| 魏毅君,张荣军,罗文颖,杨晓亮,李孝伟,唐 政,王晓峰.补骨脂酚通过抑制凋亡、氧化应激和炎症反应缓解小鼠脓毒症脑病[J].,2018,(20):3840-3844 |
| 补骨脂酚通过抑制凋亡、氧化应激和炎症反应缓解小鼠脓毒症脑病 |
| Bakuchiol Alleviates Septic Encephalopathy in Mice via Attenuating Apoptosis, Oxidative Stress and Inflammation |
| 投稿时间：2018-02-28 修订日期：2018-03-26 |
| DOI：10.13241/j.cnki.pmb.2018.20.008 |
| 中文关键词: 补骨脂酚 脓毒症脑病 盲肠结扎穿孔 凋亡 氧化应激 炎症 |
| 英文关键词: Bakuchiol Septic encephalopathy Cecal ligation and puncture Apoptosis Oxidative stress Inflammation |
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| 中文摘要: |
| 摘要 目的：探究补骨脂酚能否抵抗小鼠脓毒症脑病。方法：通过小鼠盲肠结扎穿孔法建立脓毒症脑损伤模型。盲肠结扎穿孔后通过腹腔注射补骨脂酚（10 mg/kg）。小鼠随机分为以下4组：假手术（Sham）组；单纯补骨脂酚处理（BAK）组；盲肠结扎穿孔（CLP）组；盲肠结扎穿孔+补骨脂酚处理（CLP+BAK）组。盲肠结扎穿孔48小时后检测脑组织水含量、血脑屏障通透性、凋亡率、IL-1β与TNF-α表达量、MDA含量、SOD与CAT活性。结果：与Sham组相比，CLP组小鼠脑组织水含量（增加21.20%）、脑组织Evans蓝含量（增加237.05%）、凋亡率、MDA含量、IL-1β与TNF-α表达量均明显增高，而SOD与CAT活性明显降低（P < 0.05）。与CLP组相比，补骨脂酚处理可明显降低脑组织水含量（下降10.94%）、Evans蓝含量（下降39.40%）、凋亡率、MDA含量、IL-1β与TNF-α表达量，而增加SOD与CAT活性（P < 0.05）。结论：补骨脂酚通过抑制凋亡、氧化应激和炎症反应，最终减轻脓毒症脑损伤。 |
| 英文摘要: |
| ABSTRACT Objective: To elucidate whether bakuchiol (BAK) could protect against septic encephalopathy in adult mice. Methods: In this study, cecal ligation and puncture (CLP) was introduced to establish the septic encephalopathy mouse model. BAK (10 mg/kg) was intraperitoneally administrated following CLP. The mice were randomly divided into four groups: Sham group, BAK group, CLP group and CLP+BAK group. The brain water content, blood-brain barrier permeability, apoptotic ratio, IL-1β and TNF-α expression, MDA content, SOD activity and CAT activity in each group were measured. Results: Compared with the Sham group, the brain water content (increased by 21.20%), Evans blue content (increased by 237.05%), apoptotic ratio, MDA content, and IL-1β and TNF-α expression were significantly increased, while the activities of SOD and CAT were significantly decreased in the CLP group (P < 0.05). Compared with the CLP group, BAK treatment significantly decreased the brain water content (decreased by 10.94%), Evans blue content (decreased by 39.40%), apoptotic ratio, MDA content, and IL-1β and TNF-α expression, and increased the activities of SOD and CAT (P < 0.05). Conclusion: BAK ameliorates septic encephalopathy mainly through inhibiting apoptosis, oxidative stress and inflammation. |
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