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.
Neuroimmunomodulation

中文翻译：

---

三七皂甙 R1 通过调节 miR-29a 表达和神经炎症对异氟醚所致大鼠神经损伤的保护作用

简介：吸入异氟醚会导致凋亡性神经变性，并进一步导致学习和认知功能障碍。据报道，三七中的主要成分三七皂甙 R1 (NGR1) 在脑或神经元损伤期间发挥神经保护作用。本研究旨在探讨 NGR1 对神经损伤的影响。方法：招募了出生后第 7 天的 64 只雄性 Sprague Dawley 幼鼠 (15-20 g)。通过Morris水迷宫测试评估空间学习和记忆，并确定神经严重程度评分。实时定量 PCR 用于检测 microRNA (miR)-29a 的表达水平。应用酶联免疫吸附试验估计海马组织中白细胞介素 1β (IL-1β)、白细胞介素 6 (IL-6) 和肿瘤坏死因子-α (TNF-α) 的水平。结果：NGR1减轻异氟醚引起的神经损伤，表现为大鼠神经功能评分和逃逸潜伏期的降低以及在原始象限停留时间的增加。NGR1 逆转了异氟醚处理诱导的 miR-29a 表达的下调。NGR1处理后，异氟醚诱导的大鼠海马组织中IL-6、TNF-α和IL-1β水平升高均显着降低。此外，通过下调大鼠中的 miR-29a，可以消除 NGR1 在神经损伤和神经炎症中的抑制作用。结论： NGR1 可防止异氟醚引起的神经损伤。NGR1的保护作用可能通过促进miR-29a的表达和阻止炎症反应来实现。
神经免疫调节