TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000250405
  • Gene Name:BCL2L2
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:qRT-PCR
  • mRNA Pathway:NA
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:NA
  • Drug Name:Tetramethylpyrazine
  • Drug Method:down-regulated the gene expression

Disease basic infommation

  • Disease:spinal cord injury
  • Tissue:patients tissues

Other information

  • Title:Tetramethylpyrazine alleviates neural apoptosis in injured spinal cord via the downregulation of miR-214-3p
  • Journal:Biomedicine & Pharmacotherapy
  • Published:2017
  • PubMed ID:28802236
  • Abstract:Objective:To evaluate the regulation effect of tetramethylpyrazine on microRNA-214-3p (miR-214-3p) in the spinal cord injury (SCI) rats model and to elucidate the neuroprotective effect and its mechanism of tetramethylpyrazine after SCI. Methods:Ten Sprague-Dawley rats were used to establish the SCI rats model, and the expression levels of miR-214-3p and Bcl2l2 were detected by qRT-PCR and Western blotting at 7 days post-SCI. BBB scoring test was performed to evaluate the motor functional recovery at 21 days post-SCI. Twenty-five SCI rats were randomly assigned to five groups: SCI negative control (NC) group, tetramethylpyrazine (TMP) group, miR-214-3p agomir group, TMP/agomir group and the sham group. The rats were given a two-week injection treatment with or without TMP. The expression levels of miR-214-3p, Bcl2l2, Bax and caspase 3 were measured by qRT-PCR and Western blotting at 7 days after injection. Terminal deoxynucleotidyl transferase (TdT) -mediated dUTP Nick-End Labeling (TUNEL) assay was performed to detect cell apoptosis in vivo. Luciferase activity was measured to verify the miR-214-3p target site in the 3'-UTR of Bcl2l2 mRNA. TMP treatment was also performed to injure primary cultured neuron cells and cell apoptosis in vitro was determined by flow cytometry. Results:MiR-214-3p was up-regulated while anti-apoptotic protein Bcl2l2 was downregulated post-SCI. TMP inhibited the apoptosis in vivo via decreasing the levels of miR-214-3p and increasing the expression level of Bcl2l2. A potential target site of miR-214-3p in the 3'UTR of Bcl2l2 mRNA was identified and validated by luciferase reporter assay. Furthermore, TMP could effectively inhibit neuron cells apoptosis in vitro. Conclusions:TMP alleviated neural apoptosis in injured spinal cord via down-regulation of miR-214-3p.