| 黄健
，张玉华
，胡国庆.薯蓣皂苷调控MAPK信号通路减轻小鼠创伤性脑损伤后小胶质细胞介导的炎性反应[J].神经损伤功能重建,2023,(8):441-445 |
| 薯蓣皂苷调控MAPK信号通路减轻小鼠创伤性脑损伤后小胶质细胞介导的炎性反应 |
| Dioscin Alleviates Microglia Mediated Inflammatory Response Following Traumatic Brain In⁃jury through MAPK Signaling |
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| DOI： |
| 中文关键词: 薯蓣皂苷 创伤性脑损伤 小胶质细胞神经炎性 MAPK信号通路 |
| 英文关键词: dioscin traumatic brain injury microglia inflammation MAPK pathway |
| 基金项目: |
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| 中文摘要: |
| 目的：采用体内与体外创伤性脑损伤（traumatic brain injury，TBI）模型评估薯蓣皂苷对TBI后小胶质
细胞表型转化、炎性反应及MAPK信号通路的调控作用。方法：SPF级C57BL/6小鼠随机分为对照组、创伤
组和薯蓣皂苷组，每组15只。利用Feeney氏自由落体法建立体内TBI模型、采用原代小胶质细胞划痕实验
建立体外TBI模型。造模后24 h采用检测脑水肿和NSS评分评估对神经功能影响；采用尼氏染色检测神经
细胞损伤水平；免疫荧光染色评估小胶质细胞活化及表型转化水平；q-PCR检测促炎因子白介素-1β（interleukin-1β，IL-1β）、白介素-6（interleukin-6，IL-6）及肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）的基因转
录水平；采用蛋白质免疫印迹法评估MAPK信号通路相关蛋白ERK1/2、JNK、p38及其磷酸化相关蛋白的
表达。结果：体内外模型中结果显示，薯蓣皂苷显著改善TBI后神经功能损害，降低神经细胞损伤比例，小
胶质细胞活化程度及表型转化（P＜0.05）；降低促炎介质IL-1β、IL-6及TNF-α的基因转录水平（P＜0.05）；抑
制MAPK信号通路相关蛋白的磷酸化水平（P＜0.05）。结论：薯蓣皂苷预处理抑制TBI后神经炎性反应及
小胶质细胞活化，可能与抑制MAPK信号通路活化有关，具有神经保护作用。 |
| 英文摘要: |
| Our work was attempted to evaluate the effect of dioscin on brain injury following traumatic brain injury (TBI) and explore its mechanism. Methods: TBI model was constructed in C57BL/6 mice
by Feeney’s free-falling method in vivo and in primary cortical neurons by wound scratch assay in vitro. Then,
TBI model was treated with dioscin in vivo and in vitro. Cerebral edema and Neurologic severity score (NSS)
were evaluated in mice 24 h post TBI construction. The nerve cell injury was assessed by Nissl staining, and the
microglia activation and phenotypic transformation were analyzed by immunofluorescence staining. The expression levels of proinflammatory factors (IL-1β, IL-6 and TNF-α) were measured by RT-qPCR assay and MAPK
pathway related proteins (p-ERK1/2, p-P38 and p-JNK) were observed by western blot. Results: Dioscin significantly attenuated TBI induced cerebral edema, neurological dysfunctions and microglia mediated inflammation,
reflected by reduced brain water content, NSS score, M1 microglia percentage and proinflammatory factors expression (all P<0.05). The levels of phosphorylated ERK1/2, P38 and JNK were obviously declined in TBI mice
after treated with dioscin (P<0.05). Conclusion: Dioscin elicited neuroprotective effect against TBI induced injury through MAPK pathway. |
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