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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...

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Bibliographic Details
Published in:Chinese medical journal 2022-04, Vol.135 (8), p.1003-1005
Main Authors: Li, Zhonghua, Wang, Wendi, Sun, Qi, Suo, Tingjiao, Zhai, Jiayi, Du, Huibo, Zhao, Zhen’ao, Li, Fulong, Niu, Chunyu, Zhao, Zigang
Format: Article
Language:English
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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