Loading…
Postconditioning of stellate ganglion block improves intestinal barrier function by inhibiting autophagy in conscious rats following hemorrhagic shock and resuscitation
[2,3] Thus, the role of autophagy in SGB protection of the intestinal barrier is unclear. [...]we speculated that SGB postprocessing suppresses the intestinal barrier damage caused by hemorrhagic shock by inhibiting autophagy activation. To verify this hypothesis, we investigated the effects of SGB...
Saved in:
Published in: | Chinese medical journal 2022-04, Vol.135 (8), p.1003-1005 |
---|---|
Main Authors: | , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | [2,3] Thus, the role of autophagy in SGB protection of the intestinal barrier is unclear. [...]we speculated that SGB postprocessing suppresses the intestinal barrier damage caused by hemorrhagic shock by inhibiting autophagy activation. To verify this hypothesis, we investigated the effects of SGB postprocessing on the survival rate, intestinal blood flow, intestinal tissue morphology, intestinal barrier function, and autophagy-related mechanisms in rats that underwent hemorrhagic shock. According to the conventional method in our laboratory,[1] the left side stellate ganglion was blocked by injecting 0.5% ropivacaine hydrochloride (AstraZeneca AB, Sodertalje, Sweden). To define the mechanism by which SGB improves the intestinal barrier, we investigated the expression of microtubule associated protein light chain 3-II (LC3-II) (a marker of autophagy activation), Beclin-1 (a key regulator of autophagosome formation) and p62 and found that there was a significant difference in the expression levels among these groups (F = 7.098, P = 0.003 for LC3; F = 9.698, P = 0.001 for Beclin-1; F = 21.874, P = 0.000 |
---|---|
ISSN: | 0366-6999 2542-5641 |
DOI: | 10.1097/CM9.0000000000001968 |