Neuroprotective effect of Scutellaria baicalensis on spinal cord injury in rats

被引:44
|
作者
Yune, Tae Y. [1 ,2 ,3 ]
Lee, Jee Y. [1 ,3 ]
Cui, Chun M. [1 ]
Kim, Ho C. [4 ]
Oh, Tae H. [1 ,3 ]
机构
[1] Kyung Hee Univ, Age Related & Brain Dis Res Ctr, Sch Med, Seoul 130701, South Korea
[2] Kyung Hee Univ, Sch Med, Dept Biochem & Mol Biol, Seoul 130701, South Korea
[3] Kyung Hee Univ, Sch Med, Neurodegenerat Control Res Ctr, Seoul 130701, South Korea
[4] Kyung Hee Univ, Coll Oriental Med, Dept Herbal Pharmacol, Seoul 130701, South Korea
关键词
apoptotic cell death; inflammation; neuroprotection; oxidative stress; Scutellaria baicalensis; IMPROVES FUNCTIONAL RECOVERY; TUMOR-NECROSIS-FACTOR; APOPTOTIC CELL-DEATH; ALZHEIMERS-DISEASE; OXIDATIVE STRESS; INFLAMMATORY ACTIVATION; FLAVONOID BAICALEIN; PARKINSONS-DISEASE; NADPH OXIDASE; NITRIC-OXIDE;
D O I
10.1111/j.1471-4159.2009.06214.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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-alpha, interleukin-1 beta, 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-alpha, IL-1 beta, 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.
引用
收藏
页码:1276 / 1287
页数:12
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