Zhenbao pill protects against acute spinal cord injury via miR-146a-5p regulating the expression of GPR17
The aim of the present study was to observe the effect of zhenbao pill on the motor function of acute spinal cord injury (ASCI) rats and the molecular mechanisms involving and G-protein-coupled receptor 17 (GPR17). ASCI rat model was established by modified Allen method, and then the rats were divid...
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Veröffentlicht in: | Bioscience reports 2018-02, Vol.38 (1) |
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Sprache: | eng |
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Zusammenfassung: | The aim of the present study was to observe the effect of zhenbao pill on the motor function of acute spinal cord injury (ASCI) rats and the molecular mechanisms involving
and G-protein-coupled receptor 17 (GPR17). ASCI rat model was established by modified Allen method, and then the rats were divided into three groups. SH-SY5Y cells were cultured overnight in hypoxia condition and transfected with
mimic or
inhibitor. The hind limb motor function of the rats was evaluated by Basso, Beattie, Bresnahan (BBB) scoring system. Quantitative real-time PCR (qRT-PCR) and Western blot were used to detect the expression of
, GPR17, inducible nitric oxide synthase (iNOS), interleukin 1β (IL-1β), and tumor necrosis factor α (TNF-α). Neuronal apoptosis was measured using flow cytometry assay. Luciferase reporter assay was performed to determine the regulation of
on GPR17. Zhenbao pill could enhance hind limb motor function and attenuate the inflammatory response caused by ASCI. Moreover, zhenbao pill increased the level of
and decreased GPR17 expression
Bioinformatics software predicted that GPR17 3'-UTR had a binding site with
Luciferase reporter assay showed that
had a negative regulatory effect on GPR17 expression. Knockdown of
could reverse the effect of zhenbao pill on the up-regulation of GPR17 induced by hypoxia, reversed the inhibitory effect of zhenbao pill on the cell apoptosis induced by hypoxia and the recovery of zhenbao pill on hind limb motor function in ASCI rats. Zhenbao pill could inhibit neuronal apoptosis by regulating
/GPR17 expression, and then promoting the recovery of spinal cord function. |
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ISSN: | 0144-8463 1573-4935 |
DOI: | 10.1042/BSR20171132 |