Paeoniflorin is a natural monoterpene glucoside from Paeoniae Radix with neuroprotective properties. However, it is still unclear whether paeoniflorin has neuroprotective effects on subarachnoid hemorrhage (SAH). This study explores the effect of paeoniflorin on early brain injury (EBI) using rat SAH model. We found that paeoniflorin significantly improves neurological deficits, attenuates brain water content and Evans blue extravasation at 72 h after SAH. Paeoniflorin attenuates the oxidative stress following SAH as evidenced by decrease of reactive oxygen species (ROS), malondialdehyde (MDA), 3-Nitrotyrosine, and 8-Hydroxy-2-deoxy guanosine (8-OHDG) level, increase of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase activity, and up-regulates the nuclear factor erythroid‑related factor 2 (Nrf2)/heme oxygenase‑1 (HO-1) pathway. Inhibition of microglia activation and neuro-inflammatory response both contributed to paeoniflorin’s protective effects. Moreover, paeoniflorin treatment significantly reduces the ratio of Bax/Bcl-2, active caspase-3/ neuronal nuclei (NeuN) and TUNEL/DAPI positive cells at 72 h following SAH. Our results indicate that paeoniflorin may attenuate early brain injury after experimental SAH.

Paeoniflorin 是一种来自 Paeoniae Radix 的天然单萜糖苷，具有神经保护特性。然而，芍药苷是否对蛛网膜下腔出血（SAH）具有神经保护作用尚不清楚。本研究使用大鼠 SAH 模型探讨芍药苷对早期脑损伤 (EBI) 的影响。我们发现芍药苷显着改善神经功能缺损，减少 SAH 后 72 小时的脑水含量和伊文思蓝外渗。芍药苷减轻 SAH 后的氧化应激，表现为活性氧 (ROS)、丙二醛 (MDA)、3-硝基酪氨酸和 8-羟基-2-脱氧鸟苷 (8-OHDG) 水平降低，超氧化物歧化酶 (SOD) 增加)、谷胱甘肽过氧化物酶 (GSH-Px) 和过氧化氢酶活性，并上调核因子红细胞相关因子 2 (Nrf2)/血红素加氧酶-1 (HO-1) 通路。抑制小胶质细胞激活和神经炎症反应都有助于芍药苷的保护作用。此外，芍药苷处理显着降低了 SAH 后 72 小时内 Bax/Bcl-2、活性 caspase-3/神经元核 (NeuN) 和 TUNEL/DAPI 阳性细胞的比率。我们的结果表明芍药苷可能减轻实验性 SAH 后的早期脑损伤。