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毛蕊异黄酮对脑出血后继发急性炎症损伤的改善作用及机制
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| 篇名： | 毛蕊异黄酮对脑出血后继发急性炎症损伤的改善作用及机制 |
| TITLE： | Improvement effect and mechanism of calycosin on acute inflammatory injury secondary to intracerebral hemorrhage |
| 摘要： | 目的 探讨毛蕊异黄酮（CA）对脑出血后继发急性炎症损伤的改善作用及机制。方法以雄性C57BL/6小鼠为对象，通过基底节注射Ⅶ型胶原酶构建脑出血模型，分为假手术组（以磷酸盐缓冲液代替胶原酶）、模型组、不同剂量（15、30、60、120mg/kg）CA组。在以改良神经功能缺损程度（mNSS）评分筛选干预剂量的基础上，检测各组小鼠的脑出血体积、脑含水量，脑组织中离子钙结合衔接分子1（Iba1）和脑组织中Toll样受体4（TLR4）及其下游炎症因子[肿瘤坏死因子α（TNF-α）、诱导型一氧化氮合酶（iNOS）、白细胞介素1β（IL-1β）]的表达情况，以及脑组织中细胞的凋亡情况。体外培养原代小胶质细胞，检测其中TLR4及其下游炎症因子的表达情况；体外共培养原代神经元与原代小胶质细胞，检测其中神经元的凋亡情况。结果选取30、60mg/kg作为CA的干预剂量进行后续实验。与假手术组比较，模型组小鼠出现了脑出血现象，脑出血体积和脑含水量均显著升高（P＜0.05），脑组织中Iba1蛋白的表达阳性率显著升高，脑组织中TLR4、TNF-α、IL-1β、iNOS蛋白的相对表达水平均显著上调，细胞凋亡率亦显著增加（P＜0.05）；与模型组比较，30、60mg/kgCA组小鼠上述指标均显著改善（P＜0.05）。CA显著降低了原代小胶质细胞中TLR4及其下游炎症因子的相对表达水平，显著减少了原代神经元与原代小胶质细胞共培养体系中神经元的凋亡（P＜0.05）。结论CA可发挥脑保护作用，可能与抑制TLR4介导的炎症反应而减轻脑出血后继发的急性炎症损伤有关。 |
| ABSTRACT： | OBJECTIVE To investigate the improvement effect and mechanism of calycosin （CA） on acute inflammatory injury secondary to intracerebral hemorrhage. METHODS Male C57BL/6 mice were injected with type Ⅶ collagenase into the basal ganglia to establish an intracerebral hemorrhage model， which were divided into sham-operation group（phosphate buffered saline instead of collagenase）， model group， and different CA dose groups（15，30，60，120 mg/kg）. Based on the modified neurological severity score （mNSS） to screen the intervention doses， the volume of intracerebral hemorrhage， brain water content， the expressions of ionized calcium-binding adaptor molecule 1 （Iba1） in brain tissue， Toll-like receptor 4 （TLR4） and its downstream inflammatory factors [tumor necrosis factor-α （TNF-α）， inducible nitric-oxide synthase （iNOS）， interleukin-1β （IL- 1β）] in brain tissue， and the apoptosis of cells in brain tissue were detected. Primary microglia were cultured in vitro， and the expressions of TLR4 and its downstream inflammatory factors were detected. Primary neurons and primary microglia were co- cultured in vitro， and the apoptosis of neurons was detected. RESULTS The doses of 30 mg/kg and 60 mg/kg were selected as intervention doses of CA for subsequent experiments. Compared with the sham-operation group， the mice in the model group had cerebral hemorrhage， the volume of cerebral hemorrhage and brain water content were significantly increased （P＜0.05）； the positive expression rate of Iba1 protein in brain tissue was significantly increased， and the relative expression levels of TLR4， TNF-α， IL-1β and iNOS protein in brain tissue were up-regulated significantly. The apoptosis rate also increased significantly （P＜0.05）. Compared with model group， the above indexes of the mice in the 30 and 60 mg/kg CA groups were significantly improved （P＜0.05）. CA significantlyreduced the relative expression levels of TLR4 and its downstream inflammatory factors in microglia， and reduced the apoptosis of neurons in the co-culture system of primary neurons and primary microglia （P＜0.05）. CONCLUSIONS CA can exert a protective effect on the brain， which may be related to relieving the secondary acute inflammatory injury after intracerebral hemorrhage by inhibiting TLR4-mediated inflammatory response. |
| 期刊： | 2023年第34卷第16期 |
| 作者： | 柳晓蕊；许智朝；王兆涛；张媚媚；简晓顺；彭怀东 |
| AUTHORS： | LIU Xiaorui，XU Zhichao，WANG Zhaotao，ZHANG Meimei，JIAN Xiaoshun，PENG Huaidong |
| 关键字： | 毛蕊异黄酮；脑出血；继发急性炎症损伤；Toll样受体4；小胶质细胞 |
| KEYWORDS： | calycosin； intracerebral hemorrhage； secondary acute inflammatory injury； Toll-like receptor 4； microglia |
| 阅读数： | 57 次 |
| 本月下载数： | 5 次 |
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