Rutin Inhibits Neuroinflammation and Provides Neuroprotection in an Experimental Rat Model of Subarachnoid Hemorrhage, Possibly Through Suppressing the RAGE–NF-κB Inflammatory Signaling Pathway

• Published in: Neurochemical research 2016-06, Vol.41 (6), p.1496-1504
• Main Authors: Hao, Guangzhi, Dong, Yushu, Huo, Rentao, Wen, Kai, Zhang, Yinsong, Liang, Guobiao
• Format: Article
• Language: English
• Subjects: Animals; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell Biology; Disease Models, Animal; Inflammation - metabolism; Inflammation - pathology; Inflammation - prevention & control; Inflammation Mediators; Male; Neurochemistry; Neurology; Neuroprotection - drug effects; Neuroprotection - physiology; Neurosciences; NF-kappa B - antagonists & inhibitors; NF-kappa B - metabolism; Original Paper; Rats; Rats, Sprague-Dawley; Receptor for Advanced Glycation End Products - antagonists & inhibitors; Receptor for Advanced Glycation End Products - metabolism; Rutin - pharmacology; Rutin - therapeutic use; Signal Transduction - drug effects; Signal Transduction - physiology; Subarachnoid Hemorrhage - metabolism; Subarachnoid Hemorrhage - pathology; Subarachnoid Hemorrhage - prevention & control
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-016-1863-7

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.