The Protective Effect of Notoginsenoside R1 on Isoflurane-Induced Neurological Impairment in the Rats via Regulating miR-29a Expression and Neuroinflammation.

IF 2.2 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Neuroimmunomodulation Pub Date : 2022-01-01 Epub Date: 2021-08-24 DOI:10.1159/000518215

Meijing Wang, Hongyan Liu, Lufeng Xu, Mengmeng Li, Ming Zhao

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引用次数: 3

Abstract

Introduction: Isoflurane inhalation leads to apoptotic neurodegeneration and further results in learning and cognitive dysfunction. Notoginsenoside R1 (NGR1), a major ingredient from Radix notoginseng, has been reported to exert neuroprotective effect during brain or neuron injury. This study aimed to investigate the effect of NGR1 on neurological impairment.

Methods: Sixty-four male Sprague Dawley rat pups (15-20 g) of postnatal day 7 were recruited. Spatial learning and memory were assessed by the Morris water maze test, and the neurological severity score was determined. Real-time quantitative PCR was used to detect the expression levels of microRNA (miR)-29a. Enzyme-linked immunosorbent assay was applied to estimate the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in the hippocampal tissues.

Results: NGR1 attenuated neurological impairment induced by isoflurane, shown by the decrease in neurological function score and escape latency and the increase in staying time in the original quadrant in rats. NGR1 reversed the downregulation of miR-29a expression induced by isoflurane treatment. After the treatment of NGR1, the elevated levels of IL-6, TNF-α, and IL-1β induced by isoflurane were all decreased significantly in the hippocampal tissues of rats. Additionally, the repressive action of NGR1 in neurological impairment and neuroinflammation was eliminated by downregulating miR-29a in rats.

Conclusion: NGR1 protects against isoflurane-induced neurological impairment. The protective effect of NGR1 might be achieved by promoting the expression of miR-29a and preventing inflammatory response.

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三七皂苷R1通过调节miR-29a表达和神经炎症对异氟醚诱导的大鼠神经损伤的保护作用

简介:吸入异氟醚可导致神经细胞凋亡性变性，并进一步导致学习和认知功能障碍。三七皂苷R1 (NGR1)是三七的主要成分，在脑或神经元损伤中具有神经保护作用。本研究旨在探讨NGR1对神经功能障碍的影响。方法:选取出生第7天雄性大鼠64只(15 ~ 20 g)。采用Morris水迷宫测验评估空间学习记忆能力，并测定神经系统严重程度评分。实时荧光定量PCR检测miR -29a的表达水平。采用酶联免疫吸附法测定大鼠海马组织中白细胞介素-1β (IL-1β)、白细胞介素-6 (IL-6)、肿瘤坏死因子-α (TNF-α)水平。结果:NGR1能减轻异氟醚所致的神经功能损伤，表现为神经功能评分和逃避潜伏期降低，原象限停留时间增加。NGR1逆转异氟烷处理诱导的miR-29a表达下调。经NGR1处理后，异氟醚诱导的大鼠海马组织中IL-6、TNF-α、IL-1β水平升高均明显降低。此外，下调miR-29a可消除NGR1在大鼠神经损伤和神经炎症中的抑制作用。结论:NGR1对异氟醚所致神经损伤具有保护作用。NGR1的保护作用可能是通过促进miR-29a的表达和抑制炎症反应来实现的。

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来源期刊

Neuroimmunomodulation 医学-免疫学

CiteScore

3.60

自引率

4.20%

发文量

审稿时长

>12 weeks

期刊介绍： The rapidly expanding area of research known as neuroimmunomodulation explores the way in which the nervous system interacts with the immune system via neural, hormonal, and paracrine actions. Encompassing both basic and clinical research, ''Neuroimmunomodulation'' reports on all aspects of these interactions. Basic investigations consider all neural and humoral networks from molecular genetics through cell regulation to integrative systems of the body. The journal also aims to clarify the basic mechanisms involved in the pathogenesis of the CNS pathology in AIDS patients and in various neurodegenerative diseases. Although primarily devoted to research articles, timely reviews are published on a regular basis.