Abstract
Severe hemorrhagic shock leads to excessive inflammation and immune dysfunction, which results in high mortality related to mesenteric lymph return. A recent study showed that stellate ganglion block (SGB) increased the survival rate in rats suffering hemorrhagic shock. However, whether SGB ameliorates immune dysfunction induced by hemorrhagic shock remains unknown. The aim of the present study was to verify the favorable effects of SGB on the proliferation and function of splenic CD4 + T cells isolated from rats that underwent hemorrhagic shock and to investigate the mechanism related to the SGB interaction with autophagy and posthemorrhagic shock mesenteric lymph (PHSML). Male rats underwent SGB or sham SGB and conscious acute hemorrhage followed by resuscitation and multiple treatments. After 3h of resuscitation, splenic CD4 + T cells were isolated to measure proliferation and cytokine production following stimulation with ConA in vitro. CD4 + T cells isolated from normal rats were treated with PHSML drained from SBG-treated rats, and proliferation, cytokine production, and autophagy biomarkers were detected. Hemorrhagic shock reduced CD4 + T cell proliferation and production of interleukin (IL)-2, IL-4, and tumor necrosis factor-α-induced protein 8-like 2 (TIPE2). SGB or administration of the autophagy inhibitor 3-methyladenine (3-MA) normalized these indicators. In contrast, administration of rapamycin (RAPA) autophagy agonist or intravenous injection of PHSML inhibited the beneficial effects of SGB on CD4 + T cells from hemorrhagic shocked rats. Furthermore, PHSML incubation decreased proliferation and cytokine production, increased LC3 II/I and Beclin-1 expression, and reduced p-PI3K and p-Akt expression in normal CD4 + T cells. These adverse effects of PHSML were also abolished by 3-MA administration, as well as incubation with PHSML obtained from SGB-treated rats. SGB improves splenic CD4 + T cell function following hemorrhagic shock, which is related to the inhibition of PHSML-mediated autophagy.
Highlights
Hemorrhagic shock is an acute and critical pathological process, which is more common in traumatic hemorrhage, postpartum hemorrhage, visceral rupture, peptic ulcer, and so on [1]
The CD4 + T cells isolated from normal rats were treated with post-hemorrhagic shock mesenteric lymph (PHSML) drained from rats treated with stellate ganglion block (SGB) or not
Administration of autophagy agonist rapamycin (RAPA) or intravenous injection of PHSML inhibited the beneficial effect of SGB on CD4 + T cells obtained from hemorrhagic shocked rats
Summary
Hemorrhagic shock is an acute and critical pathological process, which is more common in traumatic hemorrhage, postpartum hemorrhage, visceral rupture, peptic ulcer, and so on [1]. Studies have shown that the function of T cells is significantly inhibited after hemorrhagic shock. CD4 + T cell dysfunction has a vital role in the pathogenesis of immunosuppression after hemorrhagic shock. Blockage of post-hemorrhagic shock mesenteric lymph (PHSML) return reduces splenic histological injury and normalizes cellular immune function [8, 9]. Severe hemorrhagic shock leads to excessive inflammation and immune dysfunction, which resulted in high mortality related to mesenteric lymph return. The aim of present study is to verify the favorable effect of SGB on the proliferation and function of splenic CD4 + T cells isolated from rats underwent hemorrhagic shock, and investigate its mechanism focusing autophagy and PHSML
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