Item request has been placed!
×
Item request cannot be made.
×
![loading](/sites/all/modules/hf_eds/images/loading.gif)
Processing Request
Administration of all-trans retinoic acid after experimental traumatic brain injury is brain protective.
Item request has been placed!
×
Item request cannot be made.
×
![loading](/sites/all/modules/hf_eds/images/loading.gif)
Processing Request
- معلومة اضافية
- المصدر:
Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5381 (Electronic) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE
- بيانات النشر:
Publication: London : Wiley
Original Publication: London, Macmillian Journals Ltd.
- الموضوع:
- نبذة مختصرة :
Background and Purpose: All-trans retinoic acid (ATRA) is a vitamin A metabolite, important in the developing and mature brain. Pre-injury ATRA administration ameliorates ischaemic brain insults in rodents. This study examined the effects of post-traumatic ATRA treatment in experimental traumatic brain injury (TBI).
Experimental Approach: Male adult mice were subjected to the controlled cortical impact model of TBI or sham procedure and killed at 7 or 30 days post-injury (dpi). ATRA (10 mg kg-1, i.p.) was given immediately after the injury and 1, 2 and 3 dpi. Neurological function and sensorimotor coordination were evaluated. Brains were processed for (immuno-) histological, mRNA and protein analyses (qPCR and western blot).
Key Results: ATRA treatment reduced brain lesion size, reactive astrogliosis and axonal injury at 7 dpi, and hippocampal granule cell layer (GCL) integrity was protected at 7 and 30 dpi, independent of cell proliferation in neurogenic niches and blood-brain barrier damage. Neurological and motor deficits over time and the brain tissue loss at 30 dpi were not affected by ATRA treatment. ATRA decreased gene expression of markers for damage-associated molecular pattern (HMGB1), apoptosis (caspase-3 and Bax), activated microglia (TSPO), and reactive astrogliosis (GFAP, SerpinA3N) at 7 dpi and a subset of markers at 30 dpi (TSPO, GFAP).
Conclusion and Implications: In experimental TBI, post-traumatic ATRA administration exerted brain protective effects, including long-term protection of GCL integrity, but did not affect neurological and motor deficits. Further investigations are required to optimize treatment regimens to enhance ATRA's brain protective effects and improve outcomes.
(© 2020. The British Pharmacological Society.)
- References:
J Neurotrauma. 2009 Aug;26(8):1353-9. (PMID: 19344293)
Neurochem Res. 2013 Dec;38(12):2604-15. (PMID: 24158695)
Nat Rev Neurosci. 2007 Oct;8(10):755-65. (PMID: 17882253)
Glia. 2005 Apr 1;50(1):21-31. (PMID: 15602748)
J Cereb Blood Flow Metab. 2004 Feb;24(2):133-50. (PMID: 14747740)
J Neurochem. 2010 Sep 1;114(5):1511-26. (PMID: 20557428)
J Neurosci. 2018 Jun 6;38(23):5277-5288. (PMID: 29760176)
Br J Pharmacol. 2016 Feb;173(4):692-702. (PMID: 25752446)
PLoS One. 2012;7(8):e43829. (PMID: 22952778)
Stem Cell Reports. 2018 Jun 5;10(6):1705-1720. (PMID: 29805108)
BMC Neurosci. 2016 Jul 15;17(1):49. (PMID: 27422020)
J Neurosci Res. 2008 Apr;86(5):1125-31. (PMID: 17975839)
Drug Metab Dispos. 2000 Feb;28(2):205-8. (PMID: 10640519)
PLoS One. 2012;7(7):e41892. (PMID: 22911864)
Apoptosis. 2009 Nov;14(11):1289-98. (PMID: 19771521)
J Neurosci Res. 2017 Mar;95(3):897-906. (PMID: 27448243)
Cell Mol Life Sci. 2015 Apr;72(8):1559-76. (PMID: 25558812)
Eur J Pharmacol. 2010 Jun 10;635(1-3):56-61. (PMID: 20303946)
Br J Pharmacol. 2016 Feb;173(4):681-91. (PMID: 25939377)
Nature. 2017 Jan 26;541(7638):481-487. (PMID: 28099414)
Br J Pharmacol. 2019 Dec;176 Suppl 1:S297-S396. (PMID: 31710714)
