Hydrogen sulfide upregulated lncRNA CasC7 to reduce neuronal cell apoptosis in spinal cord ischemia-reperfusion injury rat - 04/02/18
, Min Yin b, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
Objective |
Hydrogen sulfide has been recognized as an important neuroprotective agent in the nervous system. The present study aimed to study the effect and the underlying mechanisms of hydrogen sulfide on spinal cord ischemia-reperfusion injury (SCII).
Methods |
The gene mRNA and protein expression were examined by RT-PCR and western blot, respectively. Spinal cord infarct zone was analyzed by Triphenyltetrazolium chloride staining. Cell apoptosis was detected by MTT assay. The relationship between miR-30c and CasC7 was analyzed by RNA immunoprecipitation (RIP) and RNA pull-down.
Results |
We observed that SCII rat model have a bigger spinal cord infarct zone than the control rat, but NaSH preprocessing could reduce spinal cord infarct zone in SCII rat. OGD/R induced cell apoptosis, and NaSH preprocessing reduced the OGD/R-induced SH5Y-SY cells apoptosis. CasC7 was decreased in SCII rat and OGD/R-induced SH5Y-SY cells, while miR-30c expression was increased. NaSH preprocessing upregulated CasC7 and downregulated miR-30c in OGD/R-induced SH5Y-SY cells. In OGD/R induced SH5Y-SY cells with NaSH preprocessing, knockdown of CasC7 could upregulate miR-30c expression, promote cell apoptosis and downregulate miR-30c’s target gene expression. The RIP and RNA pull-down demonstrated that CasC7 functioned as a miR-30c decoy, and miR-30c inhibitor could reverse the effect of si-CasC7. Moreover, intrathecal injection of si-CasC7 upregulated miR-30c expression and increased spinal cord infarct zone in SCII rat with NaSH preprocessing.
Conclusion |
Hydrogen sulfide protects spinal cord by upregulating CasC7 expression in SCII rat model.
Le texte complet de cet article est disponible en PDF.Keywords : lncRNA CASC7, miR-30c, Spinal cord ischemia-reperfusion injury, Apoptosis
Plan
Vol 98
P. 856-862 - février 2018 Retour au numéro
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