Department of General Surgery, Ningbo Zhenhai Longsai Hospital, Ningbo, Zhejiang Province 315200, China.
Comput Math Methods Med. 2022 Feb 8;2022:5262189. doi: 10.1155/2022/5262189. eCollection 2022.
Severe traumatic shock is one of the leading causes of death in young adults. A large number of studies have shown that effective volumetry resuscitation on the basis of controlled injury can not only increase the success rate of early resuscitation but also reduce systemic inflammatory response and improve the cure rate of severe traumatic shock. The study explored the effects of hydroxyethyl starch (HES) on the survival rate, lymphocyte function and proliferation of rats with traumatic shock, and the potential mechanisms.
Traumatic shock was constructed in rats as experimental model, and liquid resuscitation was performed using HES and lactated Ringer's (LR). 24-h mortality was recorded, and lymphocytes were isolated. The expressions of signaling pathway factors was detected by qPCR and Western blot. ELISA was performed to determine the expression of interleukin 6 (IL-6) and tumor necrosis factor- (TNF-) in cell supernatant.
HES for fluid resuscitation augmented the survival of traumatic shock rats, upregulated the expressions of MEK and ERK1/2, and downregulated the expressions of IL-6 and TNF-. However, inhibition of ERK signaling pathway reversed the effect of HES on the immune improvement and the 24-h survival rate of the traumatic shock rats ( < 0.05).
HES could exert the anti-inflammatory effects on lymphocytes by mediating the phosphorylation of proteins of the ERK signaling pathway. HSE demonstrated a high efficacy in effectively treating traumatic shock, thus could be used in clinical practice.
严重创伤性休克是导致年轻人死亡的主要原因之一。大量研究表明，在控制损伤的基础上进行有效的容量复苏，不仅可以提高早期复苏的成功率，还可以减轻全身炎症反应，提高严重创伤性休克的治愈率。本研究探讨了羟乙基淀粉（HES）对创伤性休克大鼠生存率、淋巴细胞功能和增殖的影响及其潜在机制。
以大鼠创伤性休克模型为实验模型，采用 HES 和乳酸林格氏液（LR）进行液体复苏。记录 24 小时死亡率，并分离淋巴细胞。通过 qPCR 和 Western blot 检测信号通路因子的表达。采用 ELISA 法测定细胞上清液中白细胞介素 6（IL-6）和肿瘤坏死因子-（TNF-）的表达。
HES 进行液体复苏可提高创伤性休克大鼠的生存率，上调 MEK 和 ERK1/2 的表达，下调 IL-6 和 TNF-的表达。然而，抑制 ERK 信号通路逆转了 HES 对免疫改善和创伤性休克大鼠 24 小时生存率的影响（<0.05）。
HES 可通过调节 ERK 信号通路蛋白的磷酸化对淋巴细胞发挥抗炎作用。HES 在有效治疗创伤性休克方面具有较高的疗效，因此可在临床实践中应用。
