Previous literature has described the significant biological and pharmacological activities of rutin in mammals. Nevertheless, there is no known function or role for Rutin in spinal cord neuroinflammation. In this research, 120 male adult Sprague-Dawley rats were randomly divided into 4 groups (n=30 per group) viz., sham operation (control group), spinal cord injury, methylprednisolone treatment and rutin treatment. Enzyme-linked immunosorbent assay analysis of pro-inflammatory cytokines, malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase were analyzed using kits. Fibroblast growth factor, neurotrophin 3, brain-derived neurotrophic factor, and nerve growth factor, messenger ribonucleic acid level were examined using real-time fluorescent quantitative polymerase chain reaction. Western blot analysis of p38 mitogen-activated protein kinase protein expression relative to the model group (spinal cord injury group), inflammatory cytokines, malondialdehyde levels, spinal cord water content, and p38 mitogen-activated protein kinase protein levels were reduced in the rutin treatment group, however, the superoxide dismutase, catalase, and glutathione peroxidase levels, fibroblast growth factor, neurotrophin 3, brain-derived neurotrophic factor, and nerve growth factor, messenger ribonucleic acid levels, and the blood-brain barrier score (24, 48, 72 h) were increased. Rutin relieves spinal cord neuroinflammation by inhibiting the p38 mitogen-activated protein kinase signaling pathway.

BACKGROUND:This paper analyzed the cases of dural arteriovenous fistula (DAVF) with spinal dural arteriovenous fistula (SDAVF) in the diagnosis and treatment process.CASE PRESENTATION:One case involving dural arteriovenous fistula (DAVF) with spinal dural arteriovenous fistula (SDAVF) from the 306th Hospital of PLA was retrospectively analyzed. The patient consulted the doctor due to lower limb sensory and motor disorders while exhibiting symptoms of urinary dysfunction. A computed tomographic angiography (CTA) and cerebral angiography confirmed the diagnosis of dural arteriovenous fistula (DAVF), necessitating surgical treatment. The patient was referred to our hospital for an magnetic resonance imaging (MRI) and a spinal angiography to obtain a confirmed diagnosis for spinal arteriovenous fistula, after which they underwent surgical fistula resection. The invasive intracranial dural arteriovenous fistula (DAVF) resection proceeded smoothly but did not ease the patient's symptoms. However, postoperative symptoms were partially relieved by the lumbar open spinal dural arteriovenous fistula adminstration.CONCLUSIONS:Since not enough is understood about these two diseases, the rate of misdiagnosis is significantly increased. Early diagnosis and treatment of spinal dural arteriovenous fistula (SDAVF) can play a positive role during the recovery from neural function damage.

Objective To explore the restorative effects and mechanisms of neural stem cell (NSC) transplantation on ischemic brain injury based on the Wnt signaling pathway.Methods Out of 102 male KM mice, 15 were randomly selected as the control group without any intervention, while the remaining 87 underwent middle cerebral artery occlusion (MCAO) using the Zea-Longa suture method. Seven mice that did not successfully model MCAO were excluded, leaving 80 mice that successfully underwent MCAO, randomized into two groups: the Ischemic Brain Injury group (n = 40) receiving 10 mu L of sterile PBS solution injected into the lateral ventricle, and the Ischemic Brain Injury + NSCs Transplantation group (n = 40) receiving 10 mu L of NSCs suspension injected into the lateral ventricle.Results Compared to the ischemic brain injury group, mice in the Ischemic Brain Injury + NSCs Transplantation group exhibited significantly alleviated edema in the middle cerebral artery supply area, with neurons displaying more normal morphological characteristics and fewer signs of degeneration and necrosis. The mice with NSC transplantation had significantly smaller infarct volume than those in the ischemic brain injury group (p < 0.05). The mice with NSC transplantation showed significantly lower Zea-Longa scores and a lower proportion of TUNEL-positive cells compared to those in the ischemic brain injury group (p < 0.05).Conclusion NSC transplantation can significantly inhibit neuronal apoptosis in the ischemic region of mice with ischemic brain injury, alleviate brain tissue edema, reduce infarct volume, and improve neurological function. The mechanism may be related to Wnt signaling pathway activation.

