Article Sidebar
Published:
May 29, 2022Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Probucol reduces the cerebral edema area and infarction volume in rat cerebral infarction model via PI3K/Akt pathway
Abstract
Purpose: To study the effects of probucol on rats with cerebral infarction through the phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (Akt) pathway.
Methods: Sprague-Dawley (SD) rats were divided into sham group (SO group, n = 7), model group (MO group, n = 7) and probucol group (PR group, n = 7). Infarction volume, messenger ribonucleic acid (mRNA), protein expressions of PI3K/Akt, neurological score, brain water content, degree of brain tissue lesions and neurological function score were determined.
Results: Neurological score was 0, 2.54 ± 0.67 and 1.34 ± 0.21 points, in SO, O and PR groups, respectively. In turning angle test, neurological function score gradually rose at 24 h after cerebral infarction in PR and MO groups, compared with that in the SO group (p < 0.05), but significantly declined at 48 h in PR group compared with that in MO group (p < 0.05). Brain water content was lowest in the SO group but highest in MO group; it was significantly lower in PR group than that in MO group (p < 0.05). The mRNA and protein expressions of PI3K/Akt were highest in SO group and lowest in MO group; the expressions were higher in PR group than those in the MO group (p < 0.05).
Conclusion: Probucol reduces the cerebral edema area and infarction volume by activating PI3K/Akt pathway, thereby exerting a significant therapeutic effect on rat model with cerebral infarction. Thus, this agent has the potential for use in the management of cerebral infarction.
