Effect of Mir-21-3p on Intestinal Injury in Rats With Traumatic Hemorrhagic Shock Resuscitated With the Sodium Bicarbonate Ringer's Solution

Abstract

Background This study aims to determine the impact and mechanism of miR-21-3p on intestinal injury and intestinal glycocalyx during fluid resuscitation in traumatic hemorrhagic shock (THS), and the different impacts of sodium lactate Ringer's solution (LRS) and sodium bicarbonate Ringer's solution (BRS) for resuscitation on intestinal damage. Methods A rat model of THS was induced by hemorrhage from the left femur fracture. The pathological changes of intestinal tissues and glycocalyx structure were observed by hematoxylin-eosin (H&E) staining and transmission electron microscope. MiR-21-3p expression in intestinal tissues was detected by real-time quantitative polymerasechain reaction (RT-qPCR). The expression of glycocalyx-, cell junction- and PI3K/Akt/NF-κB signaling pathway- related proteins was analyzed by western blot. Results MiR-21-3p expression was increased in THS rats, which was suppressed by resuscitation with BRS. BRS or LRS aggravated the intestinal injury and damaged intestinal glycocalyx in THS rats. The expression of SDC-1, HPA, β-catenin, MMP2 and MMP9 was upregulated, the expression of E-cad was downregulated and the PI3K/Akt/NF-κB signaling pathway was activated in THS rats, which were further aggravated by BRS or LRS. The side effect of LRS was more serious than BRS. MiR-21-3p overexpression deteriorated the injury of intestinal tissues and intestinal glycocalyx, increased the expression of SDC-1, HPA, β-catenin, MMP2 and MMP9 while decreased E-cad expression, and activated the PI3K/Akt/NF-κB signaling pathway in BRS-resuscitated THS rats. Conclusion MiR-21-3p aggravated intestinal tissue injury and intestinal glycocalyx damage through activating PI3K/Akt/NF-κB signaling pathway in rats with THS resuscitated with BRS.