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Inhibition of inflammation and oxidative stress by Angelica dahuricae radix extract decreases apoptotic cell death and improves functional recovery after spinal cord injury

Authors

  • Youn Joo Moon,

    1. Age-Related and Brain Diseases Research Center, Kyung Hee University, Seoul, Korea
    2. Neurodegeneration Control Research Center, Kyung Hee University, Seoul, Korea
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  • Jee Youn Lee,

    1. Age-Related and Brain Diseases Research Center, Kyung Hee University, Seoul, Korea
    2. Neurodegeneration Control Research Center, Kyung Hee University, Seoul, Korea
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  • Myung Sook Oh,

    1. Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul, Korea
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  • Youngmi Kim Pak,

    1. Age-Related and Brain Diseases Research Center, Kyung Hee University, Seoul, Korea
    2. Neurodegeneration Control Research Center, Kyung Hee University, Seoul, Korea
    3. Department of Physiology, School of Medicine, Kyung Hee University, Seoul, Korea
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  • Kang-Sik Park,

    1. Neurodegeneration Control Research Center, Kyung Hee University, Seoul, Korea
    2. Department of Physiology, School of Medicine, Kyung Hee University, Seoul, Korea
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  • Tae Hwan Oh,

    1. Age-Related and Brain Diseases Research Center, Kyung Hee University, Seoul, Korea
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  • Tae Young Yune

    Corresponding author
    1. Age-Related and Brain Diseases Research Center, Kyung Hee University, Seoul, Korea
    2. Neurodegeneration Control Research Center, Kyung Hee University, Seoul, Korea
    3. Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul, Korea
    • Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul, Republic of Korea
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Abstract

Inflammation and oxidative stress play major roles in the pathogenesis after spinal cord injury (SCI). Here, we examined the neuroprotective effects of Angelica dahuricae radix (ADR) extract after SCI. ADR extract significantly decreased the levels of proinflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) in a lipopolysaccharide (LPS)-activated microglial cell line, BV2 cells. ADR extract also significantly alleviated the level of reactive oxygen species in LPS-activated BV2 cells. To examine the neuroprotective effect of ADR extract after SCI, spinally injured rats were administered ADR extract orally at a dose of 100 mg/kg for 14 days. ADR extract treatment significantly reduced the levels of TNF-α, IL-1β, IL-6, iNOS, and COX-2. The levels of superoxide anion (O2·) and protein nitration were also significantly decreased by ADR extract. In addition, ADR extract inhibited p38 mitogen-activated protein kinase activation and pronerve growth factor expression in microglia after SCI. Furthermore, ADR extract significantly inhibited caspase-3 activation following apoptotic cell death of neurons and oligodendrocytes, thereby improving functional recovery after injury. Thus, our data suggest that ADR extract provides neuroprotection by alleviating inflammation and oxidative stress and can be used as an orally administered therapeutic agent for acute SCI. © 2011 Wiley Periodicals, Inc.

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