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柚皮油可减轻心肺复苏大鼠模型中脑NLRP3炎性小体的激活。

Pomelo peel oil alleviates cerebral NLRP3 inflammasome activation in a cardiopulmonary resuscitation rat model.

作者信息

Zou Xin-Sen, Xie Lu, Wang Wen-Yan, Zhao Gao-Yang, Tian Xin-Yue, Chen Meng-Hua

机构信息

Intensive Care Unit, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530000, P.R. China.

Department of Physiology, Guangxi Medical University, Nanning, Guangxi 530000, P.R. China.

出版信息

Exp Ther Med. 2021 Mar;21(3):233. doi: 10.3892/etm.2021.9664. Epub 2021 Jan 21.

Abstract

The NLR family pyrin domain-containing 3 (NLRP3) inflammasome, which is composed of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC) and pro-caspase-1 protein complexes, is activated by the reactive oxygen species (ROS) that are associated with ischemia-reperfusion (I/R) and are involved in brain damage. Pomelo peel oil (PPO) exhibits antioxidant activity. However, it is unclear whether PPO is able to attenuate NLRP3 inflammasome-induced inflammation and pyroptosis. Healthy male Sprague-Dawley rats were subjected to 7 min of cardiac arrest via trans-esophageal electrical stimulation, followed by cardiopulmonary resuscitation (CPR). The rats were then treated with PPO prior to reperfusion for 24 h. Hematoxylin and eosin staining was used to evaluate brain tissue and cell damage. In the brain tissues, reactive oxygen species (ROS) were assayed, immunofluorescence was used to analyze the expression of NLRP3 and western blotting was performed to determine the expression levels of neuroenolase (NSE), NF-κB, interleukin-1β (IL-1β), gasdermin D (GSDMD) and the NLRP3 inflammasome. Treatment of the rats with PPO significantly decreased the pathological damage of the brain tissue and reduced the expression of NSE, production of ROS and secretion of NF-κB, NLRP3, IL-1β and GSDMD. In conclusion, these results demonstrate the ability of PPO to protect the brain against I/R injury in rats after CPR by a mechanism involving inhibition of the inflammation and pyroptosis mediated by NLRP3 inflammasome activation.

摘要

含NLR家族pyrin结构域蛋白3(NLRP3)炎性小体由NLRP3、含CARD结构域的凋亡相关斑点样蛋白(ASC)和前半胱天冬酶 - 1蛋白复合物组成,被与缺血再灌注(I/R)相关的活性氧(ROS)激活,并参与脑损伤。柚子皮油(PPO)具有抗氧化活性。然而,尚不清楚PPO是否能够减轻NLRP3炎性小体诱导的炎症和细胞焦亡。健康雄性Sprague-Dawley大鼠经食管电刺激致心脏骤停7分钟,随后进行心肺复苏(CPR)。然后在再灌注前24小时用PPO处理大鼠。苏木精和伊红染色用于评估脑组织和细胞损伤。在脑组织中,检测活性氧(ROS),采用免疫荧光分析NLRP3的表达,并进行蛋白质印迹法测定神经元特异性烯醇化酶(NSE)、核因子κB(NF-κB)、白细胞介素 - 1β(IL-1β)、gasdermin D(GSDMD)和NLRP3炎性小体的表达水平。用PPO处理大鼠可显著降低脑组织的病理损伤,并降低NSE的表达、ROS的产生以及NF-κB、NLRP3、IL-1β和GSDMD的分泌。总之,这些结果表明PPO能够通过抑制NLRP3炎性小体激活介导的炎症和细胞焦亡机制,保护大鼠心肺复苏后大脑免受I/R损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d54b/7851623/03c20eb54c32/etm-21-03-09664-g00.jpg

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