanol extract of Scutellaria baicalensis (EESB) , after SCI. Using primary microglial cultures, EESB treatment significantly inhibited lipopolysaccharide‐induced expression of such inflammatory mediators as tumor necrosis factor‐α, IL‐1β, IL‐6, cyclooxygenase‐2, and inducible nitric oxide synthase. Furthermore, reactive oxygen species and nitric oxide production were significantly attenuated by EESB treatment. For in vivo study, rats that had received a moderate spinal cord contusion injury at T9 received EESB orally at a dose of 100 mg/kg. EESB inhibited expression of proinflammatory factors and protein carbonylation and nitration after SCI. EESB also inhibited microglial activation at 4 h after injury. Furthermore, EESB significantly inhibited apoptotic cell death of neurons and oligodendrocytes and improved functional recovery after SCI. Lesion cavity and myelin loss were also reduced following EESB treatment. Thus, our data suggest that EESB significantly improve functional recovery by inhibiting inflammation and oxidative stress after injury.