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黄芩苷通过抑制ROS/NLRP3炎性小体途径减轻脑出血后脑损伤的机制

Mechanism of Baicalein in Brain Injury After Intracerebral Hemorrhage by Inhibiting the ROS/NLRP3 Inflammasome Pathway.

作者信息

Chen Xuan, Zhou Yue, Wang Shanshan, Wang Wei

机构信息

Department of Neurosurgery, The First People's Hospital of Shangqiu, No. 292 Kaixuan Road, Suiyang District, Shangqiu, Henan, China.

Department of Neurological Rehabilitation, Yidu Central Hospital, Weifang, China.

出版信息

Inflammation. 2022 Apr;45(2):590-602. doi: 10.1007/s10753-021-01569-x. Epub 2021 Oct 8.

DOI:10.1007/s10753-021-01569-x
PMID:34625906
Abstract

Intracerebral hemorrhage (ICH) is a devastating subtype of stroke with high disability/mortality. Baicalein has strong anti-inflammatory activity. This study aims to explore the mechanism of baicalein on brain injury after ICH. The model of brain injury after ICH was established by collagenase induction, followed by the evaluation of neurological severity, brain water content, the degenerated neurons, neuronal apoptosis, and reactive oxygen species (ROS). The ICH model was treated with baicalein or silencing NLRP3 to detect brain injury. The expression of NLRP3 inflammasome was detected after treatment with ROS scavenger. The expressions of oxidative stress markers and inflammatory factors were detected, and the levels of components in NLRP3 inflammasome were detected. Baicalein reduced the damage of nervous system, lesion surface, brain water content, and apoptosis. Baicalein inhibited malondialdehyde and increased IL-10 by inhibiting ROS in brain tissue after ICH. Baicalein inhibited the high expression of NLRP3 inflammasome in ICH. ROS scavenger inhibited the NLRP3 inflammatory response by inhibiting ROS levels. Silencing NLRP3 alleviated the brain injury after ICH by inhibiting excessive oxidative stress and inflammatory factors. Overall, baicalein alleviated the brain injury after ICH by inhibiting ROS and NLRP3 inflammasome.

摘要

脑出血(ICH)是一种具有高致残率/死亡率的毁灭性中风亚型。黄芩苷具有很强的抗炎活性。本研究旨在探讨黄芩苷对脑出血后脑损伤的作用机制。通过胶原酶诱导建立脑出血后脑损伤模型,随后评估神经功能严重程度、脑含水量、神经元变性、神经元凋亡和活性氧(ROS)。用黄芩苷或沉默NLRP3处理ICH模型以检测脑损伤。用ROS清除剂处理后检测NLRP3炎性小体的表达。检测氧化应激标志物和炎性因子的表达,并检测NLRP3炎性小体中的成分水平。黄芩苷减轻了神经系统损伤、损伤面积、脑含水量和细胞凋亡。黄芩苷通过抑制脑出血后脑组织中的ROS来抑制丙二醛并增加IL-10。黄芩苷抑制ICH中NLRP3炎性小体的高表达。ROS清除剂通过抑制ROS水平来抑制NLRP3炎症反应。沉默NLRP3通过抑制过度的氧化应激和炎性因子来减轻脑出血后的脑损伤。总体而言,黄芩苷通过抑制ROS和NLRP3炎性小体减轻了脑出血后的脑损伤。

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