| 7-羟乙基白杨素对高原脑水肿的作用机制初探 |
| 投稿时间：2022-05-23 修订日期：2022-08-25 点此下载全文 |
| 引用本文：石志群,高迎春,张冬梅,陈克明,景临林,马慧萍.7-羟乙基白杨素对高原脑水肿的作用机制初探[J].药学实践杂志,2022,40(5):399~402,415 |
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| 基金项目:国家自然科学基金(81571847)；军队后勤科研计划面上项目(CWH17J010)；军队卫勤保障保障能力创新与生成专项计划(21WQ045). |
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| 中文摘要:目的 研究7-羟乙基白杨素（7-HEC）对高原脑水肿（HACE）的可能作用机制。方法 建立大鼠高原脑水肿模型，测定大鼠脑组织中超氧化物歧化酶（SOD）的活性及丙二醛（MDA）的含量，采用蛋白质印迹法检测细胞凋亡、周期及自噬相关蛋白的表达水平，探究7-HEC对高原脑水肿的保护作用及其机制。结果 与对照组相比，缺氧模型组大鼠脑组织中MDA含量显著上调，SOD活力显著下调，周期蛋白CyclinD1、CyclinE1、CDK6、CDK2，凋亡蛋白Bcl-2、PARP，自噬蛋白LC3-B相对表达下调，凋亡蛋白Bax，自噬蛋白P62的相对表达上调，差异均具有统计学意义（P<0.05）；与缺氧模型组相比，7-HEC给药组MDA含量下调，SOD活力显著上调，周期蛋白CyclinD1、CyclinE1、CDK6、CDK2，凋亡蛋白Bcl-2、PARP，自噬蛋白LC3-B的相对表达上调，凋亡蛋白Bax，自噬蛋白P62的相对表达下调，差异均具有统计学意义（P<0.05）。结论 7-HEC对高原脑水肿具有一定的保护作用，其机制可能与调控细胞周期、自噬、凋亡以及氧化应激等通路有关。 |
| 中文关键词:高原脑水肿 氧化应激 凋亡 周期 自噬 |
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| A preliminary study on the mechanism of 7-HEC on high altitude cerebral edema |
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| Abstract:Objective To study the possible mechanism of 7-hydroxyethyl chrysin (7-HEC) on high altitude cerebral edema (HACE). Methods A rat model of high altitude cerebral edema was established. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in rat brain tissues were measured. The expression levels of apoptosis, cell cycle and autophagy related proteins were detected by Western blotting to explore the protective effect of 7-HEC on high altitude cerebral edema and its mechanism. Results Compared with the control group, the content of MDA in the brain tissue of the hypoxia model group was significantly up-regulated; the activity of SOD was significantly down-regulated, the relative expression of CyclinD1, CyclinE1, CDK6 and CDK2, apoptotic proteins Bcl-2, PARP, and autophagy protein LC3-B were down-regulated; and the relative expression of apoptotic protein Bax and autophagy protein P62 were up-regulated; the difference was statistically significant (P<0.05); Compared with the hypoxia model group, the content of MDA was down-regulated and the activity of SOD was significantly up-regulated in the 7-HEC administration group. The relative expression of CyclinD1, CyclinE1, CDK6, CDK2, apoptotic proteins Bcl-2, PARP, autophagy protein LC3-B was up-regulated and the relative expression of apoptotic proteins Bax and the relative expression of autophagy protein P62 was down-regulated in the 7-HEC administration group. The difference was statistically significant (P<0.05). Conclusion 7-HEC has a certain protective effect on high altitude cerebral edema, and its mechanism may be related to the regulation of cell cycle, autophagy, apoptosis and oxidative stress pathways. |
| keywords:high altitude cerebral edema oxidative stress apoptosis cycle autophagy |
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