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 3 h 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.

严重失血性休克导致过度炎症和免疫功能障碍，导致与肠系膜淋巴回流相关的高死亡率。最近的一项研究表明，星状神经节阻滞（SGB）可以提高失血性休克大鼠的存活率。然而，SGB是否能改善失血性休克引起的免疫功能障碍仍不清楚。本研究的目的是验证SGB对失血性休克大鼠脾脏CD4+T细胞增殖和功能的有利影响，并探讨SGB与自噬和失血性休克后肠系膜淋巴相互作用的相关机制。 PHSML）。雄性大鼠接受 SGB 或假 SGB 和有意识的急性出血，然后进行复苏和多次治疗。复苏3小时后，分离脾CD4+T细胞以测量ConA体外刺激后的增殖和细胞因子的产生。用从SBG处理的大鼠中引流的PHSML处理从正常大鼠中分离的CD4 + T细胞，并检测增殖、细胞因子产生和自噬生物标志物。失血性休克减少了 CD4 + T 细胞的增殖以及白细胞介素 (IL)-2、IL-4 和肿瘤坏死因子-α 诱导蛋白 8 样 2 (TIPE2) 的产生。 SGB 或自噬抑制剂 3-甲基腺嘌呤 (3-MA) 的使用使这些指标正常化。相反，给予雷帕霉素（RAPA）自噬激动剂或静脉注射PHSML抑制了SGB对失血性休克大鼠的CD4+T细胞的有益作用。此外，PHSML 孵育可减少正常 CD4 + T 细胞中的增殖和细胞因子产生，增加 LC3 II/I 和 Beclin-1 表达，并减少 p-PI3K 和 p-Akt 表达。 PHSML 的这些副作用也可以通过 3-MA 给药以及与从 SGB 处理的大鼠获得的 PHSML 一起孵育来消除。 SGB改善失血性休克后脾脏CD4+T细胞功能，这与抑制PHSML介导的自噬有关。