Neurosurgery, Affiliated Hospital of Hebei University, Baoding, 071000, Hebei, China.
Emergency Department, Affiliated Hospital of Hebei University, Baoding, 071000, Hebei, China.
Inflammopharmacology. 2020 Oct;28(5):1327-1341. doi: 10.1007/s10787-020-00714-6. Epub 2020 May 16.
ischaemic stroke accounts for almost 11% of all deaths worldwide and has a high incidence of permanent disability among patients. Baicalein has many beneficial pharmacological properties, including anti-inflammatory and anti-oxidant effects. However, the neuroprotective effect of baicalein is still unclear. The current study scrutinizes the neuroprotective effect of baicalein against the ischaemic/reperfusion (I/R) injury via alteration of the nuclear factor kappa B (NF-kB) and AMP-activated protein kinase/nuclear factor erythroid 2-related factor 2 AMPK/Nrf2 signaling pathway. Wistar rats were used for the current study. In rats, I/R injury was caused by transient occlusion of the middle cerebral artery for 1 h accompanied by reperfusion for 24 h. The rats were divided into different groups and treated with the different doses of baicalein (2.5, 5 and 10 mg/kg). The effects of baicalein on the murine neurological function were determined via infarct volume, neurological defect scores, and brain water content. The -inflammatory cytokines and oxidative stress were estimated in the region of the cortical along with the expression of apoptosis markers, such as B-cell lymphoma 2, Bax, and caspase-3. Quantitative reverse transcription polymerase chain reaction was used for the estimation of the NF-kB, cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2) and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) expression. Baicalein significantly (p < 0.001) ameliorated the infarction volume, brain water content, and neurological outcome, and the malondialdehyde level, and reduced the level of interleukin-1β, interleukin-6, tumor necrosis factor-α, superoxide dismutase, glutathione, and catalase in a dose-dependent manner. Baicalein significantly (p < 0.001) altered the expression of COX-2, PGE2, LOX-1 and NF-kB as compared to I/R control group rats. Baicalein significantly reduced the Nrf2 and AMPK levels, and protected the rat brain against the I/R injury, suggesting a neuroprotective effect via down-regulation of NF-kB and LOX-1 expression and the AMPK/Nrf2 pathway.
缺血性中风约占全球所有死亡人数的 11%，患者永久性残疾的发病率很高。黄芩素具有许多有益的药理特性，包括抗炎和抗氧化作用。然而，黄芩素的神经保护作用尚不清楚。本研究通过改变核因子 kappa B（NF-kB）和 AMP 激活的蛋白激酶/核因子红细胞 2 相关因子 2 AMPK/Nrf2 信号通路，研究了黄芩素对缺血/再灌注（I/R）损伤的神经保护作用。本研究使用 Wistar 大鼠。在大鼠中，通过短暂阻断大脑中动脉 1 小时并再灌注 24 小时来引起 I/R 损伤。大鼠被分为不同的组，并给予不同剂量的黄芩素（2.5、5 和 10mg/kg）进行治疗。通过梗死体积、神经缺陷评分和脑水含量来确定黄芩素对小鼠神经功能的影响。在皮质区域估计炎性细胞因子和氧化应激，以及凋亡标志物（如 B 细胞淋巴瘤 2、Bax 和 caspase-3）的表达。使用定量逆转录聚合酶链反应来估计 NF-kB、环加氧酶-2（COX-2）、前列腺素 E2（PGE2）和凝集素样氧化低密度脂蛋白受体-1（LOX-1）的表达。黄芩素显著（p<0.001）改善了梗死体积、脑水含量和神经功能预后，降低了丙二醛水平，并降低了白细胞介素-1β、白细胞介素-6、肿瘤坏死因子-α、超氧化物歧化酶、谷胱甘肽和过氧化氢酶的水平呈剂量依赖性。与 I/R 对照组大鼠相比，黄芩素显著（p<0.001）改变了 COX-2、PGE2、LOX-1 和 NF-kB 的表达。黄芩素显著降低了 Nrf2 和 AMPK 水平，保护大鼠大脑免受 I/R 损伤，表明通过下调 NF-kB 和 LOX-1 表达以及 AMPK/Nrf2 通路发挥神经保护作用。