Objective:To provide the preclinical platform for stereotactic autologous neural stem cells(NSCs)transplantation to treat the sequela of encephalorrhagia,cerebral infarction and craniocerebral injury.Methods:The abandoned brain tissues from different areas were collected during open cranial surgery.Above 500 mg abandoned brain tissues in each case were primarily cultured by the modified methods and handed from generation to generation.The expression of Nestin(the marker of NSCs)was detected by immunofluorescence cytochemistry.The induced differentiation began from the 5th generation.Results:About 3 to 10 days after inoculation,stem cells sphere growth was observed in most cases.All the stem cell spheres were positive for Nestin.The 6th generation cells were collected for immunofluorescence cytochemistry with β-Tubulin(the marker of neuron),Sox10(the marker of oligodendrocyte)and GFAP(the marker of astrocyte)respectively,in which a few of the adherent cells were found to be positive as neurons,oligodendrocytes and astrocytes.The Western blotting was performed to 3rd and 6th generation cells.In 3th generation,only Nestin and a few of β-Tubulin were positive.However,in the 6th generation,the Nestin,Sox10,β-Tubulin and GFAP were all found positive on different levels.Conclusion:This study successfully obtains adult NSCs from the abandoned brain tissues in different regions during open cranial surgery and the autologous NSCs could be differentiated into neurons and gliocytes.It is possible for stereotactic autologous NSCs transplantation to repair the neural function from laboratory to clinical applications.

背景:对胎儿、胎鼠及成鼠神经干细胞培养已有大量研究,但成体人自体神经干细胞培养相关研究较少。目的:通过改进原代培养方法,从颅内动脉瘤破裂脑出血患者血肿腔周边废弃脑组织中培养和鉴定神经干细胞,并进行冻存与复苏研究,建立成人自体神经干细胞库。方法:收集3例动脉瘤破裂脑出血（2例大脑中动脉瘤及1例前交通动脉瘤）手术中血肿腔周边的废弃脑组织各约500 mg以上,采用细小组织块接种法进行原代无血清悬浮培养成人自体神经干细胞,倒置显微镜下观察细胞生长情况,免疫荧光细胞化学技术检测神经干细胞标志物巢蛋白（Nestin）的表达。培养获得的神经干细胞球以体积分数4%胎牛血清诱导其贴壁生长,待细胞增殖达到一定数量后传代培养。传代后部分细胞予以冻存建库,并复苏继续传代及诱导分化培养。体积分数10%胎牛血清诱导神经干细胞分化,通过免疫荧光细胞化学技术检测胶质纤维酸性蛋白（标记星形胶质样细胞）,β-tubulinⅢ（标记神经元样细胞）,SOX10（标记少突胶质样细胞）蛋白的表达来测定神经干细胞的分化能力。结果与结论:改进培养方法后,3例患者废弃脑组织中,在无血清培养液中均可形成Nestin阳性表达的神经球,并可在体外大量扩增和连续传代。在给予体积分数10%FBS条件下神经球可分化为神经元样细胞、少突胶质细胞及星形胶质细胞,即β-tubulin Ⅲ,SOX10及胶质纤维酸性蛋白阳性表达。经传代培养至5代后,仍呈Nestin阳性即可维持其神经干细胞特征。冻存细胞复苏后生长状态良好且呈Nestin阳性,可继续传代扩增。结果表明,从动脉瘤破裂脑出血患者不同脑区（颞极及额底）血肿腔周边废弃脑组织中可成功培养获得自体神经干细胞,并可向神经元样细胞、少突胶质样细胞及星形胶质样细胞分化,使自体神经干细胞移植促进神经功能修复从实验室到临床应用成为可能。