Leukemia. 2018 Jun;32(6):1277-1294. (PMID: 29743722)
Br J Pharmacol. 2019 Dec;176 Suppl 1:S229-S246. (PMID: 31710718)
J Neuroimmunol. 2016 Nov 15;300:21-29. (PMID: 27806872)
Mol Imaging Biol. 2018 Feb;20(1):94-102. (PMID: 28695372)
J Neurochem. 2017 Dec;143(5):523-533. (PMID: 28921587)
Br J Pharmacol. 2020 Nov;177(22):5208-5223. (PMID: 32964418)
J Neuroimmunol. 2006 Feb;171(1-2):135-44. (PMID: 16303184)
Br J Pharmacol. 2018 Apr;175(7):987-993. (PMID: 29520785)
Front Immunol. 2016 Dec 05;7:556. (PMID: 27994591)
Front Aging Neurosci. 2015 Mar 06;7:20. (PMID: 25798108)
Int J Dev Neurosci. 1990;8(3):317-26. (PMID: 2201170)
J Neuroinflammation. 2014 Jun 12;11:106. (PMID: 24924349)
Nature. 2011 Mar 10;471(7337):220-4. (PMID: 21307853)
J Neurosci. 2012 May 2;32(18):6391-410. (PMID: 22553043)
Trends Pharmacol Sci. 2010 Dec;31(12):596-604. (PMID: 21035878)
CNS Drugs. 2016 Sep;30(9):791-806. (PMID: 27339615)
Glia. 2014 Jan;62(1):26-38. (PMID: 24166800)
Mol Brain. 2018 Mar 13;11(1):14. (PMID: 29534734)
J Neurotrauma. 2011 Mar;28(3):359-69. (PMID: 21190398)
Immunity. 2017 Jun 20;46(6):957-967. (PMID: 28636962)
J Neurochem. 2019 Jul;150(2):173-187. (PMID: 30790293)
Neuromolecular Med. 2003;3(2):65-94. (PMID: 12728191)
Nat Rev Neurol. 2017 Mar;13(3):171-191. (PMID: 28186177)
J Biol Chem. 2015 Sep 11;290(37):22532-42. (PMID: 26240147)
Braz J Med Biol Res. 2017 Apr 03;50(4):e5561. (PMID: 28380213)
PLoS One. 2016 Sep 09;11(9):e0162626. (PMID: 27611191)
Brain Struct Funct. 2017 Dec;222(9):4005-4021. (PMID: 28589257)
J Neuroinflammation. 2019 Aug 31;16(1):175. (PMID: 31472680)
Glia. 2017 Feb;65(2):278-292. (PMID: 27778404)
Front Neurosci. 2019 Jan 23;13:07. (PMID: 30728762)
Neurobiol Dis. 2010 Feb;37(2):267-74. (PMID: 19909815)
J Neuroimmunol. 2013 Mar 15;256(1-2):1-6. (PMID: 23385081)
Br J Pharmacol. 2020 Aug;177(16):3611-3616. (PMID: 32662875)
Neurochem Res. 2018 Jun;43(6):1283-1296. (PMID: 29802528)
J Histochem Cytochem. 2017 Feb;65(2):69-81. (PMID: 27856824)
Cell Tissue Res. 2014 Aug;357(2):395-405. (PMID: 24715113)
J Neurosci. 2015 Nov 25;35(47):15731-45. (PMID: 26609164)
NeuroRx. 2004 Jan;1(1):5-16. (PMID: 15717003)
Br J Pharmacol. 2018 Feb;175(3):407-411. (PMID: 29350411)
J Neurotrauma. 2015 Nov 15;32(22):1777-88. (PMID: 26102571)
Matrix Biol. 2018 Aug;68-69:571-588. (PMID: 29054751)
J Neurotrauma. 2015 Oct 15;32(20):1599-607. (PMID: 25879397)
Neurobiol Dis. 2012 Jun;46(3):745-58. (PMID: 22426396)
Nat Rev Neurosci. 2013 Feb;14(2):128-42. (PMID: 23329160)
J Cell Sci. 2002 Dec 15;115(Pt 24):4735-41. (PMID: 12432062)
PLoS Biol. 2020 Jul 14;18(7):e3000410. (PMID: 32663219)
Exp Brain Res. 2009 Mar;193(4):581-9. (PMID: 19050858)
J Neurosci. 1997 Oct 1;17(19):7415-24. (PMID: 9295387)
J Neuroinflammation. 2019 Aug 5;16(1):163. (PMID: 31383034)
Pharmacol Res. 2015 Sep;99:125-36. (PMID: 26066585)
Sci Rep. 2017 Jul 3;7(1):4512. (PMID: 28674431)
Trends Neurosci. 2000 Feb;23(2):59. (PMID: 10652545)
Lancet Public Health. 2016 Dec;1(2):e76-e83. (PMID: 29253420)
J Exp Med. 2009 Sep 28;206(10):2131-9. (PMID: 19737861)
J Neuroinflammation. 2016 Jun 07;13(1):140. (PMID: 27266706)
- Grant Information:
SCHA1261/4-3 Deutsche Forschungsgemeinschaft; China Scholarship Council
- Contributed Indexing:
Keywords: all-trans retinoic acid; apoptosis; astrogliosis; axonal injury; hippocampus; neuroinflammation; traumatic brain injury
- الرقم المعرف:
5688UTC01R (Tretinoin)
- الموضوع:
Date Created: 20200923 Date Completed: 20210621 Latest Revision: 20231112
- الموضوع:
20231112
- الرقم المعرف:
PMC7588818
- الرقم المعرف:
10.1111/bph.15259
- الرقم المعرف:
32964418
No Comments.