Huangqin flavonoid extraction for spinal cord injury in a rat model

Flavonoids from Huangqin（dried roots of Scutellaria baicalensis Georgi） have anti-inflammatory effects, and are considered useful for treatment of spinal cord injury. To verify this hypothesis, the T9-10 spinal cord segments of rats were damaged using Allen＇s method to establish a rat spinal cord injury model. Before model establishment, Huangqin flavonoid extraction（12.5 g/kg） was administered intragastrically for 1 week until 28 days after model establishment. Methylprednisolone（30 mg/kg） was injected into the tail vein at 30 minutes after model establishment as a positive control. Basso, Beattie, and Bresnahan locomotor scale scores were used to assess hind limb motor function. Hematoxylin-eosin staining was used to detect pathological changes in the injured spinal cord. Immunofluorescence and western blot assays were performed to measure immunoreactivity and expression levels of brain-derived neurotrophic factor, neuronal marker neurofilament protein, microglial marker CD11 b and astrocyte marker glial fibrillary acidic protein in the injured spinal cord. Huangqin flavonoid extraction markedly reduced spinal cord hematoma, inflammatory cell infiltration and cavities and scars, and increased the Basso, Beattie, and Bresnahan locomotor scale scores; these effects were identical to those of methylprednisolone. Huangqin flavonoid extraction also increased immunoreactivity and expression levels of brain-derived neurotrophic factor and neurofilament protein, and reduced immunoreactivity and expression levels of CD11 b and glial fibrillary acidic protein, in the injured spinal cord. Overall, these data suggest that Huangqin flavonoid extraction can promote recovery of spinal cord injury by inducing brain-derived neurotrophic factor and neurofilament protein expression, reducing microglia activation and regulating reactive astrocytes.

A new look at auranofin,dextromethorphan and rosiglitazone for reduction of glia-mediated inflammation in neurodegenerative diseases

Neurodegenerative disorders including Alzheimer＇s disease are characterized by chronic in- flammation in the central nervous system. The two main glial types involved in inflammatory reactions are microglia and astrocytes. While these cells normally protect neurons by providing nutrients and growth factors, disease specific stimuli can induce glial secretion of neurotoxins. It has been hypothesized that reducing glia-mediated inflammation could diminish neuronal loss. This hypothesis is supported by observations that chronic use of non-steroidal anti-inflamma- tory drugs （NSAIDs） is linked with lower incidences of neurodegenerative disease. It is possible that the NSAIDs are not potent enough to appreciably reduce chronic neuroinflammation after disease processes are fully established. Gold thiol compounds, including auranofin, comprise an- other class of medications effective at reducing peripheral inflammation. We have demonstrated that auranofin inhibits human microglia- and astrocyte-mediated neurotoxicity. Other drugs which are currently used to treat peripheral inflammatory conditions could be helpful in neu- rodegenerative disease. Three different classes of anti-inflammatory compounds, which have a potential to inhibit neuroinflammation are highlighted below.

咖啡酸苯乙酯对抗脂多糖诱导的小胶质细胞炎症反应的作用及其机制的研究

目的探究咖啡酸苯乙酯对脂多糖诱导的小胶质细胞BV-2神经炎症反应的抑制作用及其潜在的作用机制。方法采用脂多糖(1μg·mL-1)诱导小胶质细胞BV-2活化,制作炎症反应模型,利用四甲基偶氮唑蓝法检测细胞存活率,并用酶联免疫法测定咖啡酸苯乙酯对炎症因子一氧化氮、白细胞介素-1β和白细胞介素-6合成释放的影响。然后用蛋白印迹法研究了咖啡酸苯乙酯对炎症相关蛋白(诱导型一氧化氮合酶、环氧化酶-2、IκB以及P-IκB)表达的作用。此外,进一步研究了咖啡酸苯乙酯对炎症转录因子NF-κB核转位的作用。结果咖啡酸苯乙酯与脂多糖(1μg·mL-1)同时作用于BV-2小胶质细胞,分别于温箱中孵育24、8 h收集上清液,检测一氧化氮、白细胞介素-1β、白细胞介素-6的释放量。结果显示,脂多糖(1μg·mL-1)可以造成细胞损伤,增加炎症因子释放,咖啡酸苯乙酯则可以降低脂多糖诱导的小胶质细胞对一氧化氮、白细胞介素-1β和白细胞介素-6的释放,并可抑制诱导型一氧化氮合酶、环氧化酶-2、P-IκB、P-NF-κB蛋白的表达,还可以抑制NF-κB的核转位。结论上述研究说明,咖啡酸苯乙酯(5,10,20μmol·L-1)可以通过抑制炎性因子的表达而减少对小胶质细胞的损伤,其抗炎活性可能是通过抑制NF-κB信号通路介导的炎症反应实现的。