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黄芪甲苷对神经炎症的改善作用及机制研究
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| 篇名： | 黄芪甲苷对神经炎症的改善作用及机制研究 |
| TITLE： | Improvement effects and mechanism of astragaloside Ⅳ on neuroinflammation |
| 摘要： | 目的 探讨黄芪甲苷对脂多糖（LPS）诱导的神经炎症的改善作用及机制。方法将BV2细胞分为对照组、LPS组和黄芪甲苷20、40μmol/L组以及地塞米松组（2μmol/L），给药处理后，除对照组外其余各组加入1μg/mL的LPS以诱导神经炎症细胞模型，再检测各组细胞上清液中炎症因子[白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）、一氧化氮（NO）]水平。将小鼠随机分为正常组、模型组、阳性对照组（阿司匹林肠溶片，20mg/kg）和黄芪甲苷低、高剂量组（10、20mg/kg），每组6只。各组小鼠灌胃/腹腔注射相应药物/生理盐水，每天1次，连续14d。除正常组外，其余各组小鼠每天给药/生理盐水1h后，腹腔注射LPS（250μg/kg）建立神经炎症动物模型。末次注射LPS2h后，检测小鼠血清中IL-6、TNF-α水平；观察小鼠脑组织病理学形态；观察小鼠脑皮质区诱导型一氧化氮合酶（iNOS）/离子化钙结合衔接分子1（Iba1）和CD206/Iba1的共定位情况；检测小鼠脑组织中核因子κB（NF-κB）/丝裂原活化蛋白激酶（MAPK）信号通路相关蛋白[NF-κBp65、磷酸化NF-κBp65（p-NF-κBp65）、p38MAPK、磷酸化p38MAPK（p-p38MAPK）、胞外信号调节激酶（ERK）、磷酸化ERK（p-ERK）]表达水平。结果在细胞实验中，与对照组比较，LPS组细胞上清液中IL-6、TNF-α、NO水平均显著升高（P＜0.05）；与LPS组比较，各给药组细胞上清液中IL-6、TNF-α、NO水平均显著降低（P＜0.05）。在动物实验中，与正常组比较，模型组小鼠血清中IL-6、TNF-α水平和脑皮质区iNOS/Iba1共定位阳性细胞数以及脑组织中p38MAPK、NF-κBp65、ERK蛋白的磷酸化水平均显著升高/增多（P＜0.05），脑皮质区CD206/Iba1共定位阳性细胞数显著减少（P＜0.05），脑皮质区和海马CA3区神经元细胞排列紊乱；与模型组比较，各给药组小鼠上述定量指标均显著逆转（P＜0.05），脑皮质区和海马CA3区神经元细胞排列较为整齐。结论黄芪甲苷可能通过抑制NF-κB/MAPK信号通路激活，促进小胶质细胞发生M2型极化，进而抑制神经炎症反应。 |
| ABSTRACT： | OBJECTIVE To investigate the improvement effects and mechanism of astragaloside Ⅳ （AS- Ⅳ ） on lipopolysaccharide （LPS）-induced neuroinflammation. METHODS BV2 cells were divided into control group， LPS group， AS-Ⅳ groups at concentrations of 20 and 40 μmol/L， and dexamethasone group （2 μmol/L）. Except for control group， neuroinflammation model was established with LPS （1 μg/mL） in other groups after medication. The levels of inflammatory factors [interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and nitric oxide （NO）] in cell supernatant were measured in each group. Mice were randomly divided into normal group， model group， positive control group （Aspirin enteric-coated tablet， 20 mg/kg）， AS-Ⅳ low- and high-dose groups （10， 20 mg/kg）， with 6 mice in each group. Mice in each group were administered the corresponding drug/normal saline via gavage/intraperitoneal injection， once a day， for 14 consecutive days. Except for normal group， other groups were intraperitoneally injected with LPS （250 μg/kg） 1 hour after daily administration of the drug/normal saline to establish neuroinflammation model. Serum levels of IL-6 and TNF-α were measured 2 h after the last medication； histopathological morphology of cerebral tissue in mice were observed； the co-localization of inducible nitric oxide synthase （iNOS）/ionized calcium binding adapter molecule 1 （Iba1） and CD206/Iba1 in the cerebral cortex region of mice was observed； the expressions of proteins related to the nuclear factor-κB （NF-κB）/mitogen-activated protein kinase （MAPK） signaling pathway in brain tissue of mice were also determined， including NF-κB p65， phosphorylated NF-κB p65（p-NF-κB p65）， p38 MAPK， phosphorylated p38 MAPK （p-p38 MAPK）， extracellular signal-regulated kinase （ERK）， and phosphorylated ERK （p-ERK）. RESULTS In the cell experiments， compared with control group， the levels of IL-6， TNF- α and NO in the cell supernatant of the LPS group were increased significantly （P＜0.05）； compared with LPS group， the levels of IL-6， TNF-α and NO were decreased significantly in the administration groups （P＜0.05）. In the animal experiments， compared with the normal group， the serum levels of IL-6 and TNF- α， the number of iNOS/Iba1 co-localization positive cells in the cerebral cortex， and the phosphorylation levels of p38 MAPK， NF- κB p65 and ERK proteins in brain tissue were all significantly increased/elevated in model group （P＜0.05）； the number of CD206/ Iba1 co-localization positive cells in the cerebral cortex region significantly decreased （P＜0.05）. The neurons in the cerebral cortex and the CA3 region of the hippocampus displayed a disordered arrangement. Compared with model group， above quantitative indexes of mice were all reversed significantly in administration groups （P＜0.05）； the neuronal cells in the cerebral cortex and the CA3 region of the hippocampus exhibited a relatively orderly arrangement. CONCLUSIONS AS-Ⅳ may inhibit the activation of the NF-κB/MAPK signaling pathway， promote the M2-type polarization of microglia， and thereby suppress neuroinflammatory responses. |
| 期刊： | 2026年第37卷第01期 |
| 作者： | 王咪咪；冯永岗；韩云；单凯欣；刘福宇；苗明三；方晓艳 |
| AUTHORS： | WANG Mimi，FENG Yonggang，HAN Yun，SHAN Kaixin，LIU Fuyu，MIAO Mingsan，FANG Xiaoyan |
| 关键字： | 黄芪甲苷；小胶质细胞；炎症；表型极化；神经保护 |
| KEYWORDS： | astragaloside Ⅳ； microglia； inflammation； phenotypic polarization； neuroprotection |
| 阅读数： | 80 次 |
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