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首页> 外文期刊>International journal of molecular medicine >Kappa opioid receptor agonists improve postoperative cognitive dysfunction in rats via the JAK2/STAT3 signaling pathway
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Kappa opioid receptor agonists improve postoperative cognitive dysfunction in rats via the JAK2/STAT3 signaling pathway

机译：Kappa阿片受体激动剂通过JAK2 / Stat3信号通路改善大鼠术后认知功能障碍

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摘要

Postoperative cognitive dysfunction (POCD) is a common and well-known complication following surgery, particularly cardiopulmonary bypass (CPB) surgery. There are currently no suitable treatments for POCD, which is associated with increased illness and mortality rates. The present study aimed to identify a novel treatment for POCD. The protective effect of kappa opioid receptor (KOR) agonists on POCD in rats following CPB was determined and the regulatory mechanism of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway was examined. The rats were randomly divided into five groups: Sham operation (Sham group), CPB operation (CPB group), KOR agonist + CPB (K group), KOR agonist + norbinaltorphimine (nor-BNI) + CPB (NK group), and KOR agonist + JAK2-STAT3 specific pathway inhibitor + CPB (AG group). A water maze test and neurological function scores were used to evaluate POCD. Hematoxylin and eosin staining was used to observe hippocampal neurons. ELISA was used to detect the levels of inflammatory factors, oxidative stress factors and brain injury markers. Immunofluorescence was used to visualize the neurons. TUNEL staining and western blotting were used to detect neuronal apoptosis, and western blotting was also used to detect JAK2/STAT3 pathway-related proteins. The KOR agonists significantly improved POCD. S-100 beta and NSE detection revealed that KOR agonists alleviated brain damage in CPB rats, and this result was reversed by KOR antagonists. The KOR agonists led to a significantly reduced inflammatory response and oxidative stress, as determined by ELISA detection, and attenuated hippocampal neuronal apoptosis, as revealed by TUNEL staining and western blotting, compared with the results in the CPB group. Finally, the KOR agonists inhibited the expression levels of phosphorylated (p-)JAK2 and p-STAT3, rather than total JAK2 and STAT3, compared with levels in the CPB group. Taken together, KOR agonists improved POCD in rats with CPB by inhibiting the JAK2/STAT3 signaling pathway.
机译：术后认知功能障碍（POCD）是手术后常见且众所周知的并发症，特别是心肺旁路（CPB）手术。目前没有适当的POCD治疗，这与疾病增加和死亡率增加。本研究旨在鉴定对POCD的新型治疗方法。确定了καapioid受体（KOR）激动剂对CPB之后大鼠POCD的保护作用，研究了Janus激酶2 /信号传感器和转录3（JAK2 / Stat3）信号传导途径的调节机制。将大鼠随机分为五组：假手术（假手术组），CPB操作（CPB组），Kor激动剂+ CPB（K组），Kor Agonist + NorbinalTorphimine（NOR-BNI）+ CPB（NK组）和KOR激动剂+ JAK2-STAT3特异性途径抑制剂+ CPB（AG组）。水迷宫试验和神经功能评分用于评估POCD。苏木精和曙红染色用于观察海马神经元。 ELISA用于检测炎症因素，氧化应激因子和脑损伤标志物的水平。使用免疫荧光可视化神经元。使用TUNEL染色和Western Blotting来检测神经元细胞凋亡，并且蛋白质印迹还用于检测JAK2 / Stat3途径相关蛋白。 kor激动剂显着改善了POCD。 S-100β和NSE检测显示kor激动剂缓解了CPB大鼠的脑损伤，而KOR拮抗剂则逆转该结果。与CPB组的结果相比，KOR激动剂导致炎症反应和氧化应激显着降低的炎症反应和氧化应激，并通过TUNEL染色和蛋白质印迹所揭示的。最后，与CPB组中的水平相比，kor激动剂抑制了磷酸化（P-）JAK2和P-STAT3，而不是总JAK2和Stat3的表达水平。一起服用，kor激动剂通过抑制JAK2 / Stat3信号通路，通过CPB改善大鼠的POCD。

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