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CTRP3过表达对大鼠脑出血后继发性脑损伤的影响及机制

Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats.

作者信息

Wan Yu, Wang Jieqiong, Yang Bo, Huang Conggai, Tang Xiaoqin, Yi Hong, Liu Yun, Wang Shaohua

机构信息

Department of Pathology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuang 646000, P.R. China.

Medical Experiment Research Center, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuang 646000, P.R. China.

出版信息

Exp Ther Med. 2022 Jan;23(1):35. doi: 10.3892/etm.2021.10957. Epub 2021 Nov 9.

DOI:10.3892/etm.2021.10957
PMID:34849150
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8613529/
Abstract

C1q/TNF-related protein-3 (CTRP3) is a novel adipokine that serves an important role in oxidative stress, anti-apoptosis, anti-inflammation and immune regulation. The aim of the present study was to investigate the protective role of CTRP3 against intracerebral hemorrhage (ICH)-induced brain injury. A model of autologous arterial blood-induced ICH was constructed in rats. Intracerebral infusion of a lentivirus carrying the CTRP3 gene was used to induce CTRP3 overexpression in the brain. The effects and mechanisms of CTRP3 overexpression on brain injury were investigated by detecting brain edema, blood-brain barrier (BBB) integrity, neurological function and inflammatory-associated factors 3 days after ICH. The present results demonstrated that CTRP3 overexpression ameliorated ICH-induced neurological dysfunction, decreased brain edema, maintained BBB integrity and attenuated inflammation. The protective effect of CTRP3 overexpression was associated with increased activation of silent information regulator 1 (SIRT1). In conclusion, the present study demonstrated that CTRP3 overexpression protected against ICH-induced brain injury in rats, potentially via activating the SIRT1 signaling pathway.

摘要

C1q/TNF相关蛋白3（CTRP3）是一种新型脂肪因子，在氧化应激、抗凋亡、抗炎和免疫调节中发挥重要作用。本研究旨在探讨CTRP3对脑出血（ICH）诱导的脑损伤的保护作用。在大鼠中构建自体动脉血诱导的ICH模型。通过脑内注射携带CTRP3基因的慢病毒来诱导CTRP3在脑内过表达。在ICH后3天，通过检测脑水肿、血脑屏障（BBB）完整性、神经功能和炎症相关因子，研究CTRP3过表达对脑损伤的影响及机制。目前的结果表明，CTRP3过表达改善了ICH诱导的神经功能障碍，减轻了脑水肿，维持了BBB完整性，并减轻了炎症。CTRP3过表达的保护作用与沉默信息调节因子1（SIRT1）的激活增加有关。总之，本研究表明，CTRP3过表达可保护大鼠免受ICH诱导的脑损伤，可能是通过激活SIRT1信号通路实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/142cc0456e40/etm-23-01-10957-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/1818cd3847d1/etm-23-01-10957-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/97f4a58bc8a4/etm-23-01-10957-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/3bf185a602d0/etm-23-01-10957-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/97d017f864cf/etm-23-01-10957-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/28b74cea1d50/etm-23-01-10957-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/142cc0456e40/etm-23-01-10957-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/1818cd3847d1/etm-23-01-10957-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/97f4a58bc8a4/etm-23-01-10957-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/3bf185a602d0/etm-23-01-10957-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/97d017f864cf/etm-23-01-10957-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/28b74cea1d50/etm-23-01-10957-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e6f/8613529/142cc0456e40/etm-23-01-10957-g05.jpg

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