Back to Search
Start Over
Engineered endomorphin-2 gene: A novel therapy for improving morphine reinstatement in CPP model of rats by using deficient adenovirus as the vector.
- Source :
-
Biochemical & Biophysical Research Communications . May2019, Vol. 513 Issue 1, p141-146. 6p. - Publication Year :
- 2019
-
Abstract
- Abstract Optimal therapeutics to deal with high relapse rates when discontinued is urgent for opioid dependence treatments. Endogenous endomorphin-2 (EM2) level in the central nervous system (CNS) down-regulates obviously after sustained morphine exposure, which suggested that to up-regulate the EM2 level could be a novel method for reinstatement. But the clinical applications of EM2 through conventional administration are limited owing to its short half-life. In our study, we engineered an EM2 gene to achieve the sustained release of EM-2 in CNS by utilizing a signal peptide of mouse growth factor for out-secreting EM2 and a deficient adenovirus as the vector. By intrathecally injecting engineering EM2 gene, a sustained increase of EM2 concentration in the cerebral spinal fluid (CSF) was observed along with a reduction of CPP scores. Also, the activation of astrocytes was suppressed in the hippocampus. In summary, this study provides evidence and reference for using intraspinal gene therapy with a combination of mouse growth factor and EM2 to treat morphine reinstatement. Highlights • We engineered an EM2 gene to achieve the sustained release of EM-2 in CNS. • The phenomenon of morphine reinstatement was improved effectively by intrathecally injecting engineering EM2 gene in rats. • The fusion gene of mouse growth factor and EM2 to treat morphine reinstatement shows promising effects. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 0006291X
- Volume :
- 513
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Biochemical & Biophysical Research Communications
- Publication Type :
- Academic Journal
- Accession number :
- 135928119
- Full Text :
- https://doi.org/10.1016/j.bbrc.2019.03.183