| 魏明豪,曹屹东,贾 栋,陈 宁,张 亮.和厚朴酚通过激活SIRT1/FOXO1信号通路抵抗小鼠脓毒症脑损伤[J].现代生物医学进展英文版,2019,19(10):1840-1844. |
| 和厚朴酚通过激活SIRT1/FOXO1信号通路抵抗小鼠脓毒症脑损伤 |
| Honokiol Alleviates Brain Injury in Septic Mice through Activating SIRT1/FOXO1 Signaling |
| Received:December 23, 2018 Revised:January 20, 2019 |
| DOI：10.13241/j.cnki.pmb.2019.10.008 |
| 中文关键词: 和厚朴酚 脓毒症脑损伤 凋亡 炎症 SIRT1 |
| 英文关键词: Honokiol Septic encephalopathy Apoptosis Inflammation SIRT1 |
| 基金项目:国家自然科学基金项目（81701251） |
| Author Name | Affiliation | E-mail | | WEI Ming-hao | Department of Neurosurgery, Tangdu Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710000, China | 13991810596@139.com | | CAO Yi-dong | Department of Neurosurgery, Tangdu Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710000, China | | | JIA Dong | Department of Neurosurgery, Tangdu Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710000, China | | | CHEN Ning | Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China | | | ZHANG Liang | Department of Neurosurgery, Tangdu Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710000, China | |
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| 中文摘要: |
| 摘要 目的：探究和厚朴酚是否通过激活SIRT1/FOXO1信号通路抵抗小鼠脓毒症脑损伤。方法：通过C57BL/6小鼠盲肠结扎穿孔法建立脓毒症脑损伤模型。小鼠随机分为以下6组：假手术（Sham）组；和厚朴酚处理（HKL）组；盲肠结扎穿孔（CLP）组；盲肠结扎穿孔+和厚朴酚处理（CLP+HKL）组；EX527（SIRT1特异性抑制剂）预处理+盲肠结扎穿孔+和厚朴酚处理（CLP+HKL+EX527）组；EX527预处理+盲肠结扎穿孔（CLP+EX527）组。盲肠结扎穿孔48 h后检测脑组织内水含量、凋亡率及凋亡相关蛋白Bax、Bcl-2和cleaved Caspase-3的表达情况、炎症相关分子IL-1β与TNF-α、SIRT1信号通路相关蛋白表达情况。结果：与CLP组相比，CLP+HKL组脑组织内SIRT1的表达量及活性、Bcl-2表达量明显增加，而脑组织水含量、凋亡率、Bax、cleaved Caspase-3、IL-1β与TNF-α的表达量明显降低（均P < 0.05）。EX527可明显抑制HKL的上述脑保护作用（P < 0.05）。结论：和厚朴酚主要通过激活SIRT1/FOXO1信号通路，抑制凋亡与炎症，从而缓解脓毒症脑损伤。 |
| 英文摘要: |
| ABSTRACT Objective: To elucidate the definite role of silent information regulator 1 (SIRT1)/Forkhead box protein O1 (FOXO1) signaling pathway in the protective effects of honokiol (HKL) against brain injury in septic mice. Methods: Adult C57BL/6 mice were subjected to cecal ligation and puncture (CLP) to induce sepsis-associated encephalopathy. The mice were randomly divided into six groups: Sham group, HKL group, CLP group, CLP+HKL group, CLP+HKL+EX527 (a selective SIRT1 inhibitor) group and CLP+EX527 group. Forty-eight hours after the surgery, the brain water content, apoptotic ratio and the expression levels of SIRT1, Ac-FOXO1, Bax, Bcl-2, cleaved Caspase-3, IL-1β and TNF-α in each group were measured. Results: Compared with the CLP group, HKL significantly increased the expression level and the deacetylase activity of SIRT1 and the expression level of Bcl-2. HKL reduced brain water content, apoptotic ratio and the expression levels of Bax, cleaved Caspase-3, IL-1β and TNF-α when compared with the CLP group. However, these cerebral-protective effects of honokiol were largely abolished by EX527. Conclusion: HKL attenuates sepsis-associated encephalopathy by reducing apoptosis and inflammation through the activation of SIRT1/FOXO1 signaling pathway. |
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