Open AccessDl‐3‐n‐butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF‐κB signalling
Author(s) -
He Zili,
Zhou Yulong,
Lin Li,
Wang Qingqing,
Khor Sinan,
Mao Yuqin,
Li Jiawei,
Zhen Zengming,
Chen Jian,
Gao Zhenzhen,
Wu Fenzan,
Zhang Xie,
Zhang Hongyu,
Xu HuaZi,
Wang Zhouguang,
Xiao Jian
Publication year - 2017
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13212
Subject(s) - microglia , tlr4 , neuroprotection , spinal cord injury , pharmacology , lipopolysaccharide , nf κb , in vivo , downregulation and upregulation , proinflammatory cytokine , inflammation , apoptosis , stimulation , chemistry , medicine , spinal cord , immunology , endocrinology , biology , biochemistry , microbiology and biotechnology , psychiatry , gene
In this study, we examined the neuroprotective effects and anti‐inflammatory properties of Dl‐3‐n‐butylphthalide (NBP) in Sprague‐Dawley (SD) rats following traumatic spinal cord injury (SCI) as well as microglia activation and inflammatory response both in vivo and in vitro . Our results showed that NBP improved the locomotor recovery of SD rats after SCI an significantly diminished the lesion cavity area of the spinal cord, apoptotic activity in neurons, and the number of TUNEL‐positive cells at 7 days post‐injury. NBP inhibited activation of microglia, diminished the release of inflammatory mediators, and reduced the upregulation of microglial TLR4/NF‐κB expression at 1 day post‐injury. In a co‐culture system with BV‐2 cells and PC12 cells, NBP significantly reduced the cytotoxicity of BV‐2 cells following lipopolysaccharide (LPS) stimulation. In addition, NBP reduced the activation of BV‐2 cells, diminished the release of inflammatory mediators, and inhibited microglial TLR4/NF‐κB expression in BV‐2 cells. Our findings demonstrate that NBP may have neuroprotective and anti‐inflammatory properties in the treatment of SCI by inhibiting the activation of microglia via TLR4/NF‐κB signalling.