[Effects of Butylphthalide on the expressions of HMGB1 and RAGE in frontal lobe of rats after chronic sleep deprivation].

Ying-Xia Yang, Yu-Fen Guo, Hong-Hong Huang, Ling-Xing Wang
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Abstract

Objective: To investigate the effects of Butylphthalide on the expressions of HMGB1 and RAGE in frontal lobe of rats after chronic sleep deprivation.

Methods: Chronic sleep deprivation and butylphthalide treatment was performed in Sprague Dawley(SD)rats and the rats were divided into three groups (n=6): platform control group, chronic sleep deprivation group and chronic sleep deprivation + butylphthalide intervention group. Rats suffering chronic sleep deprivation were put in multiple platforms box for 18 h per day and sleep deprivation lasted for 28 days. Rats in butylphthalide intervention group were intraperitoneally injected with butylphthalide 100 mg/(kg·d) for 14 days after sleep deprivation. After collecting brains, high-mobility group box (HMGB1) and nuclear transcription factor kappB (NF-κB)p65 were detected by immunohistochemistry. The expression of HMGB1, silent information regulator of transcription 1 (SIRT1), receptor for advanced glycation end-products (RAGE) and NF-κB in frontal lobe were determinated by Western blot.

Results: Compared with platform control group, the expression levels of HMGB1, RAGE and nuclear NF-κB p65 were increased significantly, while the expression of SIRT1 was decreased siginificantly in frontal lobe of chronic sleep deprivation group (all P<0.05). Compared with chronic sleep deprivation group, the expression levels of of HMGB1, RAGE and nuclear NF-κB p65 were decreased significantly, while the expression of SIRT1 was increased significantly in chronic sleep deprivation + butylphthalide intervention group (all P<0.05).

Conclusion: Butylphthalide can inhibit HMGB1/RAGE/NF-κB pathway in frontal lobe of rats after chronic sleep deprivation by changing the expression of HMGB1 and RAGE, and reducing the nuclear translocation of NF-κBp65.

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[丁苯酞对慢性睡眠剥夺大鼠额叶HMGB1和RAGE表达的影响]
目的:探讨丁苯酞对慢性睡眠剥夺大鼠额叶HMGB1和RAGE表达的影响。方法:对SD大鼠进行慢性睡眠剥夺和丁苯酞治疗,将大鼠分为平台对照组、慢性睡眠剥夺组和慢性睡眠剥夺+丁苯酞干预组3组(n=6)。将慢性睡眠剥夺大鼠置于多平台箱中,每天18小时,持续28天。丁苯酞干预组大鼠在剥夺睡眠后腹腔注射丁苯酞100 mg/(kg·d),持续14 d。采集脑组织后,免疫组化检测高迁移率组盒(HMGB1)和核转录因子kappB (NF-κB)p65。Western blot检测脑额叶HMGB1、转录沉默信息调节因子1 (SIRT1)、晚期糖基化终产物受体(RAGE)和NF-κB的表达。结果:与平台对照组比较,慢性睡眠剥夺组脑额叶HMGB1、RAGE、核NF-κB p65表达水平显著升高,SIRT1表达水平显著降低(均P<0.05)。与慢性睡眠剥夺组比较,慢性睡眠剥夺+丁苯酞干预组HMGB1、RAGE、核NF-κB p65表达水平显著降低,SIRT1表达水平显著升高(均P<0.05)。结论:丁苯酞可通过改变HMGB1和RAGE的表达,减少NF-κBp65的核易位,从而抑制慢性睡眠剥夺大鼠额叶HMGB1/RAGE/NF-κB通路。
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53
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