| 引用本文: | 景临林,杨颖,邵瑾,赵彤,马慧萍,贾正平.7-羟乙基白杨素对低压低氧致脑组织损伤的保护作用[J].中国现代应用药学,2020,37(9):1025-1029. |
| JING Linlin,YANG Ying,SHAO Jin,ZHAO Tong,MA Huiping,JIA Zhengping.Protective Effect of 7-HEC on Brain Tissue Damage Induced by Hypobaric Hypoxia[J].Chin J Mod Appl Pharm(中国现代应用药学),2020,37(9):1025-1029. |
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| 摘要: |
| 目的 研究7-羟乙基白杨素（7-HEC）对低压低氧诱导大鼠脑组织损伤的保护作用。方法 将52只健康♂ Wistar大鼠随机分为正常组、模型组、乙酰唑胺组、7-HEC组，每组13只。连续灌胃给药5 d，末次给药后，除正常组，将其余3组置于低压低氧动物实验舱，升至8 000 m海拔缺氧处理24 h。HE染色观察脑组织病理改变，酶标法检测脑组织中过氧化氢（H2O2）和丙二醛（MDA）水平，以及超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）和ATP酶的活力；Western blotting检测蛋白B细胞淋巴瘤-2（Bcl-2）、Bcl-2相关X蛋白抗体（Bax）及半胱氨酸天冬氨酸特异性蛋白酶3（caspase-3）的表达。结果 与正常组相比，低压低氧导致大鼠脑组织出现明显损伤，H2O2和MDA水平显著升高，抗氧化酶SOD、CAT和GSH-Px以及Na+-K+-ATPase和Ca2+-Mg2+-ATPase的活力显著降低。7-HEC预处理能够逆转这些变化。此外，低压低氧能够显著升高脑组织中促凋亡蛋白Bax和cleaved caspase-3表达，降低抗凋亡蛋白Bcl-2的表达，而7-HEC能够下调Bax和cleaved caspase-3表达，上调Bcl-2的表达。结论 7-HEC对低压低氧致脑组织损伤具有明显的保护作用，其作用机制可能与其缓解氧化应激，抑制细胞凋亡，改善能量代谢有关。 |
| 关键词: 7-羟乙基白杨素 低压低氧 脑损伤 氧化应激 凋亡 |
| DOI：10.13748/j.cnki.issn1007-7693.2020.09.001 |
| 分类号:R965.1 |
| 基金项目:国家自然科学基金项目（81872796，81202458，81571847）；甘肃省自然科学基金（18JR3RA408，1308RJYA061，145RJZA089）；中国博士后科学基金（2012M521926）；军队后勤科研计划（CWH17J010） |
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| Protective Effect of 7-HEC on Brain Tissue Damage Induced by Hypobaric Hypoxia |
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JING Linlin, YANG Ying, SHAO Jin, ZHAO Tong, MA Huiping, JIA Zhengping
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Department of Pharmacy, the 940thHospital of Joint Logistics Support Force of CPLA, the Lab of PLA for High Altitude Medicine, Lanzhou 730050, China
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| Abstract: |
| OBJECTIVE To investigate the protective effect of 7-HEC against hypobaric hypoxia(HH) induced brain injury in rats. METHODS Fifty two ♂ Wistar rats were divided in to normal group, model group, acetazolamide group and 7-HEC group, 13 rats per group. The drugs were intragastrically administrated for 5 consecutive days, except normal group, the rats in other three groups were transferred to 8 000 m in a HH chamber for 24 h after the final administrated. The brain histomorphology of rats were detected by HE staining. Hydrogen peroxide(H2O2), malondialdehyde(MDA), superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase(GSH-Px) and ATPase were evaluated using related Kits. The expression of Bcl-2, Bax and cleaved caspase-3 were assessed with Western blotting. RESULTS Compared to normal group, HH induced brain damage as evidenced by the increased level of H2O2 and MDA and the decreased of the activity of antioxidant enzyme including SOD, CAT and GSH-Px as well as Na+-K+-ATPase, Ca2+-Mg2+-ATPase. Pretreatment with 7-HEC could reverse these changes. Moreover, 7-HEC could inhibit the apoptosis induced by HH via up-regulating the expression of Bax and caspase-3 and down-regulating the expression of Bcl-2. CONCLUSION 7-HEC can suppress the HH-induced brain damage in rats by alleviating oxidative stress, inhibiting apoptosis and improving energy metabolism. |
| Key words: 7-HEC hypobaric hypoxia brain damage oxidant stress apoptosis |
