Hao Guangzhi, Dong Yushu, Huo Rentao, Wen Kai, Zhang Yinsong, Liang Guobiao
Institute of Neurology, The Graduate Training Base of the General Hospital of Shenyang Military Area Command of PLA of Liaoning Medical College, Shenyang, 110016, Liaoning, China.
Institute of Neurology, General Hospital of Shenyang Military Area Command, 83# Wenhua Road, Shenhe District, Shenyang, 110016, Liaoning, China.
Neurochem Res. 2016 Jun;41(6):1496-504. doi: 10.1007/s11064-016-1863-7. Epub 2016 Feb 11.
As is known to all, neuroinflammation plays a vital role in early brain injury pathogenesis following subarachnoid hemorrhage (SAH). It has been shown that rutin have a property of inhibiting inflammation in many kinds of animal models. However, the effect of rutin on neuroinflammation after SAH remains uninvestigated. In this study, we investigated the potential effects of rutin on neuroinflammation and the underlying mechanism in an experimental rat model of SAH performed by endovascular perforation. Adult male SD rats were randomly divided into three groups, including sham group, SAH + vehicle group and SAH + rutin group (50 mg/kg) intraperitoneally (i.p.) administered at 30 min after SAH. After sacrificed at 24 h after SAH, all rats were examined by following tests, including neurologic scores, blood-brain barrier permeability, brain water content and neuronal cell death in cerebral cortex. The level of inflammation in brain was estimated by means of multiple molecules, including RAGE, NF-κB, and inflammation cytokines. Our results indicated that rutin could significantly downregulate the increased level of REGE, NF-κB and inflammatory cytokines in protein level. In addition, rutin could also ameliorate a series of secondary brain injuries such as brain edema, destruction of blood-brain barrier, neurological deficits and neuronal death. This study indicated that rutin administration had a neuroprotective effect in an experimental rat model of SAH, possibly through inhibiting RAGE-NF-κB mediated inflammation signaling pathway.
众所周知,神经炎症在蛛网膜下腔出血(SAH)后的早期脑损伤发病机制中起着至关重要的作用。研究表明,芦丁在多种动物模型中具有抑制炎症的特性。然而,芦丁对SAH后神经炎症的影响仍未得到研究。在本研究中,我们通过血管内穿刺建立实验性大鼠SAH模型,研究了芦丁对神经炎症的潜在影响及其潜在机制。成年雄性SD大鼠随机分为三组,包括假手术组、SAH + 溶剂组和SAH + 芦丁组(50 mg/kg),于SAH后30分钟腹腔注射给药。SAH后24小时处死所有大鼠,通过以下测试进行检查,包括神经功能评分、血脑屏障通透性、脑含水量和大脑皮质神经元细胞死亡情况。通过多种分子,包括晚期糖基化终末产物受体(RAGE)、核因子κB(NF-κB)和炎症细胞因子来评估脑内炎症水平。我们的结果表明,芦丁可显著下调蛋白水平升高的RAGE、NF-κB和炎症细胞因子水平。此外,芦丁还可改善一系列继发性脑损伤,如脑水肿、血脑屏障破坏、神经功能缺损和神经元死亡。本研究表明,在实验性大鼠SAH模型中,给予芦丁具有神经保护作用,可能是通过抑制RAGE-NF-κB介导的炎症信号通路实现的。