Department of Anesthesiology, Tianjin Medical University NanKai Hospital, Tianjin, China; Department of Anesthesiology, Tianjin NanKai Hospital, Tianjin, China.
Department of Anesthesiology, Tianjin Medical University NanKai Hospital, Tianjin, China.
J Surg Res. 2020 Dec;256:258-266. doi: 10.1016/j.jss.2020.06.056. Epub 2020 Jul 23.
Sepsis-associated encephalopathy (SAE) is a common complication of sepsis. Although sepsis is effectively managed with the administration of antibiotics and source control, which may include surgical intervention, SAE usually leads to prolonged cognitive dysfunction affecting the quality of life of the patients. In this study, we investigated the possible effect of electroacupuncture (EA) on cognition in a model of SAE induced by cecal ligation and puncture (CLP).
The rats were randomly divided into four groups: the control group, the CLP group, the CLP with EA treatment group (CLP + EA), and the CLP with sham EA treatment group (CLP + sham EA). EA at DU20, LI11, and ST36 or sham EA was performed 30 min daily for 10 consecutive days starting from 2 days before CLP. Then cognitive function was examined by the Morris water maze test. On day 14 after CLP surgery, the synaptic injury, neuron loss, and oxidative stress were studied.
Rats with EA treatment showed improved survival rate, spatial learning, and memory abilities. The dendritic spine density, the synaptic proteins, and the hippocampal neuron number were also increased after EA treatment. Furthermore, EA suppressed oxidative stress through regulating the level of malondialdehyde and superoxide dismutase and enhanced the expression of antioxidant nuclear factor erythroid-2-related factor-2 and hemeoxygenase-1. But sham EA did not have the same effect.
EA may protect against SAE-induced cognitive dysfunction by inhibiting synaptic injury, neuronal loss, and oxidative stress, and the nuclear factor erythroid-2-related factor-2/hemeoxygenase-1 signaling pathway may be involved in this effect.
脓毒症相关性脑病(SAE)是脓毒症的常见并发症。尽管通过给予抗生素和控制感染源(包括手术干预)可以有效治疗脓毒症,但 SAE 通常会导致认知功能障碍延长,从而影响患者的生活质量。在本研究中,我们通过盲肠结扎穿孔(CLP)模型研究了电针对 SAE 模型中认知功能的可能影响。
将大鼠随机分为四组:对照组、CLP 组、CLP 加电针(CLP+EA)组和 CLP 加假电针(CLP+ sham EA)组。从 CLP 前 2 天开始,每天进行 30 分钟,连续 10 天,电针于 DU20、LI11 和 ST36 进行或进行假电针。然后通过 Morris 水迷宫测试检查认知功能。CLP 手术后第 14 天,研究突触损伤、神经元丢失和氧化应激情况。
电针治疗组大鼠的存活率、空间学习和记忆能力均有所提高。电针治疗后,树突棘密度、突触蛋白和海马神经元数量也增加。此外,电针通过调节丙二醛和超氧化物歧化酶的水平抑制氧化应激,并增强抗氧化核因子红细胞 2 相关因子 2 和血红素加氧酶-1 的表达。但假电针没有相同的效果。
电针可能通过抑制突触损伤、神经元丢失和氧化应激来保护 SAE 诱导的认知功能障碍,核因子红细胞 2 相关因子 2/血红素加氧酶-1 信号通路可能参与这一作用。