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SGB Postconditioning Improves Intestinal Barrier Function by Inhibiting Autophagy in Conscious Rats Following Hemorrhagic Shock and Resuscitation

Authors :
Ting-Jiao Suo
Qi Sun
Zhong-Hua Li
Jia-Yi Zhai
Hui-Bo Du
Zhen-Ao Zhao
Chun-Yu Niu
Zigang Zhao
Fu-long Li
Wen-Di Wang
Publication Year :
2021
Publisher :
Research Square Platform LLC, 2021.

Abstract

Background Intestinal barrier dysfunction is the critical link of distant organ injury caused by hemorrhagic shock. The role of autophagy in ischemic intestinal injury has been paid more and more attention. Prophylactic treatment of stellate ganglion block (SGB) reduces intestinal barrier dysfunction induced by haemorrhagic shock. This study investigated the role of SGB post-processing on improved bowel barrier function and autophagy-related mechanisms of action after haemorrhagic shock. Methods The model of hemorrhagic shock in conscious rats was established, and the rats were treated with SGB, autophagy inhibitor 3- methyladenine (3-MA) at the time of fluid resuscitation. We detected the survival rate, intestinal loop blood flow, intestinal barrier permeability, intestinal morphology, wet/dry ratio (W/D), the intestinal barrier and autophagy marker proteins. Simultaneously, we also observed the effect of autophagy activator rapamycin (RAPA) on SGB. Results SGB postconditioning significantly prolonged the overall survival and enhanced survival rate of 72 hours in rats after hemorrhagic shock. SGB post-processing and 3-MA administration improved the intestinal morphology and intestinal permeability, increased the intestinal loop blood flow and expression of ZO1, Occludin and Claudin-1, and decreased the intestinal W/D and LC3 and Beclin-1 expressions, expected for increased P62. Meanwhile, RAPA partially inhibited the effect of SGB on above indices in haemorrhagic shock rats. Conclusion SGB postconditioning alleviates the intestinal barrier dysfunction caused by haemorrhagic shock, which is related to the inhibition of excessive autophagy.

Details

Database :
OpenAIRE
Accession number :
edsair.doi...........ad9067eb5d21f351920d12976a45625f